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THE UNIVERSITY 
 OF ILLINOIS 
 
 LIBRARY 
 616.12 
 
 Cit 
 
Return this book on or before the 
 Latest Date stamped below. A 
 charge is made on all overdue 
 books. 
 
 U. of I. Library 
 
FACTS 
 
 On 
 
 fel rE A. Re P 
 
 By 
 RICHARD C. CABOT, M.D. 
 
 Professor of Medicine and of Social Ethics 
 at Harvard University 
 
 ILLUSTRATED 
 
 PHILADELPHIA AND LONDON 
 
 W. B. SAUNDERS COMPANY 
 1926 
 
Copyright, 1926, by W. B. Saunders Company 
 
 MADE IN Use Se Ae 
 
 PRESS OF 
 We Be SAUNDERS COMPANY 
 PHILADELPHIA 
 
ee 
 
 x 
 aN 
 
 taka tal a a. 
 6IGSE 
 eee + 
 eet ee Ol 
 
 PREFACE 
 
 I cannot too strongly insist that a large part of this book 
 represents not my work but that of others. The necropsies and 
 
 )necropsy records of the 1906 cases on which my conclusions rest, are 
 
 the work of Drs. James H. Wright and Oscar Richardson. A good 
 many of these necropsies I have witnessed. AI of their protocols I 
 have studied in whole or in part. But my task has been merely to 
 
 collect, arrange, and at times to interpret the results of these pathol- 
 
 ogists’ labors so far as they relate to cardiovascular disease. JI have 
 made no attempt to decide for myself any question of gross or micro- 
 scopic pathology but have gratefully accepted and tried to utilize 
 the decisions of those who did the work. 
 
 On the clinical side I have studied and have had abstracted the 
 ward records of 1906 cases decisively diagnosed post-mortem. 
 Starting from the post-mortem diagnoses I have worked back into the 
 clinical records corresponding. A good many of these clinical records 
 depict the sufferings of patients who were under my charge in the 
 wards and in a fair number I wrote the record of the cardiovascular 
 examination and clearly recall the patients. In the great majority of 
 instances however, the patients were cared for by other members of 
 our staff and I am confined to a study and interpretation of other 
 men’s work. Iam indebted to Drs. Paul D. White, Hugh Cabot, 
 Edward L. Young Jr., William H. Smith, William D. Smith and 
 Maurice Fremont-Smith for some of the printed discussion of cases. 
 
 In abstracting the clinical and pathological records many have 
 assisted me. Dr. Harry Taylor, now in China, Dr. J. H. Newburgh 
 of Ann Arbor, Michigan, Dr. Byron C. Darling of New York, Dr. 
 Mary W. Lawson of New London, Conn., Dr. James H. Young, 
 Dr. E. H. Heath and Dr. W. R. Redden of Boston, Mr. John M. 
 Porter of the Harvard Medical School and, above all, my secretaries, 
 Miss Alice G. O’Gorman and Miss Florence Painter, have gathered 
 
 and arranged material for me. 
 
 My own task has been to put ane and edit this material, 
 since no one else appeared anxious to undertake so prosaic and 
 time-consuming a task. 
 
 9 
 
 614079 
 
IO PREFACE 
 
 I appreciate clearly that the data here gathered together would 
 have been far more valuable in many ways had they represented 
 throughout the observations of one man. But had this been so, one 
 set of preconceptions and leading ideas would have guided and per- 
 haps to some extent marred the observations. There is some advan- 
 tage as well as a considerable disadvantage in the fact that most of 
 the observations on which I rest were made without any idea of the 
 use to which they might later be put. 
 
 To all of those whose names are mentioned above, as well as to the 
 staff of the Massachusetts General Hospital, I acknowledge my 
 gratitude and indebtedness. I trust that this book may to some 
 extent carry out their interests as well as mine. 
 
 Especially to Dr. Oscar Richardson I am indebted, not only as 
 one of those by whose daily labors I have profited, but for the time and 
 pains he has taken in re-reading and interpreting pathological records 
 and sometimes in re-examining old specimens to clinch or expunge a 
 diagnosis. 
 
 The book differs from all those previously written on heart disease 
 (so far as I know) in basing its conclusion wholly on the study of 
 cases which came in the end to necropsy. The chapter on syphilitic 
 aortitis, for example, was written by abstracting all the necropsies 
 from 1897 to 1919 in which this lesion occurred and then finding what 
 was recorded and remembered about them on the clinical side. 
 
 It is true that the pathologist may have overlooked something 
 or mistakenly identified some lesion. But considering the care with 
 which the necropsies were made and the systematic and detailed 
 records that were dictated from them at the time, I believe the 
 percentage of error is small. 
 
 If anyone reads and compares the statistical tables, he may be 
 puzzled to see that the total number of cases of a particular disease 
 as given in the early tables differs from the same total given in 
 later tables. This is due to the incompleteness of our records. In 
 relation to age and sex, for instance, we may be able to prepare a 
 table based on complete data from 1oo% of the necropsies of that 
 disease. Yet in relation to the examination of the heart we may 
 be able to study only 75% of these. Hence the totals of the latter 
 table will be smaller. 
 
 Obviously there is very little about treatment in these pages. 
 Most of the little that I know on that subject is to be found in the 
 records or discussions of some of the illustrative cases. 
 
PREFACE 1 a 
 
 Very few people should even try to read the whole of this book. 
 
 I should advise most readers to read the opening and the closing 
 
 chapters, and the summaries at the end of each section, and then 
 
 to look over as many of the illustrative cases as seem interesting. 
 RICHARD C. CABOT. 
 
 CAMBRIDGE, MaAss., 
 February, 1926. 
 
CONTENTS 
 
 CHAPTER I 
 PAGE 
 REVIEW OF 4143 LESIONS IN 1906 CASES OF CARDIAC DISEASE. TABLES OF 
 PREQUENCY:./§. .. 17 
 I. In Examining a Patient enced to trays Heart Disense What are the 
 Diagnostic Expectations Which Experience Justifies?. . . . .... #17 
 dieeeiew a terial rere ptudietiawt aie uu ei ero ae ee AY be ARE, fh o9 
 III. Manifest Cardiovascular Lesions. . . . i ORS Ree 
 IV. Relative Frequency of the Different Garlioumentrs Tesncs eee 26 
 V. Variations of Necropsy Diagnoses at Different Periods. ....... 28 
 CHAPTER II 
 RUSUMATICE HEART DISEASE. “KATA CHOREA.. 8 oie si, le es ep gO 
 PERIL ENOSS cr UTS ANG COMPUCOLCUC UO On htc te bs (eee Rane wes, eels. 3a 
 IML ieay dave: eSIONG oy Nag nen Ai carton sone ys Pa og’ te ae OIAR 
 EEC AImari CAOLLIC LCN Osia man ee aoe tel Strat dr Mee ie ae Soe ue My TAL 
 iopremecmbinediLesiOnsmeren a etka ean ek el oe Te, peg 
 Aortic Stenosis and Remeeention: eRe cat mis Ts encase Nighy ica ta a aOS 
 Pure Aorticukeguroitationiwithout stenosis tc. ei eee 3. B52 
 WittrAleheQrvilation we mes ee ee ah Ae aa we ot Pe eee) oe 280 
 SERRE ORGA ci, 7, os, 1 age mem gan eli oe Need wb eae We ok an ae chee AGES 
 CHAPTER III 
 SECRET TIGR LLEART  IISEASE tent i ILS EN Sel Se cad RNID Maa.) 322 
 Sypnilizic: Aortitis.- .-2 . us ORE autee >. ht ida eos a cee: Ame 322 
 Diagnosis of the Disease in Life. . .. . Ste Ween ee Reber meee uk hae: 26 
 Cardiac Hypertrophy in Syphilitic ernie: TAR Me eae) at) Cate’ 330 
 General Cardiac Symptoms of Dac AOTUUSH en Attn) oR Lame 331 
 Cause of Death. .... 1 SOR OE WO CN OPER S Sea ane FE 
 Special Symptoms of ears ROR, Fe rn ew nan Mae Vi awe keno gin® 333 
 Dee MACTOSISUOr AN CULISMat, siemtr nme de Nc clea tot let kein wee te 3A 
 Serv aaculats Om PuCALIONS tamminnr se hen ho bourne) ay Sealy as. 5) 330 
 SOOT SHI GaN (Ste FY Ok: OA a ME A el ena LE Mey Ue. singe) ek w Ae uk 3390 
 DDG k Meek el ee cee ne EE le | ety (av faa, ws 402 
 Dissecting nen rar El ee eh FASS Pe oh a) Se Nice al ste. 4 E2 
 Septic or Mycotic Aneurism ....... ea Re Sheer AL2 
 CHAPTER IV 
 HYPERTENSIVE HEART DISEASE ..... hi PETE Tey 7028 Uae AUG ae eee Tey bo) 
 I. Definition. . . . Pe meaner eee mee ive Pee, ATO 
 II. Hypertensive (urdinacniar aban Ce a nate’. ae ALO 
 III. Latent vs. Manifest Cases of Hypertensive Heart Tee ae ar Pie: ees ASO 
 TV The Etiology.of Cardiac Enlargementio0) eo. ie he whe) s 42T 
 
 13 
 
14 
 
 CONTENTS 
 
 PAGE 
 
 . Hypertrophied and Dilated Heaits Occurring in Young Persons 
 
 Without Nephritis or Arteriosclerosis . . 428 
 
 VI. The Largest Hearts. . 429 
 
 VII. Degrees of Cardiac Fe entrnts in ipiffereat Lesions. 5 Age 
 
 VIII. Cardiac Failure in Hypertrophy and Dilatation... .. ? nea 
 
 EX. Physical Signgy eee eer : . 444 
 
 X. Blood-pressure and other Data in Ween ; . 445 
 
 XT. Diagnosis Actually made in these Cases. . Re 
 
 XII. Summary and Conclusions. » 452 
 
 GHAPTER®: V 
 
 MYOCARDITIS 340) eae ey wae Salted tla cian . 404 
 
 I. Chronic Fibrous Manet Ge ER A AS - 404 
 
 Il; Myocardial Iniarction.y-e) 14. pasta 
 
 IH. Myocardial Abscess. . .~. . . mA: 
 
 IV. Cardiac Aneurism . s yet 
 
 V. Rupture of the Heart. . 546 
 CHAPTER VI 
 
 ANGINA PECTORIS . ; . 548 
 
 Angina and Myocarditis, Son 
 
 Blood-pressure and Angina. ...... Ree 
 
 The Cessation of Angina with the Advent of General Paachte Contestina 5g Rae 
 
 Coronary Thrombosis and Acute Blocking of the Coronary. ....... Son 
 CHAPTER VII 
 
 ACUTE AND SUBACUTE ENDOCARDITIS. ... . Star 
 
 Definition and Terminology . YomenOr Dy. PBOx 
 
 Types of Acute and Subacute Madecarditis Fein, ol: it S568 
 
 Age and Sex. ED ee eI I Oh gts og . 563 
 
 Valve Affected. : . 564 
 
 Nature of the Inflammatory Pieces ; . 566 
 
 Clinical Manifestations . . . . ye. 
 
 Symptoms on the Part of the crcnltion ie Sa 
 
 Weight of HeartataNecropsy sy 9.9: 7am, <> . 578 
 
 Bacteriology. , S878 
 
 Associated Lesions . . . ay A, 
 
 Duration . 2 Sex 
 
 Summaryos. 2 tees . 582 
 CHAPTER VIII 
 
 CHRONIC NON-DEFORMING VALVULAR SCLEROSIS OR ENDOCARDITIS . . 628 
 
 Euology. 92 ie . 629 
 
 Conclusions . . . . 634 
 CHAPTER IX 
 
 ACUTE. PERICARDITIS): Ss 4a4t Sc Oss 
 
 Age and Sex. = 035 
 
 Associated Lesions . . . . 636 
 
CONTENTS 
 
 Fever and Leucocytosis . 
 
 Diagnosis . 
 
 Septic Heart F milurs iad Diopey UGpronie Hanctee Convention) 
 Acute or Chronic Passive Congestion . . . 
 
 Pericardial Effusion 
 
 Bacteriology. 
 
 Murmurs in Acute Berea ME eh ering 
 Cardiac Hypertrophy in Acute Beprerditie SF Re 
 Summary . 
 
 CHAPTER X 
 
 CHRONIC PERICARDITIS . . EEPyatre 
 Chronic Vestigial Becodiie Sore ha eee 
 Primary Rheumatic Group. .... . 
 Secondary Rheumatic Group. 
 
 “Age and Sex. 
 Diagnosis . 
 Diagnostic ierpiote 
 
 CHAPTER XE 
 
 THYROCARDIAC DISEASE. é See; 
 I. The Over- ationstte Heat ce ae, 
 II. Early Congestive Heart Failure in Miro Disease! 
 lil. Toxic Death. 
 
 IV. Late Congestive Failure in Pitas. insane ond Teophttahnic Gotan 
 
 CHAPTER XII 
 
 GONGENITAL- HEART DISEASE |. 3 >? 
 
 DUMMABY OF THE BOOKS isha. caer: 
 I. As Regards Heart Disease as a euhole. 
 II. As Regards Rheumatic Valvular Disease . 
 III. Aortic Stenosis. 
 IV. Syphilitic Heart Die 
 V. Hypertensive Heart Disease. 
 VI. Myocarditis . 5. Pea ae 
 VII. Acute and Subacute Bndoetniie Smee S eae soe 
 VIII. Acute Pericarditis . 
 IX. Chronic Pericarditis. 
 X. Thyrocardiac Disease. 
 XI. Angina Pectoris and Cardiac Tntarcts 
 
 T5 
 
 PAGE 
 
 . 636 
 7,020 
 . 037 
 . 638 
 . 638 
 . 640 
 . 640 
 . 643 
 a .OA5 
 
ae ae 
 
 ‘aay, | 
 
FACTS ON THE HEART 
 
 CHAPDER SL 
 
 REVIEW OF 4143 LESIONS IN 1906 CASES OF CARDIAC 
 DISEASE. TABLES OF FREQUENCY 
 
 I, IN EXAMINING A PATIENT SUPPOSED TO HAVE HEART DISEASE, WHAT 
 ARE THE DIAGNOSTIC EXPECTATIONS WHICH EXPERIENCE JUSTIFIES? 
 
 The first point on which this book hopes to shed light is this: 
 when a physician is called to attend a patient who seems to be suffer- 
 ing from cardiovascular disease, what are the important probabilities 
 and the more remote possibilities which he should consider? If we 
 have some basic knowledge about what is rare and what is common, 
 it may give us valuable clues. 
 
 The first and in some ways the most important point of all is to 
 know that 
 
 Most “Heart Disease” is imaginary. 
 
 Those who think or fear that they have heart disease usually turn out 
 on careful examination to be free from it. Nearly 10% of Harvard 
 freshmen in one of the classes examined by Dr. Roger I. Lee and his 
 assistants believed themselves to have a ‘‘weak heart” orsome more 
 definite heart disease. 14 out of 18 successive patients sent to me by 
 their physicians quite recently for supposed heart disease, had, in my 
 opinion, perfectly sound hearts. The patient with ‘‘effort syndrome,”’ 
 complaining of his dyspnea, cardiac pain and palpitation, yet with 
 a normal heart, is not the commonest type. More often it is a 
 patient who has fainted or been dizzy or had a little precordial pain 
 and whose physician has heard a (quite harmless) systolic murmur 
 somewhere in the precordia. 
 
 That such cases are more numerous than those with organic 
 heart disease is difficult to prove, though strongly suggested by the 
 experience of anyone who has examined many college students and 
 middle-aged women. But whether or not this pseudo-heart disease, 
 this groundless fear of heart disease, is as common as I believe it to be, | 
 it is certainly common enough to make the thought of it an essential 
 
 2 17 
 
18 FACTS ON THE HEART 
 
 part of our mental furniture whenever we begin the examination of a 
 supposedly cardiovascular case. For the needless sufferings and 
 sacrifices of such patients are often very great. To my knowledge 
 boys have given up their chosen life work, girls their prospect of 
 marriage, business men their favorite projects because of a false. 
 diagnosis of heart disease. The fears, disappointments and ailments 
 resulting from such a diagnosis may be enough to render a person’s 
 life miserable. And all this one can sweep away by a clear and 
 positive reassurance based on a thorough examination.’ I know few 
 greater services that a physician can perform, few that give him 
 livelier satisfaction. 
 
 Narrowing the Field.—Next to this fundamental knowledge of the 
 frequency of supposed but unreal heart disease, one is helped by 
 a narrowing of the field of possibilities. That we do not need any 
 longer to consider and search for fatty degeneration of the heart, 
 fatty overgrowth upon the heart, brown atrophy, myocarditis, the 
 senile heart, etc., simplifies our work and makes us more apt to make 
 a correct diagnosis. 
 
 The Commonest Lesions.—This series of 1906 necropsied cases, 
 (see Table 1) covering all the cardio-vascular material in the 4000 
 necropsies done at the Massachusetts General Hospital between 
 1896 and 1919 is enough, I think, to constitute a fair sample and give a 
 fairly accurate picture of heart disease as one may expect to find it in 
 most parts of the United States. Certain districts where syphilis or 
 endemic goiter are especially prevalent will have a higher incidence of 
 syphilitic or thyrotoxic heart disease, but in most parts of the country 
 the proportion of the different types will be found, I think, to be 
 about the same as in New England.” 
 
 (a) For example our conclusion that 77% of all heart disease 
 is due to simple hypertrophy and dilatation of the heart (or hyper- 
 tensive cardiovascular disease) without valve lesions wil!, I believe, 
 be found to represent approximately the facts in any large series of 
 necropsies made in the United States and Canada. 
 
 Further results of this study are: 
 
 * Of course no comparisons are of value except on the basis of necropsy statistics, 
 which so far as I know do not exist in this country. 
 
SUMMARY OF MATERIAL IQ 
 
 TABLE I1.—SUMMARY OF MATERIAL 
 
 A. Total cardiovascular lesions, 4143 in 1906 persons, (out of 4000 necrop- 
 sied from 1896 to 1919). 
 
 B. All cases showing cardiac hypertrophy and dilatation.............. 1209 cases 
 Adlecasesa without ypertrophoy and dilatation | 3. 5 «<0 ste «cela» sielets 697 cases 
 CLOTS ee me eeveret FO ele, wrt Myoihtu afta MEM Sie, RAS etek ensia a, rl eid ert eaten s euthekere 1906 cases 
 
 { with other lesions 1053 1200 cases 
 . 2 * 
 ie Hvpeciropnyy alld CiUAtatiONi is <a. eves sls el a are | hia Smee cee 
 
 *Referred to in the rest of this table as “H & D.” 
 
 J with H. & D. 668 ro51 cases 
 
 Ta MPATCCTIOSCIELOSIS . cht 1o 8 elas seis vite chsis alee ere/ebe. sistas pwithoutiHee Des 
 
 J with H. & D,.. 93 142 cases 
 
 III(b) Arteriosclerosis with artscl. degen. kidney....... Seer rStt ye ek aiS 
 
 { with H. & D. 275 377 cases 
 
 ote ie . 
 IV. Nephritis,~ acute, subacute and chronic......... ierehoutHe ania ha 
 
 V. Chronic non-deforming endocarditis............. fowith © Tae ab Cabee 
 
 \ without H. & D. 93 
 VieeACute and stipacute endocarditis. sc. a... cis «ch ae es e a 4. 180 cases 
 MEE DSANY Reve IatONS es V%. 6 0. See Mend Sta fia kates oa fe aie Ee : 24 on a nace pone 
 VILL. EWeGnIC PETICATCITIS a. es eae all Ml eee Thee pages fs % at n | A CASES 
 Pe A CUGETIOTICRLCICIS:.. cunts soatibetensaicis wh eteel scssskanehys ee es . ra - 186 cases 
 X. Myocarditis incl. Riccees Cus nntarcta(26)m amen ae, 2 A at A of oe ha 
 Be erittic nortitia vs.) Macatee eck eo oes, ore aka See ae 
 Pali @Perhiqous anemiay.. 12.01 hes. eee Ss eae = Fi as iss go Gases 
 Pay ARSE ae CO dC a cA ie as eG Rata. as 
 Dal Vell VOOpIASLiGNaOrta:. .\. wsaysuletn ool meet eo oe ee ae H.&D. 8 19 cases 
 \ without H. & D. 11 
 eves Golem with cardiac results... /5.5 : wis vas aie sd hiss aa a : A : Bo cases 
 a Vis (Congenital heart disease 55 5.6 os ade ae «oon +0 2 | with eT Ochi ; 10 a 
 PEC RONG RAL MN RICHLS Wee § uM tie ee pee ee eae pk et San oko er eal ahve Rie g 4143 
 
 * Nephritis is here included as a local vascular lesion producing in most cases a cardiac effect 
 through the changes in its glomerular capillaries or in its larger vessels. 
 
 (b) That rheumatic valvular disease is approximately twice as 
 common as all the varieties of syphilitic aortitis combined, or 
 
20 FACTS ON THE HEART 
 
 (c) five times as common as syphilitic valvular disease (aortic 
 regurgitation). 
 
 (d) That mitral stenosis, existing alone or combined with other 
 valve lesions, is about three times as common as all other rheumatic 
 valve lesions combined, 
 
 (e) That mitral stenosis uncomplicated is about twice as common 
 as any other single valve lesion. 
 
 I believe, this picture is what anyone who looks for the facts will 
 find to be true in any part of this country and probably in many parts 
 of the other continents. 
 
 Il. THE MATERIAL HERE STUDIED 
 
 The Probable Error in Table 1.—These figures have been verified 
 and re-verified again and again until they are as nearly correct as I 
 can make them. It is sometimes a matter of judgment, however, 
 whether a slight puckering on a valve shali be considered sufficient to 
 throw it into the group of deforming valvular lesions with a genuine 
 obstruction or leak, or whether it shall be placed with the cases of 
 chronic non-deforming endocarditis. Valve measurements alone do 
 not settle it. A valve may have considerably less than the average 
 circumference (considering the age, development and musculature 
 of the individual) and yet show no deformity and be in fact normal. 
 In another case a valve may have the normal circumference and yet 
 be so rigid and adherent as to be incompetent. Some balancing 
 of conflicting evidence, then, and some chance for error enter these 
 statistics (and all other statistics) not because of inaccurate counting 
 but because the assignment of each case to a particular pile-to-be- 
 counted involves questions of judgment which may be very difficult. 
 Most of them, however, are simple and so the possible error from this 
 source 1s not great. For example: most cases of acute endocarditis 
 are easy to recognize at necropsy. It is only in the occasional case 
 that we are uncertain as to the nature of a few minute tags on a valve. 
 In most cases of syphilitic aortitis the lesions can be readily and 
 positively identified by an experienced pathologist. But in a few 
 cases in every hundred he will remain in some doubt as to the nature 
 of the lesions, since the treponema pallida is not often to be found 
 within the time that can be devoted to the search for it. 
 
 Having myself gone over the evidence on which all these patholog- 
 ical diagnoses were based and having discussed with the pathologist 
 his reasons for the more doubtful divisions, I am confident that the 
 error in any of the figures of this table does not exceed 5%, an error 
 
THE MATERIAL HERE STUDIED 2I 
 
 which will not invalidate any of the conclusions or predictions which 
 are based upon them. 
 
 Comments and Conclusions Drawn from the Whole Material.— 
 (a) Nearly half of all the individuals necropsied at the Massachusetts 
 General Hospital during approximately a quarter of a century had 
 suffered from some cardio-vascular lesion. Some of these lesions are 
 trifling. For example, some of the cases show only arteriosclerosis 
 (slight or considerable) without any cardiac enlargement or other 
 important lesions. Such cases of slight and isolated arteriosclerosis 
 amount to 265 out of our total ros51 cases of arteriosclerosis. So far 
 as we know, these scleroses did no harm to the cardiovascular system 
 and were of no importance to the circulation. Adding to these the 
 71 cases of nephritis without cardiac hypertrophy, pericarditis or 
 other cardiovascular lesion, 39 cases of chronic non-deforming endo- 
 carditis uncomplicated, ro cases of hypoplastic aorta without cardiac 
 enlargement, and 5 other odds and ends, we reach a total of 390 
 cases to be subtracted from the gross total of 1906 in order to ascertain 
 the net total of patients with important cardiovascular lesions; 1516 out 
 of 4000, or 38%. 
 
 It must be further borne in mind, however, that although the 
 cardiovascular lesion was, I believe, a factor in producing death in all 
 these 1516 persons, it was sometimes a minor factor, not the only or 
 the chief one. Some of the 1g cases of acute endocarditis and some 
 of the 12 cases of acute pericarditis without other cardiovascular 
 lesions, (Table 4) were of the terminal type, the main underlying 
 cause of the patient’s illness and death being a cancer or a diabetes. 
 But the above figures show, somewhat to my surprise, that these 
 restrictions apply to but a few per cent of the cases, so that with less 
 than 5% of error, one can say: @ cardiovascular lesion 1s an wmpor- 
 tant factor in 38% of all deaths. 
 
 (b) In 1846 of the persons here studied, there were 4037 cardiovas- 
 cular lesions, or more than 2 apiece, on the average. As a matter of 
 fact the 16 lesions in Table 1 occur in 209 different combinations. 
 Only 644 out of the 4037 lesions occurred singly. There were 625 
 cases with two cardiovascular lesions, one member of the combination 
 being hypertrophy and dilatation in 502 cases and arteriosclerosis 
 in 248. 
 
 In 379 cases there were three lesions,* 359 including hypertrophy- 
 and-dilatation as one of the two, and 261 of this 359 including hyper- 
 trophy-and-dilatation and arteriosclerosis as two of the three. 
 
 *Tn all the figures of Paragraph (b) a heart with valve lesions counts as one, even 
 when two, three, or four valves were affected. 
 
22 FACTS ON THE HEART 
 
 157 cases had four lesions; all but two of these included hyper- 
 trophy-and-dilatation as one member of the combination; 130 of the 
 155 included hypertrophy-and-dilatation and arteriosclerosis as two 
 of the four in the combination; and 53 of these 130 cases had hyper- 
 
 trophy-and-dilatation, arteriosclerosis, and nephritis as three mem-: 
 
 bers of the quartet of lesions. 
 
 36 cases had five lesions, of which hypertrophy-and-dilatation 
 was a member of 34; arteriosclerosis and hypertrophy-and-dilatation 
 were members of 28 of these 34; nephritis, arteriosclerosis and hyper- 
 trophy-and-dilatation were members of 13 of these 28. 
 
 Five cases had six lesions. In four of these the combination of 
 hypertrophy-and-dilatation, arteriosclerotic nephritis (or arterio- 
 sclerotic kidney) and chronic endocarditis recurred. 
 
 Singlestesions .s6 a3 vis s hus el elae a Pathan clas a> Wt cpa Rea eae ee 644 
 TWO JOSIOMS 2e bsp) 0 abe ans fon cl Supra SIRS aur ge ane 625 
 “Three lesions sor cee nies mele c Saeed ae oe ee ee 379 
 Four lesions...04 es fe su besten ek 0k he eee ae ae 157 
 Five, lesions ¢ Wai. tbo aig Lo Dae aes eo eae ee 36 
 Six-Lesions i oie on G sk sacks Sees a eo eis wale eh hee ae 5 
 
 1846 
 
 The chronic infections (rheumatic and syphilitic) affected 665 
 persons. 
 
 The acute infections (endocarditis, pericarditis, myocardial abscess) 
 affected 358 persons. 
 
 The chronic degenerative changes (arteriosclerosis, hypertrophy 
 and dilatation of the heart, myocarditis) affected 809 persons. 
 
 The congenital deformities cut very little figure. There was a 
 hypoplastic aorta in 19 cases; Io occurring as the only cardiac lesion 
 and g with other lesions; the other congenital lesions of the heart 
 occurred alone in only four cases (10 cases in all had congenital 
 lesions).* So that the infections, acute and chronic and the 
 degenerative-reparative lesions divide the whole material into three 
 main groups: 
 
 (1) {Chronic infection (rheumatism, syphilis).... 665—36% 
 (2) Acute infection (pericarditis, endocarditis).... 358—19% 
 (3) Degenerations (hypertrophy and dilatation of 
 the heart, arteriosclerosis, myocarditis)...... 809—44.3% 
 (4) Congenital lesions occurring alone (29 in all) 14—7% 
 1846 100% 
 
 * 29 congenital lesions in all or 1% including 19 of hypoplastic aorta and 5 of 
 harmless valve anomalies. 
 
 + I have included here the cases of chronic pericarditis and chronic non-deforming 
 endocarditis. 
 
 ee — 
 
 —_—— — 
 
MANIFEST CARDIOVASCULAR LESIONS 23 
 
 II. MANIFEST CARDIOVASCULAR LESIONS 
 
 But though all but a few of the lesions here listed doubtless 
 had some effect on the heart’s powers, we get another and probably a 
 fairer view of cardiac disease as a whole if we confine ourselves to 
 manifest lesions, i.e., those in which there is at necropsy and in life 
 definite evidence of deficient heart power as shown in dropsy of the 
 
 TABLE 2.—No. oF CASES AND PERCENTAGES OF HYPERTROPHY AND DILATATION AND 
 oF CHRONIC PASSIVE CONGESTION IN ALL LESIONS 
 
 & ode H. & D:* ge C.P.CF 
 
 ota eee ingle 
 
 cases cause Remarks 
 No. | % No.| % 
 
 Mitral Stenosis: ......... 
 
 Mitral & aortic stenosis. 
 
 Combined valve lesion... 
 
 Aortic stenosis.......... 28 23|82 
 Nephritis, chronic.......] 198 107|54 
 Nephritis, subacute ..... 66 
 Nephritis, acute......... ae 
 Nephritis, amyloid...... 21 I 
 Pericarditis, chronic.....] 112 34/30 (Several with valve or other les- 
 ions such as to make C.P.C.) 
 OTe Patt k eee Sees 10 5/50 
 PGCE II ae ety ar che (td. 9 4 
 Pernicious anemia....... 23 12150 
 Endocarditis, acute ..... 180 80/56 (In many, the C.P.C. was ac- 
 ; counted for by other lesions. ) 
 Pericarditis, acute.......| 186 67/36 (31 accounted for by other les- 
 ions, the rest unexplained) 
 Endocarditis chronic non- 
 Cerormtne aes eee |. 6237 67/28 
 Arteriosclerotic kidney..| 175 6 
 Arteriosclerosis.......... IO5I 
 Wy OCATOIES: 6 cise cetue sents: OL 56/63 (Many had other causes for H. & 
 D. and for C.P.C. present) 
 Syphilitic aortitis....... 92 26|27 
 Congenital heart........ 10 1/10 
 Pure mitral regurgitation 10 5|50 
 Pure aortic regurgitation 13 11| 8 
 H. & D. with other dis- 
 eases 
 (a) With Artscl....... 343 
 (b) Without Artscl....] 164 230/45 
 Odds and ends _ | 
 ‘TDiupericarditis: ; is... 2 2 
 Pulmonary artscl...... 2 2 
 Amyloid degen. kidney 2 . ‘ j . 
 Artscl. degen. kidney.. 2 ||(without arteriosclerosis elsewhere) 
 Hypoplasia of aorta... 19 8 |42 | 
 
 * Hypertrophy-and-dilatation. 
 + Chronic passive congestion. 
 
24 FACTS ON THE HEART 
 
 serous. cavities and in general chronic passive congestion. From 
 Table 2* we can separate out the cases with chronic passive conges- 
 tion in each group, giving the results shown in Table 3a. 
 
 Among the degenerations referred to on page 22. I have 
 bracketed together arteriosclerosis, myocarditis and hypertrophy, 
 with dilatation because it seems to me probable that most of them 
 belong to a single group, namely, hypertensive heart disease—with 
 enlarged but finally failing heart, the acute infections being terminal 
 events and the other lesions historical landmarks of no significance 
 in weakening the heart. In some of the cases of extensive 
 myocarditis this may not be true, but the number of these exceptions 
 is small. 
 
 TABLE 3a.—CAUSES OF MANIFEST HEART DISEASE WITH CHRONIC PASSIVE CONGES- 
 TION 
 
 Valvular heart disease (including luetic aortic regurgitation) 
 Chronic pericarditis 
 
 Acute endocarditis (with hypertrophy and dilatation and probably 
 with hypertension) 
 Acute pericarditis (ditto) 
 
 Chronic non-deforming endocarditis (ditto) 
 Myocarditis (ditto) 
 
 Hypertrophy and dilatation (with and without nephritis; ““ hyper- 
 tensive heart disease’’) 
 
 *T have omitted here 12 cases of Pernicious Anemia, 4 of Leukemia, and 5 of Thyroid disease. 
 all of which showed passive congestion at necropsy. I am not sure how these should be classified, 
 
 TABLE 3b.—PREDOMINATING LESION IN 465 CASES OF MANIFEST HEART DISEASE 
 
 Cardiac hypertrophy and dilatation 
 Valvular lesions 
 
 Chronic pericarditis 
 
 Acute endocarditis 
 
 Acute pericarditis 
 Myocarditis 
 
 * Although for Table 1 we have included all the cases catalogued in the path- 
 ological records, in Table 2 and in the subsequent chapters which elaborate the 
 different items of this table we have often analyzed in detail a number smaller 
 than the total as given in Table 1. 
 
MANIFEST CARDIOVASCULAR LESIONS 25 
 
 Of our 1906 cardiovascular cases, then, only 465, or one-quarter, 
 produced heart failure. The /atency of many cases of heart disease is 
 apparent in all the types. (See Table 2.) For example, out of 262* 
 cases of valvular disease as found post mortem, only 169—or 63%— 
 had produced heart failure, as shown in chronic passive congestion. 
 Out of 112 cases of chronic pericarditis only 34—or 30%—were 
 manifested in dropsy. 
 
 Only in a minority of the cases that I am here referring to did any 
 single lesion, such as rheumatic valvular disease or chronic pericardi- 
 tis—occur alone. ‘There are 207 different combinations and over- 
 lappings in numbers mentioned on p. 22. In view of this difficulty 
 the 465 cases of manifest heart disease just referred to have been 
 divided up according to what seemed to be the dominating lesion 
 when several were present. In the production of death from chronic 
 passive congestion, the following lesions predominated in the 
 proportion expressed by the figures in Table 3a. 
 
 Acute endocarditis and acute pericarditis are here put down 
 because they were the only anatomical lesion present after death in 
 the cardiovascular system in association with 18 cases and to cases, 
 respectively, dying a congestive death. In these, as in others of the 
 smaller items in this table, there may well have been an earlier 
 hypertension producing the cardiac hypertrophy and leading to the 
 final breakdown. 
 
 But dropsy is of course an extreme, sometimes terminal, manifesta- 
 tion of heart disease. Let us take hypertrophy and dilatation as 
 evidence that extra work has in some way been thrown upon the 
 heart. 1209 cases out of 1906, or 63%, showed hypertrophy and 
 dilatation, the causes for which will be discussed in detail later. 
 Here one may merely note that of these 1209 cases of hypertrophy 
 and dilatation only 184 are due to valvular disease and 88 to chronic 
 pericarditis. The vast majority (34 of all) are cases of ‘‘simple 
 cardiac hypertrophy” associated with nephritis and with arterio- 
 sclerosis, often combined with acute terminal lesions like acute 
 endocarditis and acute pericarditis, or with historical landmarks 
 like myocarditis and the non-deforming valve scars. 
 
 Still, it is hard to get a fair picture of heart disease from these 
 figures, because there are so many combinations and interweavings 
 of the different lesions. When a patient dies with valvular disease, 
 chronic nephritis and chronic pericarditis, with which of these three 
 
 * 220 cases of rheumatic valvular disease,-plus 42 of syphilitic aortitis with aortic 
 regurgitation. 
 
26 FACTS ON THE HEART 
 
 are we to class it when we come to separate the different types of 
 cardiac trouble? In view of these difficulties, we have separated 
 out the uncomplicated cases in which we can deal with single lesions. 
 The results appear in Table 4. Here again simple cardiac hyper- 
 
 trophy, with or without arterio-sclerosis and nephritis, is vastly the . 
 
 commonest lesion. It makes up 469 cases out of 656 or 71% of 
 the whole. Rheumatic valvular disease comes next with 69 cases. 
 These two items together amount to 538—or 82%—of the 654 cases 
 in which these single lesions had produced hypertrophy and dilata- 
 tion as evidence of interference with the heart’s action. Among the 
 other 116 cases serious enough to produce hypertrophy and dilatation 
 chronic pericarditis (16) and syphilitic aortitis (20) are the important 
 items, though they only amount to 2%-+ each of the whole. In 
 most of the remaining 78 cases the diagnoses represent terminal or 
 vestigial lesions, the real cause of the trouble being probably the same 
 as that producing the 469 cases of enlarged heart without local lesions 
 to explain it,—1.e., ypertension, the great cardiac malady. 
 
 TABLE 4.—1145 SINGLE LESIONS (WITH AND wiTHouT H. & D.) 
 
 Without With 
 
 Arteriosclerosis 
 
 Chronic non-deforming endocarditis 
 
 Acute endocarditis 
 
 Valve lesions 
 
 Acute pericarditis 
 
 Chronic*pericarditisye.. arma stare ar, et 
 Arteriosclerotic degeneration, kidney...... ....... 
 Luetic aortitis 
 
 Myocarditis (with abscess and infarct)............ 
 Hypoplastic aorta 
 
 Pernicious anemia 
 
 Leukemia 
 
 Goitre 
 
 Nephritis 
 
 Hypertrophy and dilatation alone 
 
 IV. RELATIVE FREQUENCY OF THE DIFFERENT CARDIOVASCULAR LESIONS 
 
 Haven Emerson* found that among 4566 patients treated for 
 
 heart disease in nine New York hospitalst during 1920 or 1921 
 (twelve months) the diagnoses of the primary condition stood: 
 
 * “The Nation’s Health,”’ Vol. V, No. 6, June, 1923. 
 + Bellevue, King’s County, Metropolitan, City, Neurological, New York, Presby- 
 terian, St. Luke’s, and Mt. Sinai. 
 
 lit te 
 
« 
 
 DIFFERENT CARDIOVASCULAR LESIONS 27 
 
 Lesions as diagnosed in New York hospitals 
 
 Valvular disease 
 Myocarditis 
 Endocarditis 
 
 Cardiac hypertrophy 
 Arrhythmia 
 Pericarditis 
 
 * Not mentioned among ‘‘complications,’’ hence this number 28 appears to represent all the 
 cases so diagnosed. 
 
 Comparing these with our findings in 465 cases of manifest heart 
 disease (i.e., those with chronic passive congestion post-mortem) 
 there were: 
 
 Lesions (Manifest Heart Disease) as found at necropsy 
 
 Valvular disease 
 Myocarditis 
 
 Hypertrophy and dilatation (hypertensive heart disease). ... 
 Chronic pericarditis 
 
 Acute endocarditis 
 
 Acute pericarditis 
 
 Others 
 
 Taking our cases, manifest and latent (1230), we find the results not 
 very different: 
 
 Valvular disease (including 42 syphilitic, 220 rheumatic)............... 262 or 21% 
 Dee Ltt ren, OR et, MPR ec Meee rn, US SoD MR ae wy a aiden 89 or 7% 
 Hypertrophy and dilatation (with chronic nephritis, acute endocarditis, 
 
 acute pericarditis, chronic pericarditis, chronic non-deforming endo- 
 
 Parent LeLioscierosis and COMbINALIGNSs.... ccs. 65 1s P perce ea see 879* or 71% 
 And since myocarditis is not a clinical entity we may say that 77-+-% 
 of heart disease is non-valvular and 22+% is valvular. 
 
 The forty-one aneurisms in our 1906 cases is in marked contrast 
 with Dr. Emerson’s thirty-eight aneurisms in 4566 cases, as is also the 
 186 cases of acute and 114 of chronic pericarditis in our 1906 cases, 
 
 minus Syphilitic disease with H. & D. 63 
 minus Myocardial disease with H. & D. 83 
 
 * 1209 cases of hypertrophy and dilatation minus Valve disease with H. & D. ‘sf 
 879. 
 
 3390 
 
e 
 
 28 FACTS ON THE HEART 
 
 while in the 4566 New York diagnoses of cardiovascular disease, 
 there are only forty-six cases of pericarditis (presumably acute in the 
 vast majority of cases). 
 
 Our percentage of acute pericarditis (10%) is ten times as great as 
 theirs, which apparently (like ours) does not include any that were 
 treated only as out-patients and is therefore comparable. Some 
 years ago I found that at the Massachusetts General Hospital we 
 recognized one case in five. In New York they apparently recog- 
 nize about one in ten. Of aneurisms we recognized twenty-five out 
 of forty-one or 60%. In New York if the same percentage held, our 
 forty-one aneurisms in 1230 cases, (3%) would correspond to 137 
 aneurisms of which 38 were recognized, or 28%. Myocarditis was 
 recognized six times as often as it was present, valvular disease twice 
 as often. 
 
 V. VARIATIONS OF NECROPSY DIAGNOSES AT DIFFERENT PERIODS 
 
 In Table 5 I have separated the post-mortem diagnoses into four 
 groups, taking each thousand necropsies by itself so that we can exam- 
 ine the variations in our recognition of the different lesions during 
 the four periods, 1896-1903, 1903-1907, 1907-1912, and 1912-1919. 
 
 The figures show a falling off in the cases of rheumatic valvular 
 disease after 1907. This is not to be accounted for by any known 
 change in the types of patients received at the hospital or coming to 
 necropsy. The same pathologists have applied the same diagnostic 
 criteria to this part of the necropsied material throughout the 
 whole period from 1896 to 1919. ‘Therefore these statistics show 
 that in this group of cases there has been a diminution in the amount 
 of fatal rheumatic heart disease during these twenty-three years. So 
 far as I know, this group of cases may be taken as a fair sample, at 
 any rate for the north-eastern part of the United States. 
 
 It is notable that the diagnoses of aortic stenosis have noé 
 decreased in number, while those of mitral stenosis, and of mitral- 
 and aortic stenosis combined ave fallen from forty-six (in the period 
 1903-1907) to twenty, or less than half, in the period from 1912-19109. 
 
 On the other hand there is no falling off in the amount of 
 pericarditis which is ordinarily included with the valvular stenoses 
 as a “‘rheumatic”’ lesion. 
 
 The sudden drop in the number of cases of ‘‘non-deforming 
 endocarditis” in the last thousand necropsies is I believe of no 
 significance and represents merely a change in the pathologist’s 
 views as to the term “endocarditis.”” Slight thickenings of the 
 
DIFFERENT CARDIOVASCULAR LESIONS 29 
 
 valves, especially in elderly persons, are now not called endocarditis 
 or noted in our anatomical diagnosis. 
 
 The apparent increase in fibrous myocarditis is also not 
 significant, and represents probably a slightly altered terminology. 
 
 The diagnoses of syphilitic aortitis in the cases belonging to the 
 earlier years were made by re-examining old specimens after the 
 pathologists had come to recognize this lesion. Naturally the cases 
 thus identified are relatively few, so that the increase in the later 
 years means an increase not in the cases of syphilitic aortitis but 
 in the diagnoses of this lesion. 
 
 TABLE 5.—NECROPSY DIAGNOSES IN EACH 1000 AUTOPSIES TAKEN CONSECUTIVELY 
 FROM 1896 TO 1916 
 
 1896 to | 1903 to | 1907 to | I9g12 to 
 1903 1907 IQI2 I9QIQ 
 
 Disease Nears Necropsy| Necropsy|Necropsy| Total 
 PSY) number | number | number 
 number 
 roor- | 2001- | 3o001- 
 I-I000 
 2000 3000 4000 
 
 Pure mitral disease (stenosis) . . . 16 
 Mitral and aortic (stenosis) .... 
 
 Combined valve lesions 
 
 Aortic stenosis 
 
 Acute pericarditis 
 
 Chronic pericarditis 
 
 Acute endocarditis............. 
 
 Chronic non-deforming endocar- 
 
 Fibrous myocarditis 
 Myocardial abscess............ 
 Myocardial infarct 
 
 Pure aortic regurgitation (rheu- 
 
 Syphilitic aortitis......... 
 
 * In the text two more cases from another series have been used. 
 + In the text one more case has been used from another series. 
 
CHAPTER II 
 RHEUMATIC HEART DISEASE. FATAL CHOREA 
 
 The Material Used.—In all cases I have started from the demon- 
 strated post-mortem lesions and worked back to the clinical findings 
 corresponding. I have paid no special attention to the clinical 
 diagnosis in deciding which cases to include under each group, but 
 have based all classifications and statistics on the measurements and 
 descriptions of the necropsy records. 
 
 A valve has been considered obstructed or stenosed when its 
 circumference was found to be markedly diminished either by the 
 rigid end results of chronic endocarditis, by soft vegetations, or by the 
 combination of both. When soft vegetations were not in such a 
 position or of such a size as to produce obstruction the case has been 
 studied not as a valve lesion but in the chapter on “Acute and 
 Subacute Endocarditis.” 
 
 Hypertrophy and dilatation of the heart has been judged and 
 classified (like the valve lesions) wholly on the post-mortem data,— 
 the weight of the heart, the thickness of its walls, and the size of its 
 cavities all considered in relation to the size of the individual. A big 
 man has a big heart. ‘The same cardiac dimensions if existing in a 
 small woman or in a child would be considered evidence of 
 hypertrophy. 
 
 Terms.—1. When the mitral valve alone was found at necropsy 
 to be diseased, or when the disease of other valves was so slight as 
 apparently not to interfere with the opening and closing of the 
 valve, I have called the cases “ pure mtiral”’ or simply “‘ mztral.” 
 
 2. When there are important deformities both in the mitral and 
 in the aortic valves I have called the cases ‘‘mitral-and-aortic,” 
 emphasizing by the two hyphens the fact that I am not here referring 
 to two separate groups of cases but to one set of combined lesions. 
 
 The cases grouped as “‘pure mitral’? number 107 and those called 
 ‘‘mitral-and-aortic”’ come to 4o. 
 
 3. Isolated disease of the aortic valve is called “‘ pure aortic,”’— 
 28 cases. 
 
 4. The cases in which the mitral-aortic-and-tricus pid valves were 
 all involved, (23 examples), those with lesions in mitral-aortic-tri- 
 
 30 
 
RHEUMATIC HEART DISEASE 31 
 
 cus pid-and-pulmonary valves (2 cases), the combination of mitral-and 
 tricuspid disease (6 cases), and of pulmonary-and-tricus pid (2 cases) 
 have here been all lumped together under the term ‘“‘OTHER 
 COMBINATIONS.” 
 
 In all the cases classed under these four groups—208 in total— 
 sienosis was the lesion anatomically demonstrated post-mortem. 
 This is all that the necropsy can demonstrate. But from the half- 
 open position in which the diseased valves were rigidly fixed, it 
 seems clear that there must have been some regurgitation as well as 
 some obstruction of the blood stream. A valve fixed half open will 
 not open fully, but neither will it shut. 
 
 A valve lesion, single or combined, means therefore in the following 
 section, a deformity believed to have caused stenosis and regurgitation 
 although it may sometimes be called simply a “‘lesion,”’ a ‘‘disease”’ 
 or a ‘‘stenosis.” 
 
 The rare cases of regurgitation alone, due to rheumatic endocar- 
 ditis will be discussed separately. They make up only 23 cases in all. 
 
 By the terms ‘“‘rheumatism”’ and “‘rheumatic”’ I mean a disease 
 believed to originate as a general septicemia (point of entrance 
 unknown), which may “‘settle”’ in the joints (‘‘rheumatic fever’’) in 
 the subcutaneous tissues (‘rheumatic nodules’’) or in the tonsils 
 (tonsillitis), may cause brain symptoms (Sydenham’s chorea) or may 
 be implanted in the pericardium, in the myocardium or on the heart 
 valves without any other localization. Ordinarily when the disease 
 affects the heart it has had some earlier localization (in the joints, 
 tonsils, or brain, sometimes in the subcutaneous tissues also). But 
 it does not seem strictly true to say that the rheumatic joint trouble 
 causes the endocarditis which so often follows. Both are presumably 
 caused by the same organism—the same septicemia—which may 
 localize its activities first in the heart and later in the joints, or in 
 the reverse order. In case the heart lesion appeared first (as is not 
 very rarely the case) we should not say that the heart trouble caused 
 the joint trouble. It is as incorrect, I think, to say that acute 
 polyarthritis causes endocarditis. Both manifest a single cause. 
 
 The proof of a septicemia is not yet to be obtained. 
 
 No “‘arthritis”’ has been considered “‘rheumatic”’ in the analysis 
 of these cases unless it involved many joints, produced marked 
 prostration, ran a short course and left the joints sound in the end. 
 The chronic, stiffening, apparently afebrile lesions often called 
 rheumatism, especially in elderly people, have received no considera- 
 tion here. 
 
32 FACTS ON THE HEART 
 
 The Type of Endocarditis Found Post-mortem in 208 Cases.—- 
 I include here under ‘‘Rheumatic Valvular Heart Disease”’ as the 
 subject of this chapter (see Table 6), any valvular obstruction, 
 whether produced by a soft, acute, vegetative process (ten cases in 
 208), by the chronic deforming end-result of an earlier acute 
 endocarditis, or by the combination of both.* 
 
 I have included these acute cases in part because in 53 out of 208 
 cases, or 25%, the chronic process was overlaid at the time of death 
 by a fresh endocarditis. In some cases (see Table 48) this acute 
 septic process, involving in its effects the myocardium and all the 
 organs of the body, may be assumed to be the immediate cause of 
 death as, in earlier stages of the disease, similar acute exacerbations 
 are believed to produce many of the decompensations formerly 
 explained by mechanical overstrains. f 
 
 Valvular lesions (such as mitral obstruction) are here conceived 
 to be produced (a) (as is usually the case) by the hardened, shrunken, 
 adherent end-results of an acute endocarditis; (b) by acute soft 
 inflammatory vegetations: (c) by a combination of both. 
 
 TABLE 6.—TyYPE OF ENDOCARDITIS 
 
 ce M-A | M-A-T| M-T | Aortic | P-T |4 valves] Total 
 
 Since there appear to be all possible transitions between the 
 various types, and all sorts of combinations of them, it seems best to 
 include them all under a single heading, “rheumatic valvular heart 
 disease.’ Very probably there are differences, at the extremes quite 
 marked differences, both in the type of micro-organism and in the 
 clinical course of acute cases as contrasted with chronic. But the 
 
 *Tt is often impossible to decide the chronicity of the so-called verrucose endo- 
 carditis. Sometimes the character of the minute masses, such as softness, reddening, 
 and fragility, is apparent, and the process is of course acute. But frequently this is 
 wanting, and they appear as firm, grayish to gray-red, warty granules apparently 
 organized, and in these instances are chronic in nature, but of more recent origin 
 
 than the usual accompanying, underlying chronic endocarditis. (Note by Dr. Oscar 
 Richardson.) 
 
 {See Breaks in compensation from Endocarditis: Charles Hunter Dunn, Jour. } 
 Amer. Med. Assoc., Feb. 9, 1907. 
 
MITRAL STENOSIS, PURE AND COMPLICATED 33 
 
 border-line cases are so many that I doubt the wisdom of separating 
 them. 
 MITRAL STENOSIS, PURE AND COMPLICATED 
 
 Age of Onset.—In Table 7 I have endeavored to estimate the 
 age at which the cardiac lesion started in this group of necropsied 
 cases. This estimate is made by assuming that the first attack of 
 rheumatism or chorea known to the individual or his parents coin- 
 cided with the beginning of the endocarditis; or, when no history of 
 rheumatism or chorea could be obtained, by dating the cardiac 
 disease from the onset of cardiac symptoms. Obviously this last 
 measure is misleading since there is in most if not in all cases a latent 
 or symptomless period, often lasting for years. The frequency with 
 which (especially in women) we find mitral stenosis in the course of a 
 routine physical examination undertaken by reason of complaints 
 unconnected with the heart proves the existence of this latent period 
 in many cases, perhaps in all except the acute vegetative types of 
 endocarditis. 
 
 Taking the figures of Table 7 as they stand, with all the errors 
 inherent in them, it appears in 42 out of 63 cases, or 67% that the 
 heart disease began before the thirtieth year (‘‘pure-mitral’’ cases). 
 When the mitral stenosis was complicated by stenosis at other valves 
 the disease began before the thirtieth year in 77%. Taking all the 
 well-studied cases in one group, 73% of them began before thirty. 
 
 Compare these figures with the estimates in 239 similar ambulant 
 cases examined by me. There 104 out of 130 well studied “‘pure- 
 mitral’ cases or 80% began apparently before the 30th year. Of the 
 mitral-and-aortic cases 85% began before the 30th year. Although 
 the diagnosis in these cases was not verified by necropsy the histories 
 are probably better than those in the necropsied series. So that I 
 am inclined to believe that the true percentage of mitral cases 
 beginning before 30 is nearer 82% than 73%. 
 
 Sex in Relation to the A ge of Onset.—In males the disease apparently 
 begins earlier than in females if the indication of my rather scanty 
 figures 1s borne out by larger statistics. Thus in Table 7, 90% 
 of the males with mitral-and-aortic disease and 70% of the “pure 
 mitral’ cases began before the thirtieth year, while in women only 
 60% of the pure mitrals and 71% of the mitral-and-aortic cases 
 began before thirty. Combining all groups we find: 
 
 LOU Meer ete eoe Moers St en, sc a ature less 77% before 30 
 Tt rennet ter mrt. Meyer. Sls, 68% before 30 
 
34 FACTS ON THE HEART 
 
 In the ambulant cases examined by me in life but not at necropsy, 
 88% of the men and only 76% of the women were under the 3oth 
 year. This correspondence with the figures in necropsied cases is 
 striking. 
 
 TABLE 7.—NECROPSIES. AGE OF ONSET 
 
 Mitral | petra Other comb. 
 
 and Aortic 
 
 TABLE 8.—LIvING CASES. AGE OF ONSET IN 239 CASES OF RHEUMATIC HEART DISEASE, 
 EXAMINED IN OutT-PATIENT DEPARTMENT FOR THE YEARS I9Q1Q, 720, ’21, ’22 
 
 Mitral Mitral and Aortic Total 
 Age 
 Male | Female} Male | Female| Male Female 
 
 Oo 9 13 15 14 
 10-19 16 27 Zs 
 20-29 12 21 
 
 30-39 3 15 
 40-49 4 
 50-59 
 60-69 
 
 Unknown 
 
 DURATION OF LIFE 
 
 Out of 36 pure-mitral necropsied cases, 27 (or over 24) are esti- 
 mated as having lived ten years or more since the onset of the disease. 
 Six lived apparently 25-35 years with their stenoses. 
 
 The term of life in the mitral-and-aortic cases is strikingly shorter. 
 In more than half the cases, the disease appeared to have killed the 
 patient in one year. The average duration in the 31 cases is three 
 
DURATION OF LIFE 35 
 
 years as compared with 15 years in the pure mitral cases. Only 
 one lived more than ro years. 
 
 In the other ‘‘combined lesions” (with fewer cases involving the 
 aortic valve) the prognosis seems to be better than in the mitral-and- 
 aortic cases, though worse than in the pure-mitral cases. Nine out 
 of 28 lived ro years or more, only two of 28 succumbed within the 
 first year and the average duration of the disease was Io years. 
 
 Average duration in pure-mitral cases = 15 years 
 Average duration in mitral-and-aortic = 3 years 
 Average duration in combined lesions = 10 years 
 
 In the living cases the figures are of course not compared. (See 
 Table ro.) 
 
 TABLE 9.—ESTIMATED DURATION OF LIFE IN 95 CASES OF RHEUMATIC HEART DISEASE 
 EnpING MosTLy By PASSIVE CONGESTION 
 
 Years | Mitral | Mitral and aortic Other comb. | Total 
 
 16 
 
 | 
 I 
 
 WwW HH O HH H 
 
 3 
 fo) 
 fe) 
 fo) 
 2 
 I 
 2 
 3 
 4 
 2 
 fo) 
 I 
 2 
 I 
 2 
 ° 
 I 
 I 
 I 
 I 
 I 
 2 
 fo) 
 ° 
 
 WiO GeO Orta: OFM O50. 0° 0 o> O00 0. O- 02 08080 0/008 
 Om Om Om Hay Om On Olen Hi OMOMISs OF OL MeN § OR HLH. Weir miles 
 
 wW 
 io 
 
36 FACTS ON THE HEART 
 
 The lesion dated supposedly from a rheumatic attack in seventy- 
 two, and from a choreic attack in six cases. The estimated duration 
 of the lesion was as in Table 9. 
 
 This group of cases with a known cause appears to occur in 
 younger people than the group in which no cause is clear (see below). 
 
 The average age of the thirty-six patients with “‘pure-mitral” dis- 
 ease is thirty-five years, and the average duration of the lesion 15 
 years. Most of these cases died from passive congestion (‘‘con- 
 gestive death’’). 
 
 TABLE 10.—LIVING CASES. ESTIMATED DURATION OF LIFE IN 239 CASES OF RHEUMATIC 
 HEART DisEASE EXAMINED BY ME IN THE OUT-PATIENT DEPARTMENT IN THE 
 YEARS I91Q, 1920, I92I, 1922 
 
 Mitral Mitral and aortic 
 Total 
 
 is 
 = 
 = 
 
 M F 
 
 2 VOATS Mee) Lik PC ee ae ee ee 
 APVCATS 025 HE ha ote dea ey ae ee 
 SEATS. | aah Ber cose ee 
 
 O VEAaTSi is. cigs so tee eee eee 
 AT OATS coe certs ode ee oe ee 
 SO: Vears ce vay, 
 
 9 years 
 
 LO V eats ee 
 
 TTUVCATS yh. 2. RUS pee ee 
 EA yearsie sae ee a eet 
 IZVVCATS Aan Oke ee ee 
 EALY CATS) uk Leon eae ee 
 TORyears oes tele aes teers eee 
 TO VCATS? AG shes eee da ne eee 
 17 years 
 
 EO *VEAIS SS, Via ee eae 
 TO “VEaTS /" eet (pie ae eee ea 
 DO: VEATSi7 tua ape ce ae ae eae 
 25 years 
 
 20 VeaTSia% os moet a ees et 
 
 BR ALY CATS Muveron REA SCs. Staats Ben 
 SRV eATS te oa ieee 
 
 H # HH O DD BH AH OW HH HH OO HW dN W PW HB CON NY DS CC 
 
 Or (Oe ie Oe O AO -- 0) OOS et 0 Se Sei RG ONO (bs WON 
 OVO Se He eH OFF 69 700-0 Go Fe Bt O91 et G1 00 "06 Us 
 
 OH O RH O HK HR OO OO H HR HR HR RW AB RR RW OO HW HR Re DD 
 
 Many years 
 Unknown 
 
DURATION OF LIFE 37 
 
 Age and Length of Life in Rheumatic Heart Disease.—1. Age. 
 The figures in Table 7 show that rheumatic valvular heart disease 
 (defined as above) occurs at every age, lasts till old age, and is 
 compatible with long life. In the 10% ‘‘pure-mitral’”’ cases, 33 or 
 30% were over fifty years of age at the time of death; while of the 
 40 mitral-and-aortic cases 14 or 35% had survived the fiftieth year. 
 From the point of view of prognosis in youthful cardiac sufferers 
 these facts are somewhat reassuring, though the majority (in ‘‘pure- 
 mitral’ cases 70%) die before fifty. 
 
 The worst decade for mitral cases is that between thirty and forty, 
 while the danger-point for mitral-and-aortic is fifty to sixty. 
 
 Males with ‘“‘pure-mitral”’ stenosis and combinations of this with 
 pulmonary and tricuspid disease die usually before forty; only one- 
 fourth survive the fiftieth year. But if they have both mitral and 
 aortic stenosis they are slightly older at death than with mitral alone. 
 
 Aortic stenosis is the longest-lived lesion of the rheumatic group. 
 76% of the cases lived beyond forty, and almost 50% survived the 
 fiftieth year. Ji zs a lesion of elderly men, but when women have it 
 (which is rare) they live even longer than men. 
 
 2. Duration of Disease—(a) The actual number of years occupied 
 in each case by the disease before death and the causes of death 
 (congestive or non-congestive) are shown in Table 9 and Table 48. 
 The first of these points—the duration of the disease—can be settled 
 only with an approximation to accuracy. We may surmise that 
 the disease began at the date of the first (often the only) attack of 
 acute rheumatism or chorea, a date which can be fixed with approxi- 
 mate accuracy in 86 of our cases. Assuming this to be true we can 
 say that 35, or 40%, of our cases lived ten years or more. 
 
 (b) The table of ages at the time of death in necropsied cases (Table 
 II) represents the only certain data that I have. But it is of some 
 interest to compare with this the ages of 315 cases diagnosed as 
 rheumatic heart disease by me in out-patient practice or in private 
 practice (see Table 12). These ages given at the time the patient 
 was first seen, are to be taken as representing a point near the time at 
 which symptoms first appeared. In this group (see Table 12) the 
 decade from ten to nineteen is the most important one. It is striking 
 that only 17 or 5% fall within the first decade of life while 87 or 
 nearly 27% come for advice within the next ten years, and 173 or 
 55% before the thirtieth year. 
 
38 FACTS ON THE HEART 
 TABLE 1t.—AGE (AT THE TIME OF DEATH) AND SEX 
 
 Mitral M-A M-A-T M-T Aortic Poly 4 valves Total 
 
 SCH OH NOW O 
 SCOnR N COB HO 
 OO AO UOMO ne. 
 
 0 
 5 
 3 
 6 
 6 
 4 
 I 
 2 
 
 27 
 
 Set leSetha eae ee 
 tislkctar cose weotS 
 Ail en eae Chl Nee 
 nl 
 
 uw HAM NT DN OW H 
 Bell oweree Cees 
 si [ets es a es ee 
 ress ak dat otter ee ae 
 
 H 
 n 
 
 Females.... 
 
 Returning now to the necropsied cases (Table 11) we see that the 
 end of the disease comes most often in the years from thirty to 
 thirty-nine. Its earliest symptoms (if the ante-mortem diagnoses 
 of Table 8 are correct) come twenty years earlier. I refrain from 
 concluding that the average length of the disease is twenty years. 
 The two sets of figures cannot legitimately be combined in this way. 
 Moreover, only in the death-age figures are we certain of the 
 diagnosis. 
 
 3. Sex.—It has usually been stated that mitral stenosis (pure or 
 combined with other lesions) is commoner in women than in men. 
 In this series of 180 proved mitral cases (‘‘pure” and combined) there 
 were 84 males to 96 females. But as in our necropsies from all 
 sources males make up 65.4% these figures certainly show a consider- 
 able excess of females. Women do not come into our wards as 
 often as men do. The difference in the number of autopsied cases 
 may well be accounted for by women’s greater unwillingness to 
 trust themselves to a hospital, or by their relatives’ greater unwill- 
 ingness to grant necropsy in the case of a female than in that of a 
 male.* 
 
 *The actual number of deaths from heart disease of all sorts is about the same 
 
 in women and in men. See for example the Statistical Bulletin of the Metropolitan 
 Life Insurance Co., June, 1925 (Vol. VI, No. 6). 
 
DURATION OF LIFE 39 
 
 TABLE 12.~~LIVING PATIENTS 
 
 Age and Sex 
 
 Age at first consultation 
 
 Mitral 
 private cases 
 
 Mitral Aortic 
 
 Males | Females} Males | Females} Males | Females| Males | Females 
 
 Males... 
 Females. 
 
 Comparing these figures with those obtained in out-patient work 
 and in private practice, we find that (see Table 12) in the living out- 
 patient and private cases there is a considerable excess of females, 
 181 to 134 males, even though among all the patients coming for all 
 causes to our Out-Patient Department there are but fifty-eight 
 women to every seventy-one men. Hence this excess of women with 
 mitral stenosis is greater than the’figures show. 
 
 Taking now the Out-Patient Department figures of heart disease, 
 chorea, and rheumatism in children up to sixteen, we find that 59% 
 of those treated as ‘‘rheumatic cardiac disease” in 1921 and 61% of 
 those treated either as rheumatic heart disease, as chorea, or as 
 rheumatism, were girls. 
 
49 FACTS ON THE HEART 
 
 TABLE 13.—SOURCE OF CASES 
 
 Mitral | M + A | Aortic | Total 
 
 (a) Out-Patient Department (for years 1910, 
 TO2O; 21,522) See ee eee ee Bean 
 (b) Private practice 
 
 In the ‘“‘pure-mitral”’ cases of all ages the females are more than 
 twice as numerous (149 to 68) so long as we confine our attention to 
 living (and therefore doubtful) cases. In the necropsied cases of 
 ‘‘pure mitral” disease there were sixty-two females to forty-five 
 males. But as already said this gives too slight an impression of the 
 excess of females, since our necropsied series is not a fair sample of the 
 sick adult population, but contains a disproportionate number of 
 males. Putting together all our facts: 
 
 (a) as to necropsied cases in a “‘selected”’ material, 
 
 (b) as to all living cases examined by me, 
 
 (c) as to all out-patient cases of rheumatic heart disease, 
 
 (d) as to all out-patient cases of rheumatic heart disease in 
 children, 
 
 (e) as to all out-patient cases of chorea, 
 
 (f) as to all out-patient cases of acute rheumatism, 
 we may conclude that the female sex is a strong factor in determining 
 the incidence of mitral disease, whether ‘‘pure”’ or combined. 
 
 I have already called attention to the fact that in the mitral-. 
 and-aortic lesions the males predominate, while in the pure aortic 
 lesions females are the exception. 
 
 Relation of Sex to Duration of Diseases.—When we study 
 the relation of sex to the age at which the fatal illness occurred, we 
 see that males break down earlier than females. Thus in Table 11 it 
 appears that in females only 40% (24 of 62 cases) of the pure mitral 
 and 59% (22 of 37 cases) of those associated with other valve lesions 
 died before their fortieth year. Combining both groups we find that 
 in only 47% of the 96 (not counting the cases of “‘pure’’ aortic steno- 
 sis) female cases did death occur before forty. In other words more 
 than half of them (53%) get by the fourth decade. 
 
 Of the 84 men (not counting aortic stenosis) only 40% (33) lived 
 past forty. 60% (27 of 45 cases) of the ‘‘pure mitral” and 76% 
 (39 of 51) of the remaining cases in men died under forty. 
 
ETIOLOGY IN MITRAL STENOSIS 41 
 
 We may surmise that this is due to the greater muscular activity 
 called for by the men’s occupations, but for reasons stated elsewhere 
 I doubt whether this explanation holds. I cannot explain the 
 women’s greater tenacity of life. 
 
 ETIOLOGY IN MITRAL STENOSIS 
 
 The Relation of These Lesions to Rheumatism, Chorea, and 
 Tonsillitis.—In 92 cases the records on this point are fairly complete. 
 They show that rheumatic arthritis was a factor in 73 or 78%; that 
 chorea was remembered in only 7 cases or 6%, while tonsillitis seemed 
 important in 7 cases or 7%. In the remaining 7 cases none of these 
 evidences of infection was recorded. 
 
 The surprising thing to me in these cases is the small number of 
 choreas. Perhaps chorea, even when fatal (see page 312), causes a 
 type of endocarditis not apt to lead to serious deformities of the 
 valves. I find that only in 7% of cases seen clinically did definite 
 mitral stenosis follow chorea in patients without joint symptoms. 
 Thus in rr6 living cases of “pure mitral” disease, and in 73 mitral- 
 and-aortic disease there were but eight cases with a history of chorea 
 without rheumatism, that is, only 7%, which corresponds closely 
 with 6% in the necropsied cases. 
 
 As to the importance of fonszllitis in these cases it is difficult to 
 say anything definite, on account of the frequency of this infection in 
 all sorts of people. Our records do not clearly separate the cases in 
 which tonsillitis has been frequent and severe from those in which it 
 was merely remembered to have occurred once or more in the individ- 
 ual’s lifetime. Our records show only g of 174 autopsied cases and 
 31 of 170 clinical cases with records of tonsillitis. This is no more 
 than would be found in any series of healthy people. 
 
 Number of Attacks of Rheumatism (or Chorea).—An attempt was 
 made to ascertain how many attacks of rheumatism or chorea had 
 occurred during the lifetime of these patients. The memory of such 
 events is notoriously faulty and the following table is therefore of 
 very little value. 
 
42 FACTS ON THE HEART 
 
 TABLE 14.—NUMBER OF ATTACKS OF RHEUMATISM (OR CHOREA) IN MiTRAL DISEASE 
 “PURE”? OR OCCURRING WITH OTHER LESIONS 
 
 Mitral Mitral & Aortic Other combinations 
 No. of 
 
 ttack 
 Ss y Males Females Males Females Males Females 
 
 Rheum. 13 Rheum. 9 | Rheum. : Rheum. 11 | Rheum. 7 | Rheum. 46 
 Chorea 2 Chorea 4 Chorea I Chorea 3 | Chorea 10 
 
 Rheum. 17 
 Chorea I 
 
 Rheum. 6 
 
 Rheum. 
 Rheum. 
 Rheum. 
 
 Rheum. 
 
 Previous Infections Other than Rheumatism.—In Table 15 are 
 listed the infections remembered by the individual, or in the case of 
 children by the parents, as having occurred in the course of his pre- 
 vious life. It seems to me apparent from these figures that no infec- 
 tion other than that manifested in rheumatism and chorea can as yet 
 be definitely correlated as an etiological factor in mitraldisease. The 
 histories of any 173 people with the same age and sex distribution 
 would contain, I think, at least this number of pneumonias, scarlet 
 fevers, etc. Doubtless some cases of scarlet fever complicated by 
 streptococcus infection may be the precursors of some types of heart 
 disease. But for scarlet fever alone these figures show no connection 
 to endocarditis. 
 
 Pneumonia in fatal cases shows a fair percentage of acute endocardi- 
 tis, especially when the streptococcus is present (as in the ‘‘influenza”’ 
 pneumonias). But on the whole when we consider the great fre- 
 quency of pneumonia and the relative rarity of mitral disease at all 
 ages, it is difficult to put down pneumonia as an etiological factor, 
 even a minor one. 
 
 Equally groundless in these cases is the theory that syphilis or 
 
 arteriosclerosis can produce the peculiar lesions of mitral stenosis. 
 Lesions of syphilis recognizable post-mortem were not found in a 
 single case, and the percentage of known syphilitic infections was 
 notably below the figures to be found by questioning hospital patients 
 in general. (See R. C. Cabot: Relative Frequency of the Different 
 Diseases Prevalent in Boston and its Vicinity; Shattuck Lecture, 
 Mass. Medical Society, June 13,1911.) A calcified column (“‘bone’’) 
 was found at the root of the mitral valve in three cases and seemed 
 
 ll 
 
ETIOLOGY IN MITRAL STENOSIS 43 
 
 like a lesion which might be explained by arteriosclerosis. But 
 these calcified masses caused no stenosis. (See page 204.) 
 
 TABLE 15.—PREvIOUS INFECTIONS OTHER THAN RHEUMATISM IN 173 CASES OF RHEU- 
 MATIC HEART DISEASE 
 
 Other 
 
 Mi 
 itral M+A ine 
 
 Scarlet fever 
 M easl@s. 
 
 Pneumonia........ 
 
 Typhoid 
 
 Smallpox 
 Diphtheria 
 ePOPPUGRIS . Sec hy 
 
 Oxts= Bee to Ls Ca ON 
 POOH WBW ON WW BA 
 O= O°. OF. O.42O.8N. CO Dw Onsite 
 
 TABLE 16.—TUBERCULOSIS, ACTIVE OR OBSOLETE 
 
 Mitral 
 Mitral and 
 Aortic 
 
 Other 
 comb. 
 
 The idea fathered by some French writers that tubercu- 
 losis 1s an etiological factor in rheumatic heart disease finds no 
 support in these figures. Moreover there is but one case in which 
 an active phthisis has accompanied or complicated rheumatic heart 
 disease. There were two miliary cases, one affecting the pleura and 
 liver, one of “‘pseudo-miliary”’ tuberculosis in the kidneys, and one of 
 active tuberculosis of the right adrenal. 
 
 Even obsolete tuberculosis, though carefully searched for in 176 
 necropsies, was found in but twenty-three cases. 
 
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SYMPTOMS OF MITRAL STENOSIS 45 
 
 Earliest Symptoms (Necropsied Cases).—Table 17 shows as 
 might be expected that dyspnea, either alone or in company, was 
 present at the onset of symptoms in fifty-three out of sixty-one 
 cases of “pure-mitral” stenosis in which this point was carefully 
 inquired into. In thirty-four cases, or over half, dyspnea appeared 
 alone, was the earliest symptom, and often persisted for years before 
 any other symptoms were noticed. 
 
 In the mitral-and-aortic cases, twenty-three out of twenty-seven 
 had dyspnea alone or in combination as their first symptom, while 
 in the other combined stenoses 18 of 21 began in the same way. 
 In the total group of 109 carefully questioned patients, 94 began with 
 dyspnea, alone or accompanied. 
 
 Earliest Symptoms (Out-Patient Cases).—In the living cases 
 (Table 18) dyspnea was the first complaint in sixty-one out of eighty- 
 five carefully questioned “‘pure mitral’’ cases, and in thirty out of 
 forty-seven “mitral-and-aortic” cases, i.e. in about three-quarters of 
 all cases. 
 
 Palpitation was noticed first in ten out of thirty-three “‘pure 
 mitral’’ cases and in ten out of twenty-six ‘mitral and aortic,” i.e. 
 in one-third of the total cases. 
 
 Cough was the earliest symptom in eleven out of twenty-seven 
 ‘‘pure mitral’’ and five out of twelve ‘“‘mitral and aortic,” i.e. in 
 about one-third. 
 
 Precordial pain of some sort was the earliest complaint in eight 
 out of twenty-five ‘‘pure mitral’ and sixteen out of twenty-seven 
 “mitral and aortic.’’ The mitral-and-aortic cases show a higher 
 percent of pain,—over one-half. 
 
 Edema was the first point noticed in four ‘‘mitral” cases out of 
 twenty-one, and five ‘mitral and aortic” out of fifteen. 
 
 TABLE 18.—TABULATION OF THE EARLIEST CARDIAC SYMPTOM 
 Living Cases 
 
 Symptom Mitral M+A 
 
 Dyspnea 
 BITECOLGLAL Wal vrei oi. se Nake ke Rents ee 
 
 160 cases 
 
46 FACTS ON THE HEART 
 
 Taking all symptoms noted, whether early or late, their relative 
 frequency in this whole group of living mitral cases. with or with- 
 out aortic disease, was as follows: 
 
 Dyspneat chew eas oo ls ae 132 
 Palpitations os Metviteecc Oats. os a ae a 59 
 Precordial pathic... its. 0.08. le ee 52 
 1 (6 (e100 F: Snead ar 36 
 
 In contrast with the necropsied cases most of which were studied 
 only at the end of life, these relatively early cases (though their diag- 
 nosis is never quite certain) seem to show a much greater frequency 
 of pain as a complaint (especially in the “‘mitral-and-aortic”’ cases). 
 The relation of pain to dyspnea is as fifty-two to one hundred and 
 thirty-two in the early (living) cases, while it is only as twenty-one to 
 one hundred and twelve in the late (necropsied) cases. 
 
 Palpitation and dyspnea were noted together at the onset of 
 twenty-three cases or about one-fourth. 
 
 In most respects these tables show no notable differences of 
 symptomatology as between the “‘pure-mitral” and the mitral-and- 
 aortic cases. 
 
 The percentage of patients who noticed edema at some time 
 before hospitalization is 12 out of 40 in the mitral-and-aortic series, 
 as compared with 43 out of 107 in the mitral series and 17 out of 
 33 in the other combinations,—1.e. the mitral and aortic cases showed 
 early edema in 30%, the pure mitral in 40%, and the other 
 combinations in 51%. 
 
 Symptoms in General.—The figures of Table 19 refer to the 
 patient’s complaints before entering the hospital, not to the terminal 
 sufferings. The familiar symptoms of cardiac patients here occur 
 in very much their familiar order. It is perhaps significant that in 
 the mitral-and-aortic cases dyspnea is relatively more frequent (75%) 
 than in the mitral (50%). The “‘combined”’ stenoses give the high- 
 est of all (82%). | 
 
 The fact that only 55 out of 107 “‘pure-mitral’’ patients are known 
 to have had any dyspnea at all before entering the hospital is surpris- 
 ing, indeed almost incredible. But if it represents the truth it goes 
 toward explaining why the diagnosis was altogether missed in about 
 the same percentage of cases. Examining this similarity more 
 closely we find that 7m 40 out of 52 of the undiagnosed cases dyspnea 
 was absent. Under these conditions the cardiac histories may 
 well have been less searchingly taken. 
 
SYMPTOMS OF MITRAL STENOSIS 47 
 
 Palpitation; Early or Never.—Another notable fact is that palpi- 
 tation (often, perhaps usually, equivalent to auricular fibrillation) 
 appears either early or not at all. It was noticed in only eighteen 
 ‘pure mitral”’ cases but in 12 of these it was noticed as early as any 
 sympiom. In seven out of eleven mitral-and-aortic cases the same 
 “early or never’”’ tendency appears, while in the remaining ‘‘com- 
 bined stenoses” palpitation came early or never in five of the 9 
 _ recorded cases. So that (combining the three groups) we may say: 
 In mitral disease (with or without other valve lesions) palpitation is 
 recorded only 38 times among 180 cases, but in 24 of these 38 or 63%, 
 this palpitation appeared either as the earliest symptom or with the 
 earliest symptoms. [These data do not agree with those of the Out- 
 Patient Department series wherein only one-third of those with pal- 
 pitation manifested it as a ‘‘first complaint.”’] 
 
 These figures as to palpitation may be compared with our rather 
 scanty data on the pulse as recorded during the patients’ stay in the 
 hospital. Of the mitral cases 41 out of 67 cases with definitely 
 recorded pulse observations showed arrhythmia. In all but three of 
 these the arrhythmia is so described as to make it highly probable 
 that auricular fibrillation was present. But it is certainly surprising 
 that only 41 out of 67, or approximately 61%, should have manifested 
 this obvious change in any such degree as to get it into our hospital 
 records. Arrhythmia has been, throughout the years covered by 
 this series of cases, one of the points most clearly expected and looked 
 for by physicians and internes in sick patients of all types, especially, 
 but not only, in those believed to have heart disease. It is not usu- 
 ally difficult to recognize the existence of some arrhythmia when one 
 feels the pulse as often as is the routine practice of physicians, internes 
 and nurses at the Massachusetts General Hospital. 
 
 In the “mitral-and-aortic”’ cases, 24 had regular and to irregular 
 pulses while in the other “combined stenoses”? 15 were regular and 
 12 irregular. Combining the three groups, we have 63 of 127 or 
 almost exactly 50% with irregular pulses. The greater part of these 
 I believe (knowing the conditions of observation, and the character- 
 istics of internes and nurses at the Massachusetts General Hospital) 
 would not have been recorded as “irregular”? unless an absolute 
 arrhythmia or auricular fibrillation were present. Hence I think 
 we may conclude that 50% of arrhythmias (mostly fibrillations) is 
 not far from the correct figure in hospitalized cases of mitral disease. 
 But we must realize that a large number of these cases were hospi- 
 talized not for heart disease but for all sorts of medical and surgical 
 
48 FACTS ON THE HEART re 
 
 TABLE 19.—FREQUENCY OF CERTAIN SyMPTOMS IN RHEUMATIC HEART DISEASE 
 Necropsied Cases ; 
 
 ; Comb. 
 Symptoms Mitral M+A lestae Total 
 
 Cos ON Sy 
 oo nv 
 
 Palpitahom.s <a ate Maes oe 
 Vomiting 
 
 Precordial pain or distress 
 Orthopnea 
 
 Abdominal pain 
 ANGIZESEOR Ie era, Cees aes eee oe 
 Nausea 
 
 Chills 
 
 (FAS ATC OOLIC Meta tar parece oh * ate 
 Headache 
 
 Vertigo 
 
 Malaise 
 
 21 
 21 
 I 
 
 Of if eto NN bb -GA. oR O7 Oo 3 
 H O H O O H O ND HB BB 
 
 OFORO TOs Om hi Os ta One Cxasts 
 H HHH NHN BP C]OMO NN 
 
 TABLE 20.—FREQUENCY OF CERTAIN SYMPTOMS IN RHEUMATIC HEART DISEASE 
 Living: Cases 
 
 Symptoms Mitral M+A 
 
 Dyspnea 85 
 
 Palpitation 33 
 det CCOT CI ale tttlant eer teeyeemn olns, Gite ae oe 25 
 27 
 21 
 
 conditions, the heart disease appearing at necropsy as a surprise. 
 In a group of cases hospitalized for heart disease itself the figures 
 would be quite different. 
 
 This 50% represents to a considerable extent the terminal events. 
 It may be that the discrepancy between the 63 arrhythmias noticed 
 in the hospital and the meagre 38 observed by the patients as “‘pal- 
 pitation”’ represents a late onset of fibrillation. It seems more prob- 
 able, however, that minor degrees of arrhythmia, including many 
 fibrillations, passed unnoticed by the patients. 
 
 Aside from this early or never feature in the patient’s awareness 
 of his heart-beats, the other symptoms listed in Table 19 call for 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 49 
 
 little comment. The abdominal pain may represent congestion of 
 the liver. The precordial distress only once presented definitely 
 anginoid characteristics. In this case, No. 810, a patient forty-two 
 years of age, without history or physical evidence of syphilis, had for 
 three months intense squeezing and boring pain in the left chest and 
 shoulder, sometimes lasting thirty-six hours at a time. The coro- 
 naries, aorta and myocardium showed nothing remarkable at 
 necropsy. 
 
 The absence of bowel disturbances is only what experience leads us 
 to expect in all types of cardiac disease. It is nevertheless remarkable 
 that the definite and obvious congestion which necropsy almost 
 always shows in these cases should have no correlation with diarrhea, 
 with obstinate constipation, or with abdominal pain. 
 
 If orthopnea really occured but 17 times in 149 patients previous 
 to their hospitalization it is remarkable. I strongly suspect, how- 
 ever, that better history taking would have changed this figure. 
 
 PHYSICAL SIGNS OF MITRAL STENOSIS 
 
 General Physical Examination.—1. Nutrition was good or fair 
 in 65% of the uncomplicated cases. (See Table 21.) When emacia- 
 tion was present it was usually explainable by complications such as 
 malignant endocarditis, diabetes, abscess of the lung, cancer of the 
 pancreas, gullet, uterus, breast, gall-bladder, etc. The remaining 
 21% of poorly nourished patients had presumably suffered unusually 
 from loss of sleep, pain, or nausea. Sepsis may well have been a 
 factor also. 
 
 TABLE 21.—STATE OF NUTRITION 
 
 Mitral M+A Comb. Total 
 
 DOS PIVEN... sa os 
 
 2. Jaundice—(Table 35.) Only 6 cases showed icterus. Of 
 
 these one showed cancer of the pancreas, one gallstones, one cirrhosis 
 4 
 
5° FACTS ON THE HEART 
 
 of the liver. Of the remaining 3 cases, one was of the ulcerative 
 type of endocarditis, one had a terminal infection. Thus it appears 
 that in only one case out of 180 are we forced to fall back on 
 hepatic stasis and so on the mitral stenosis itself as an explanation 
 of jaundice. : 
 
 3. Cyanosis.—In slight degree this was noted in 10 out of 180 
 cases, in marked degree in 62, or 72 in all. On the other hand its 
 definite absence was noted only in 37 out of 180 cases, so that in fact 
 it may be the rule though in our records it was usually not noted. 
 
 4. Leucocytes—(Table 40.) We have studied 123 cases. Asa 
 rule only one count, made at the patient’s entrance to the hospital, 
 is recorded, though in febrile cases counts are usually recorded once 
 a week or more. Out of these 123 cases, 102 were free from non- 
 cardiac complications such as might cause leucocytosis. Among 
 these 102 there were 28 or about one-fourth which showed a leucocy- 
 tosis of over 15,000. 
 
 Correlating these 28 cases with the conditions found post-mortem, 
 we find that leucocytosis, like fever (see p. 67) was generally asso- 
 ciated with embolism and thrombosis, with complicating pneumonia, 
 meningitis, acute endocarditis, pericarditis, or general sepsis. Occa- 
 sionally no cause could be found. Sometimes acute endocarditis is 
 present without leucocytosis (nine of twenty-eight cases in this 
 group). 
 
 Cardiac Enlargement.—The data are collated in the following 
 table: 
 
 TABLE 22.—CARDIAC ENLARGEMENT 
 
 Comb. 
 
 Necropsied cases Mitral |M-+A : 
 lesions 
 
 Heart not enlarged transversely 
 
 Heart slightly enlarged transversely........... 
 Heart markedly enlarged transversely......... 
 Heart greatly enlarged transversely 
 
 Heart enlarged considerably downward........ 
 
 Living cases 
 
 Heart showing ‘‘definite enlargement” 
 Heart showing no ‘‘definite enlargement” 
 
PHYSICAL SIGNS OF MITRAL STENOSIS SI 
 
 “Slightly enlarged’? means that the apex was not over 2 cm. 
 beyond its normal position. 
 
 “Markedly enlarged’? means that the apex was 2 cm. to 4 cm. 
 beyond its normal position. 
 
 “Greatly enlarged’? means that the apex was not over 4 cm. 
 beyond its normal position. 
 
 “Enlarged considerably downward” means that the apex was in 
 the sixth, seventh, or eighth interspace. 
 
 Comment.— 1. The mitral-and-aortic cases and the “other com- 
 binations” fail to show, as might be expected, any greater frequency 
 and degree of enlargement than the “‘pure mitral” cases. Thus 60+ 
 % (20 of 33) of the mitral-and-aortic cases were “‘markedly’’ or 
 “‘oreatly’’ enlarged, as compared with 60—% (52 of 87) of the 
 mitral cases. But at the other end of thescale, 25% of the mitral cases 
 manifested no cardiac enlargement in life, while only 9% of the 
 mitral-and-aortic cases, and 18% of the ‘‘other combinations”’ 
 failed to show hypertrophy. 
 
 2. In both groups the apparent enlargement was mostly trans- 
 verse. Only 16 of 87 mitral cases, four of forty-two mitral-and- 
 aortic cases, and g of the combined lesions showed an apex impulse 
 in the sixth, seventh, or eighth space. It is contrary to the usual 
 teaching that the cases complicated by aortic disease should show no 
 more lowering of the apex impulse than the “‘pure mitral’ cases. In 
 fact there seemed to be actually less downward enlargement (5%) 
 in the “‘aortic-and-mitral”’ than in the “‘pure mitral” cases (18%). 
 But these figures are probably not significant. 
 
 _ Comparing these estimates with the facts found regarding enlarge- 
 ment post-mortem, we find the following. Clinically the heart 
 appeared to be of normal size in 25% of the necropsied pure mitral 
 cases and 15% of the living cases. At necropsy there were 16% of 
 normal sized hearts. 
 
 In the mitral-and-aortic group, 9% of the necropsied cases 
 appeared to have hearts of normal size, while in the living cases the % 
 appeared to be also g. At necropsy there were 7% in this group. 
 In the 30 combined lesions 6 (or 20%) seemed to show hearts of 
 normal size, while at necropsy there was but one out of thirty-three 
 that was free from hypertrophy, though considerably dilated. 
 
 At the other extreme the comparisons are as follows: 
 
52 FACTS ON THE HEART 
 
 PurE MITRAL 
 Markedly + (2-4 cm. out) ante-mortem = 20% of 87 cases 
 500-600 grams post-mortem = 22% of 104 cases 
 
 Greatly + (over 4cm. out) antemortem = 20% of 87 cases 
 600 grams or more post-mortem = 6% of 104 cases 
 MITRAL + AorTIC 
 
 2-4 cm. out in 30% ante-mortem 
 500-600 grams in 25% post-mortem 
 
 Over 4 cm. out in 30% ante-mortem 
 Over 600 grams in 22% post-mortem 
 
 On the whole the agreement is fairly close. 
 
 TABLE 23.—WEIGHT OF HEART AT NECROPSY 
 
 Mittal sl a eee Total 
 lesions 
 
 200-300 grams 
 
 300-400 grams 
 
 400-500 grams 
 
 500-600 grams 
 
 600-750 grams 
 
 Overi7s0. 0a nistn eee ee 
 
 TABLE 24.—HYPERTROPHY AND DILATATION AT NECROPSY 
 
 Mitral | Al Comoe 
 lesions 
 
 Hypertrophy and dilatation present........... 
 
 Hypertrophy and dilatation absent............ 
 Hypertrophy present 
 Dilatation present 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 53 
 TABLE 25.—DILATATION OF CAVITIES 
 
 Riierat | Meroe! [ee oa ler otal 
 lesions 
 
 All cavities greatly dilated 
 
 All cavities greatly dilated, right more than left. 
 
 All cavities dilated 
 
 All cavities dilated, right more than left 
 
 All cavities dilated, left more than right 
 
 All cavities dilated, auricles more than ventricles 
 
 All cavities dilated esp. right auricle & left 
 ventricle 
 
 All cavities dilated esp. left auricle............ 
 
 All cavities dilated esp. right auricle 
 
 All cavities dilated esp. right ventricle 
 
 All cavities dilated esp. left ventricle... 
 
 Right auricle and ventricle dilated. . 
 Right auricle and ventricle and left auricle 
 
 Right auricle and ventricle and left ventricle. .. 
 
 Right and left auricle dilated.. hes 
 Right and left auricle and ast) mentees 
 Right and left auricle and left ventricle 
 
 Right and left ventricle:dilated....0..0..4..... 
 Right and left ventricle and left auricle 
 Right ventricle and left auricle 
 
 Left auricle and ventricle dilated........ 
 Left auricle and ventricle and right auricle 
 Left auricle and ventricle and right ventricle... 
 
 Left auricle alone 
 Right auricle alone....... 
 
 Left ventricle 
 
 No dilatation present........ 
 
 1660—(Mitral-aortic-and-tricuspid) extreme dilatation of auricles, right ventricle 
 also dilated, left contracted. 
 303—(Pulmonary Stenosis) three cavities dilated, especially right auricle. 
 3945—(M-A-Stenosis) three cavities dilated, especially left ventricle. 
 Heart Weights —What can we conclude from Table 23? 
 The obvious and outstanding fact is that mitral stenosis produces 
 less hypertrophy when alone than when it is linked with similar 
 
54 FACTS ON THE HEART 
 
 disease in other valves. There are fifteen small hearts in 107 cases 
 of pure mitral disease, or 14%, and there are forty-seven (including 
 these fifteen) which are not much enlarged, 43%. In the mitral- 
 and-aortic cases only 27% fall in the corresponding group and in 
 ‘other combinations” only 18%. 
 
 At the other end of the scale there are very few “pure mitral” 
 hearts weighing over 600 grams, (6%) while in the mitral-and-aortic 
 cases 25% of the hearts weighed 600 grams or more. 
 
 Yet on the whole the differences are Jess striking than might have 
 been expected. Only at the extremes is there a striking contrast. 
 
 Table 24 however makes these differences considerably sharper. 
 If we take into account the relation of heart-weight to the size of 
 the whole body, as is done in deciding whether a heart is hypertro- 
 phied or not, it appears that in eighteen of 107 pure mitral cases hyper- 
 trophy was absent. This is 16%, or nearly one-sixth of all cases. 
 In the mitral-and-aortic cases the corresponding percentage is but 
 7%, and in the “other combinations” zero. 
 
 General Dilatation (in 35 to 40%).—As regards the dilatation of 
 the several heart chambers Table 25 shows on the whole surprisingly 
 little preponderance of right-sided change. In seventy cases out of 
 180 rheumatic valve lesions of all sorts, the dilatation affects all the 
 chambers alike. This is 39%. In the pure mitral cases the per- 
 centage of general dilatation is thirty-five—not much less. 
 
 Preponderance of Dilatation (Table 25).—When there is any differ- 
 ence between the two sides of the heart in respect to the amount of 
 dilatation, the right side is more dilated in 40 cases out of 180,-the 
 left side in 21. Taking the pure mitral cases alone, the correspond- 
 ing figures in 104 cases are twenty-five and twelve. 
 
 Lop-sided Dilatations—When the pathologist finds no general 
 dilatation but certain chambers picked out by the disease, *‘ pure mitral” 
 is usually the lesion. ‘Thus there are thirty-four of these lop-sided 
 dilatations in the 107 ‘‘pure mitral”’ cases, only four in forty mitral- 
 and-aortic cases, and six in the thirty-three “other combinations.” 
 
 The favorite specialization of the dilatation in ‘‘pure mitral” 
 cases is in the right auricle and ventricle with the left auricle (ten 
 cases), next in the right and left auricle (7 cases), and next in the 
 right auricle and ventricle (five cases). Jn all these groups the left 
 auricle is included thirty-two times, so that it seems to be the chamber 
 hardest hit. But the right auricle (thirty-one times) is a very close 
 second. 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 55 
 
 When all cavities were dilated the right side was more stretched 
 than the left in ten cases and the left auricle more than the right in 
 only five. | 
 
 On the whole, then, these observations, accurate and reliable 
 as we have every reason to believe, show that in the “‘ pure mitral” 
 cases there 1s very little preponderance of right-sided dilatation, while 
 in the “combined valve lesions” right sided preponderance was more 
 striking than in the pure mitral cases. 
 
 TABLE 26.—CARDIAC MuRMURS 
 
 Combined 
 
 Mitral : 
 lesions 
 
 Necropsied cases 
 
 oP TOG ae aa an De 
 
 No murmurs L206 30% 
 Systolic murmur only 7 or 18% 
 Presystolic murmur only... Lor 2% 
 Presystolic + Systolic.... 3 or 7% 
 Systolic + Diastolic 10 or 25% 
 Mtwee MULMUIS A. 6 or 15% 
 Diastolic only lor 2% 
 
 12 or 36% 
 6 or 18% 
 5 or 15% 
 
 1 ae UE seer Rae nee 33 
 
 TABLE 27 
 
 Mitral Private 
 
 Living cases 
 
 APT IAUES ce sale. ate 
 
 Systolic murmur only 
 
 Presystolic murmur only... 
 
 Diastolic murmur only.... 
 Presystolic & diastolic 
 Presystolic & systolic 
 Diastolic & systolic 
 
 3 murmurs....... 
 
 POUA ER ess wane te eas 
 
 4% 
 7% 
 34% 
 4% 
 19% 
 18% 
 1% 
 13% 
 
 30r 3% 
 Ir or 12% 
 10 or 11% 
 17 or 19% 
 35 OF 39% 
 oor 0% 
 30r 3% 
 Io or 11% 
 
 89 
 
 (mitral) 
 
 5 or 7% 
 5or 7% 
 25 or 37% 
 oor 0% 
 13 or 19% 
 17 or 25% 
 ror 1% 
 Ofer 
 
 Comments. 
 
 Cardiac Murmurs.—1. The 45% of necropsied pure mitral cases 
 in which presystolic or diastolic murmurs were heard at or near the 
 apex corresponds closely with the 48.5% in which the diagnosis of 
 mitral stenosis was made during life. 
 
 a 
 
56 FACTS ON THE HEART 
 
 2. We know that in many cases of mitral stenosis a systolic 
 murmur at the apex is all that we hear uwuless we stir up the heart and 
 bring out the presystolic or diastolic by exertion (or by a drug like 
 amyl nitrite), or listen carefully for a mid-diastolic in the recumbent 
 position. This we should be unlikely to do unless we suspected 
 the presence of the stenosis. In many cases of this series (surgical 
 cases) there was no such suspicion. . But such suspicions should be 
 aroused (as apparently they were not in fifty-four of these cases) : 
 
 (a) By any history of rheumatism or chorea. 
 
 (b) By an unusually sharp, slapping or thumping quality of the 
 first heart sound. 
 
 (c) By the “explosive” quality of the systolic murmur. 
 
 (d) By the absence or feebleness of the second Bier sound at the 
 apex and in the second right interspace. 
 
 (e) By the doubling of the second sound in the pulmonary area, 
 at the apex, and along the left sternal border (third heart sound). 
 
 (f) By the age of the patient (youth). 
 
 (¢) By the evidence of auricular fibrillation, decompensation, or 
 passive congestion not otherwise explained. 
 
 In the necropsied mttral-and-aortic cases a presystolic or diastolic 
 murmur was heard in 21 out of forty (or 52%) so that our diagnostic 
 average was higher than in the pure mitral cases. As a rule we 
 heard in this group either a systolic murmur alone (18%) or no mur- 
 Mit atealle 3007). 
 
 In the ‘‘other combinations,”’ though their total is but 33 cases, 
 we did rather better, recognizing a presystolic or diastolic murmur 
 in 71% of them, a systolic only in 21% and no murmur in the 
 remainder. But of the multiplicity of the lesions we had no idea. 
 In the whole group of 180 cases our success in recognizing some mitral 
 lesion appears to be expressed as 50%. 
 
 To explain the 50% of failure we may say that: 
 
 In the present group of cases there were many elderly and 
 moribund patients without rheumatic or choreic histories, patients 
 entering the hospital for surgical or other non-cardiac complaints. 
 
 Heart Sounds.— Moreover our records show that the suggestive 
 changes in the heart sounds (see 0, d, and e above) often most helpful 
 (in that they lead us to search for a presystolic or diastolic murmur, 
 at rest in the recumbent position or after physical or pharmacal 
 stimulation of the heart) were not often looked for at all in this 
 group of cases. Thus there is no record whatever of the quality of 
 the apical first sound in 74 out of 107 “pure mitral” necropsied 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 57 
 
 cases, and in 30 out of forty mitral-and-aortic cases. In other words 
 this suggestive sign of mitral stenosis (“‘sharp first sound’’) was 
 ignored in 34 of the examinations. 
 
 Doubling of the 2nd sound at the or along the left sternal margin 
 (third heart sound) was apparently not looked for. 
 
 TABLE 28.—HEART SouNDS (NECROPSIED CASES) 
 
 Necropsies Mitral |M-+A 
 
 First sound sharp 
 
 First sound accentuated 
 
 First sound loud 
 
 First sound thumping 
 
 RUMOUR FOULS oo. 5 io bin ck 5 a sdtarh # one Dene Oe ees 
 First sound not clear 
 
 First sound valvular 
 
 BEEN AIIDULG. 3 oh) is sa cacns Re 
 First sound not heard 
 
 First sound snapping 
 
 First sound negative or no record............. 
 
 H HH AH SB NY HR 
 
 2d at apex present 
 
 2d at apex absent 
 
 2d at apex diminished 
 
 em ACEC DY TMUTINUT ya 5..84'c 20, bs ale Me eect cs 
 ERE C COLO COs od tety wie 8p. OR win eine eee 
 
 A comparison with the living cases (though of course their diagno- 
 sis is never certain) shows what, with expectant attention, one might 
 have heard in most of the cases coming to necropsy. Thus in 134— 
 or 89% out of 150 pure-mitral cases—examined in life by me, the 
 first sound at the apex was “‘sharp”’ or accentuated, and in only 
 fourteen was it normal, diminished or absent. 
 
 In the mitral-and-aortic living cases this sign was not so fre- 
 quently present. 63 out of 89 (70%) showed an accented first sound, 
 while in twenty-one it was normal or absent. 
 
 Accentuation of the pulmonic 2nd sound was present in 60 out of 
 150. 
 
58 FACTS ON THE HEART 
 
 TABLE 29.—HEART Sounps (LivING PATIENTS) 
 
 Heart sounds Mitral | M+ A 
 
 First sound sharp or | 
 First sound accentuated J 
 First sound doubled 
 
 First sound Absentic i.) semua ete cay.) oun 
 First sound normal 
 
 2d at apex present 
 
 2d at apex absent 
 
 2d at apex doubled 
 
 2d at apex diminished........ 
 2d at apex not recorded 
 
 Aortic 2d doubled 
 
 Aortic 2d accentuated....... 
 AGrticvedediminished tne a. aceas the eee c Cee ae ee 
 Aortic 2d absent 
 
 Aortic 
 
 Aortic 2d questionable 
 
 Aortic 2d not recorded 
 
 Pulmonic 2d greater than Aortic 2d......... 
 
 Aortic 2d greater than P2 
 
 Pulmonic 2d equal to A2 
 
 Pulmoniesd and “Ava bsenit fig ot cb elecs ae tar Pee ee 
 Pulmonic 2d not recorded 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 59 
 
 Doubling of the 2nd sound to the left of the sternum—or a third 
 heart sound—(I cannot always distinguish these if, indeed, they are 
 different) was present in 83 out of 150 living patients. 
 
 Diminution or absence of the 2nd sound at the apex I noted in 
 36 out of 150 cases. 
 
 Our records in the necropsied cases are woefully meagre as regards 
 that very helpful confirmatory sign, doubling of the second sound (or a 
 third heart sound) to the left of the sternum. In only six of ro4 
 necropsied mitral cases, and four of the 40 mitral-and-aortic cases 
 was any attention paid to this sign. Yet as already stated I believe 
 that this is a much more common and valuable sign than accentua- 
 tion of the pulmonic sound. It was noted in 55% of the living pure 
 mitral cases. 
 
 The same is true of a third helpful sign, the weakening or oblitera- 
 tion of the apical second sound. It was noted as weak or absent in only 
 thirteen cases out of 149, and present in five cases. In the remaining 
 131 cases, 87%, the whole matter was ignored. I believe from clinical 
 experience that this sign grows more and more frequent as the case 
 progresses in severity, i.e. as decompensation increases. In the 
 moderately or entirely compensated pure-mitral cases seen by me in 
 private or out-patient practice, 36 out of 150 or 26% showed this 
 change. 
 
 Accentuation of the pulmonic second sound is a sign which I have 
 found of little value in the diagnosis of mitral disease or indeed of 
 any other disease. 
 
 Of the living cases in only 40%—a small minority—could I find 
 any distinct accentuation. The frequency and value of this sign 
 has certainly been much exaggerated. I regard it as rather rare in 
 ambulant cases. 
 
 The diastolic murmurs in these mitral cases are sometimes early 
 diastolic but more often mid-diastolic. They are the rule in the 
 moderately advanced and far advanced stages of the lesion, while 
 presystolic (or /ate diastolic) murmurs are what we expect (at any 
 rate after exertion) in the earlier stages of the lesion. Some very 
 early cases show only a mid-diastolic obtained best after rest in the 
 recumbent position. 
 
60 FACTS ON THE HEART 
 
 TABLE 30 
 
 Palpable Thrill 
 
 In 183 ambulatory mitral cases there was a thrill in ninety-three or 50%: 
 
 CASES 
 
 Thrill feltebest-at- apex an) 3), /0 2. . ess fois yee ee 57 
 Thrill felt best atjapex, extending to aortic, 225 94, ie ene 
 Thrill felt best at‘apex, extending to base of heart.) 7) ae I 
 Thrill felt.at aortic-areaalone., : 5.0.15 5552 aes ee I 
 Thrill felt at*palmonicaréa alone... >. 2.5 ae. se oe I 
 Noirecord. Of place 22.74. west: sents sk tn ae te eee 32g 
 Thrill felt. during presystolie period... ..: 0.45. Gee 67 
 Thrill felt-durine systole alone... .>..: ..am(s5 ee te 6 
 Thrill felt“during ‘diastolealones.< ).c.c.te. oe ee ete ee 6 
 
 ING TECOTALOTAMIMEN ts caa cacy wre eicsh itn: Shige ARE ieee T42.%03 
 
 In 89 ambulatory mitral-and-aortic cases twenty-six showed thrill: 
 CASES 
 a rill felttine Renee 0 Soe 1A a eee 24 
 Doublerthrill felines sscex hine fae eis ae ee 2 226 
 Systolic and: presystolic at apexss:.\. cues oe eee I 
 Systolicrat Apex cic. seers tea cba hs kya Mines I 
 PresystohiGatia pex mecat tyxctuest GS $0. ka eae Gee sip he 8 
 Presystolicat apex, systolic at.aortic areas:.: 2.00. «eee ee 
 Diastolee rata pex: ty sie mte Lsciee say, i aie lant ge ee eee 2 
 Diastolic at pulmonic area. 07.5. 2 oa ne amen es I 
 Diastolic no*record of ‘place, 20.0... 2 eaeort ad I 
 Systolic teortic cm. sence ceo wel « aise 1 uses OR de 9 
 Systohcing Tecords0l/ Placa. -auinn t) totus a oe ee ee “2 
 rm 
 
 Thus in 119 out of 272 ambulatory cases the diagnosis rested in 
 part on the presence of a purring thrill palpable after exertion or at 
 rest. Ina few cases (fifteen) this thrill was not confined to the apex 
 region but could also be felt at the base of the heart. I suppose this 
 variation depends chiefly on how violent the vibrations are. 
 
 The Pulse.—Out of 107 necropsied ‘‘pure mitral”’ cases our records 
 are of some value in sixty-seven. Of these twenty-six showed regular 
 pulses, most of them small in volume and of low tension* but a good 
 many entirely normal in all respects. There is no characteristic pulse 
 of mitral disease. 
 
 Forty-one were arrhythmic, and of these thirty-eight are described 
 so that it is probable that absolute arrhythmia, and so auricular 
 fibrillation, was present i.e. in about 50% of the well-recorded cases. 
 
 * Two are described as of high tension. 
 
" PHYSICAL SIGNS OF MITRAL STENOSIS 61 
 
 The three remaining are called “intermittent”? and may have repre- 
 sented other types of arrhythmia. 
 
 In three cases the word ‘‘Corrigan”’ is used, and twice a capillary 
 pulse is recorded. These cases are of special interest because we 
 know that no chronic aortic disease, no arteriosclerosis, or hyper- 
 thyroidism was present. In one case the pulse is easily explained by 
 the presence on the aortic valve of large fresh vegetations which 
 probably caused regurgitation. In another chronic pericarditis, that 
 universal confuser of all circulatory signs, was present. The third case 
 was not accounted for. 
 
 Comparing the pulses in the two groups of cases in Table 31, it 
 seems that arrhythmia ts nearly twice as common in the pure-mitral 
 cases as in the mitral-and-aortic. Why this is so I have no idea. In 
 the mitral-and-aortic cases the regular pulses greatly out-number 
 the irregular by 2 to 1; in the “other combinations” also the regular 
 pulses are slightly but definitely in the majority. It would seem to 
 follow, if these figures are correct, that “‘pure mitral”’ disease is more 
 apt to be associated with arrhythmia than any of the more com- 
 plicated lesions. 
 
 The Corrigan Pulse in the mitral-and-aortic series was noticed 
 only ten times or 22%. ‘This figure is of considerable interest. It 
 shows (if the clinical records are correct) that when we are in doubt 
 whether or not an aortic lesion is present beside the recognized mitral 
 lesion, we cannot often count on the Corrigan pulse as an indication 
 of aortic disease. In four-fifths of the cases the associated stenosis 
 at the mitral (and usually at the aortic) valves prevents the pulse 
 from jerking and collapsing. 
 
 TABLE 20-2 HE PULSE 
 
 - Necropsies 
 
 Other 
 Mitral M+A combi- 
 
 nations 
 
 Regular 
 BELAY eee ee ev os rig sk Once eas ea be 
 
 ISS: hea ees on oe gre 5 a 
 Capillary 
 
 High tension 
 
 PEP ATUENSION® oy ates fd eo eke 
 Fair tension 
 
 RereNEACA LOTISION A, GaN haces a Oo Rae 
 
62 FACTS ON THE HEART 
 TABLE 32.—LIVING CASES 
 
 Pure-Mitral and Mitral-and-Aortic* 
 
 Corrigan 
 Capillary 
 
 Pistol shot 
 Durdziers: 5.0. eee ee 
 Waterhammer....%.;..... 
 Normalior n0-tecord 4504. 3ee 
 
 TABLE 33.—CONDITION OF THE ARTERIES 
 
 Necropsied cases Mitral 
 
 Palpable 
 
 Thickened, brachials tortuous 
 Palpable and sclerosed 
 
 Not palpable 
 
 Bounding, not palpable 
 
 No record 
 
 Blood Pressure.—Nothing definite or characteristic can be made 
 out. It is noteworthy, however, that the presence of mitral stenosis 
 does not prevent very high pressures in cases complicated by chronic 
 nephritis. Thus in Case 3283 (complicated by glomerulonephritis 
 
 TABLE 34.—BLOOD PRESSURE 
 Living Cases 
 
 Mitral (59 measured). 
 Highest diastolic pressures: 155, 120 (2), 115, 110 (2), 105 (3), 100.... 10 Cases 
 Highest systolic pressures: 210 (2), 195, 185, 180 (2) 6 cases 
 Highest pulse pressures: 105, go. 
 
 Mitral-and-aortic (45 cases measured). 
 Systolic blood pressure 100-120 14 cases 
 Systolic blood pressure 120-130 13 cases 
 Systolic blood pressure 130-140 g cases 
 Systolic blood pressure 140-150 2 cases 
 Systolic blood pressure 150-160 6 cases 
 
 Brachial *1 20/36, popliteal 100/20. wn: Ws; Bee eye atte sao ie oe 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 63 
 
 in a patient of twenty-three) pressures of 210/130, 220/130, 280/110, 
 and 210/140 were recorded during the twelve days of his life in the 
 hospital. The mitral orifice measured eight cm. and showed a well 
 . marked stenosing deformity. 
 
 In another mitral stenotic patient dying at sixty-four of a cerebral 
 hemorrhage with complicating pneumonia, the systolic pressure 
 reached 175. In thirty other valve lesions there were only six records 
 of systolic blood pressure ranging from 105 to 180, with three records 
 of diastolic pressure, 50, 65, and 80. 
 
 The living patients illustrate the same point. 
 
 Hoarseness and Aphonia.—Only one of the cases here analyzed 
 necropsy 3422 showed during life either of these symptoms, though Dr. 
 Paul D. White* has shown them to be not infrequent clinically in 
 mitral cases which did not happen to come to necropsy. Probably 
 poor observation accounts for this discrepancy. 
 
 TABLE 35.—PoST-MORTEM EVIDENCES OF PASSIVE CONGESTION 
 
 107 cases 40 cases 33 Cases 180 cases 
 
 + Present | 
 
 PA bent Mitral Other comb. Total 
 
 + + 
 
 ByANOSIS..... 80555 
 
 MIME, la ate a ops 
 WetaSaTCAs sm. «'s 
 
 Hydropericardium 
 
 Pav TOUIOTAX. 1. 3... 6). 
 
 Ascites 
 
 OTHER 
 Mitra. M+ A Comes. Torta 
 us lahitebdoysotong: beh bal deh hese 5. a eter lrg rr ery 6 Six nC eCart 8 3 3 14 
 PMI TOLMOTAK a lent ame. Wyeast ecsud ist silos oj areicledebee ebeus eve setae 6 2 2 Io 
 iva roohOrax maOUDlE raat a Matters cs a ntete eeLMebe oes 30 14 8 52 
 Reerornoras, Nidca Nos stated)... cn. sy Coen Meads pen > 3 3 
 
 79 cases. 
 
 * Paralysis of the left recurrent laryngeal nerve associated with mitral stenosis, 
 Paul D. White, M.D. and Joseph Garland, M.D., Archives of Int. Med., Sept., 1920, 
 Vol, 26, p. 343. 
 
64 FACTS ON THE HEART 
 
 Evidences of Passive Congestion at Necropsy.—Anasarca was 
 recorded twenty-two times in the 107 pure mitral cases and four 
 times in the 40 mitral-and-aortic cases. 
 
 Hydropericardium was recorded twenty-seven times in ing 107 
 mitral cases. In the other cases we have no record. 
 
 Hydrothorax forty-five times in the 107 mitral cases and 19 times 
 in the 40 mitral and aortic. Thus the two series show no significant 
 difference in the % occurrence of this symptom. Aortic disease 
 when added to mitral disease neither increases nor diminishes the amount 
 of terminal pulmonary congestion produced by mitral disease alone. 
 
 What seems most surprising in these figures is that 56% of the 
 cases Show no hydrothorax at all! 
 
 In the positive cases the fluid was confined, or largely confined to 
 the right chest in fourteen cases and to the left in ten cases—a 
 discrepancy favoring the right side less than clinical observation 
 would lead us to suppose. 
 
 In nineteen out of forty cases the hydrothorax was not recognized 
 in life. Part of this error may be due to a reluctance to disturb dying 
 patients in order to establish a fact which is of little or no use to prog- 
 nosis or treatment. Twice hydrothorax was diagnosed in life but 
 not found at necropsy. Four times we found it in life only on the 
 right side while the pathologist found it on both sides. 
 
 Ascites was also rather surprisingly infrequent in both mitral 
 and mitral-and-aortic cases. It was present in thirty-five of 107 
 mitral cases and 17 of 40 mitral-and-aortic cases,—practically identi- 
 cal fractions, each representing about one-third of the group. In 
 the ‘‘combined lesions’”’ it was twice as frequent (20 of 33). 
 
 In two-thirds of all cases the ascites was recognized in life. In 
 the remainder we missed it. In four cases we “‘found”’ ascites when 
 it was not there. 
 
 The spleen was firm and elastic at necropsy in 68 cases, soft in 33 
 out of a total of ror cases in which a definite observation is recorded. 
 Thus two-thirds show passive congestion and one-third suggest 
 infection. In life the spleen was felt but five times in 144 cases. 
 In one of these five, infarction was found at necropsy. 
 
 These cases seem to show that as a rule death does not occur in 
 mitral disease by means of decompensation and passive congestion. 
 
 When “pure mitral” disease is itself the cause of death, decom- 
 pensation is usually present. But mitral disease is often present 
 not as a cause of death but as an historical landmark, harmless so far 
 as we know, to the individual. In our series this was the case 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 65 
 
 in 60 cases out of 107— or nearly three-fifths—an astonishing result. 
 (Further analysis of the non-congestive deaths is given on page 77). 
 
 How Explain the Cases without Dropsy.—Sixty of 107—or 36 
 of the pure mitral cases died without any hydrothorax and with little 
 or no dropsy elsewhere. In most cases this fact is explained by the 
 fact that compensation was good to the last, the patients dying of 
 embolism and thrombosis (ten), pneumonia (five), sepsis (five), acute 
 endocarditis (four), general peritonitis (four), cancer (four), apoplexy 
 (three), meningitis (two), leukemia, uremia, and hemorrhage, each 
 one. In four cases death was unexplained. 
 
 In the 40 Mitral-and-Aortic cases, 21 or over half showed no 
 hydrothorax; among the “‘combined lesions,” 18 of 33 were also free of 
 hydrothorax. 
 
 TABLE 36.—CONDITION OF THE LIVER IN LIFE 
 
 107 cases 40 237 Comps 180 
 mitral M+A lesions total 
 
 Liver enlarged (felt below ribs) 14 19 
 Setetetitcss alsO. 11)... . 42.) sees ce 2 (9) (8) 
 Not demonstrably enlarged 17 10 
 0 Tete) ss [o's I 9 4 
 
 TABLE 37.—CONDITION OF THE SPLEEN *AFTER DEATH 
 
 107 40 33 comb. 
 mitral M+A lesions 
 
 Beemer. TUDDEry) (sf. ass 4" 
 
 RESO Leer teri Pts yn so 5. Peyote. 
 Bers reASLOT INA Lge aed wy he ars, eS 
 Bae TIVETST PEC aie fete eit arated Vo was 
 Spleen not recorded 
 
 Condition of the Liver.—The figures in Table 36 seem to show that 
 during life hepatic enlargement is obvious in slightly under one-half 
 of the pure mitral cases, over one-half of the mitral-and-aortic cases 
 and nearly 24 of the ‘‘other combinations.”’ 
 
 The decompensating power of multiple valve lesionsis very slightly 
 greater than that of mitral stenosis alone. This is only what we 
 should expect and bears out what is shown in the post-mortem records 
 of passive congestion (Table 35). There we see that hydrothorax 
 
 is produced by pure mitral disease in 42% of cases, by mitral and 
 5 
 
66 FACTS ON THE HEART 
 
 aortic disease in 47.5%, and by the ‘‘other combinations” in 45%. 
 Ascites occurred in 33% of pure mitral cases, in 42.5% of mitral-and- 
 aortic cases, in 40% of “‘other combinations.” The records of 
 hydro pericardium are incomplete. 
 
 The Spleen.—The necropsy record of a firm and ‘‘rubbery”’ 
 spleen represents passive congestion. Enlargement is mentioned in 
 only six cases and is relatively slight, especially in length and breadth, 
 although the organ is often plumper than normal. Its lack of longi- 
 tudinal enlargement accounts for the fact that in heart disease we 
 can so rarely feel its tip during life unless an infarct is lodged there. 
 
 The soft spleens are usually associated with acute endocarditis or 
 other septic complications. 
 
 Urinalysis.—The cases showing definite glomerulonephritis and 
 those associated with renal infarcts are collated in Tables 42 and 45 
 which show that about 14 of all cases of mitral disease (‘“‘pure” or 
 complicated) are associated with nephritis of some type. In 4o 
 uncomplicated cases eight showed normal urine and thirty-two 
 showed albumin and casts. In only four of these thirty-two was the 
 albumin or the casts in unusual amount, i.e., more than the traces 
 of albumin and the few hyalin and granular casts to be expected as 
 a result of passive congestion. ‘These four cases showed the following: 
 
 TABLE 38.—URINE IN PASSIVE CONGESTION DUE TO MITRAL DISEASE 
 
 Pathological state Albumin Casts 
 
 Simple passive congestion Large trace | Many 
 Simple passive congestion Many 
 Meningitis as complication Many 
 General peritonitis as complication Slight trace | Many 
 
 Comments —Considering these cases in connection with those 
 complicated by definite nephritis, it is obvious that urinary examina- 
 tion does not enable us to distinguish nephritis from the conditions 
 accompanying (a) passive congestion of the kidney, (b) acute infec- 
 tious diseases with cloudy swelling of the kidney. This conclusion I 
 proved many years ago* but until recent years it was been unfash- 
 ionable in medical circles to admit it. 
 
 * Cabot, R. C.: The Diagnosis of Renal Functions, N. Y. Med. Journ., May 12, 
 1906. 
 
PHYSICAL SIGNS OF, MITRAL STENOSIS 67 
 
 Fever.—Fever was present (continued or remittent) during most 
 or all of the hospital stay of seventy-six out of 180 patients (see 
 Table 39). The probable explanation in 55 cases was as follows: 
 
 Peetcormolicating pHeuUmMonia...22..c0.-- yess ss s.. OT 
 DPPPETITRONCOCAPCILIS: 6.0 ele Piece eves oa vas ro (or possibly rr) 
 MUIR CLS tae Opts Bees SY chatter hehite wits Bohs 4 
 BPEL AI SOD SIS Weta) aide «AS cect toed x toe Sida 12 
 MME MeT LIS. pdt yee ne oi ere Sauit beth ew Des 3 
 6. General peritonitis, arthritis, leukemia, uremia, 
 PURO CACM PONG weit boku es oe ei i: 
 55 
 
 Thrombus—F ever. —In addition to these there remains an interest- 
 ing group of thirteen cases in which nothing was found post-mortem 
 to explain fever except thrombz, embolt, fresh infarcts and their results. 
 In six of these the thrombi were confined to one or both auricular 
 appendages (the left in five). This association of thrombi with 
 fever may not be a causal one. Certainly thrombi are sometimes 
 associated with bacteria. In other cases the disintegration of a clot 
 might cause a protein fever. On the whole it seems not improbable 
 that ball thrombi or other clots in the auricles are part of a process 
 which not infrequently causes fever. 
 
 TABLE 39.— TEMPERATURE 
 
 Temperature Mitral M+A 
 
 Subnormal 
 Dorma. (under 00). isi ih. eek. 
 
 ETLONLOS 22h n.d: 
 RLTARLOA Witte afi ek NAY Fs Fe Yon 
 Peeree Not, Tecorded........5..%... 
 
 Ordinarily when an unexplained fever arises in a case of valvular 
 heart disease we begin to speculate on the possibility of acute endo- 
 carditis, and regard this possibility as strong if embolic phenomena 
 subsequently appear. But from this series of cases it appears that 
 unexplained fever in cardiac cases is associated as often post-mortem 
 
——— 
 
 68 _ FACTS ON THE HEART 
 
 with intracardiac clots or visceral infarcts as it is with fresh valvular 
 endocarditis. 
 
 Leucocytosis.—Leucocytosis usually accompanied these fevers 
 of all types. There was nothing of special interest about it in these 
 cases except that in eight out of twenty-one “‘acute”’ cases of endo- 
 carditis leucocytosis was absent. 
 
 TABLE 40.—LEUCOCYTE COUNT 
 
 Leucocytes Mitral M+A One Total 
 comb. 
 
 O- 5,000 
 6,000— 7,000 
 8,000- 9,000 
 10,000-I 1,000 
 I 2,000—1 3,000 
 14,000-I 5,000 
 16,000-1 7,000 
 18,000—-19,000 
 20,000- 21,000 
 2 2,000-30,000 
 31,000-50,000 
 Slight leucocytosis 
 Moderate leucocytosis............. 
 Marked leucocytosis 
 
 2. 2 
 I oo 
 2 4 
 Zz, I 
 3 4 
 2 3 
 3 I 
 2 
 
 3 
 
 TABLE 4I 
 
 Mitral M+A 
 
 Total scases an ethe cat oe tres eee 83 135 
 
 Of these there was leucocytosis in 66 105 
 or 80% 
 
 No cause for leucocytosis outside the 
 heart in : 13 89 or 85% 
 
 _ Comments.—t1. In terminal stages, from two-thirds to four-fifths 
 of the cases in each group showed fever. 
 
 2. In one-fifth of the cases this fever might be explained by the 
 acute endocarditis found post-mortem. Other common causes are 
 pneumonia and general sepsis. 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 69 
 
 3. In the remainder thrombosis occurred thirteen times, leaving 
 two cases with fever quite unexplained. Thrombosis thus appears 
 to be associated with most of the “unexplained”’ fevers of mitral 
 disease. 
 
 4. Nearly four-fifths of all cases showed a leucocytosis, particu- 
 larly marked in the “combined lesions.” The cause of this 
 -leucocytosis was usually within the heart (clot or endocarditis). 
 
 Infarction of the Kidneys, Lungs, and Spleen.—Whatever the 
 precise cause of infarcts, however they are related to embolism, to 
 thrombosis, or to simple passive congestion, the data of these necrop- 
 sies regarding them may well be presented here (Table 42). 
 
 TABLE 42.—INFARCTS 
 
 Infarcts in the Mitral M+A 
 
 39 
 33 
 
 23 
 
 Total no. of cases with infarctions in 7 19 20 96 
 these organs. (of 107) (of 40) (of 33) (of 180) 
 
 From these figures it is clear that: 
 
 (1) In 57 out of 107 cases infarctions were present, ordinarily of 
 the lungs, kidneys, spleen or liver. 43 of this 57 were in uncom- 
 pensated cases with general dropsy and congestion. Only 14 occurred 
 in well compensated, non-congestive cases. 
 
 (2) Infarcts occur in 19 out of 4o or about 1% the “mitral-and- 
 aortic cases and in 20 of 33 or 43% of the “‘other combinations.” 
 
 (3) Infarcts are slightly commoner in the kidneys than elsewhere, 
 perhaps because they are easier to see in this organ than in the lungs. 
 
 The Diagnosis of Infarctions 
 
 Pulmonary infarction one may recognize clinically in about one- 
 third of the cases, those namely in which it leads to an hemoptysis 
 not otherwise explained. This was the case in nine out of the thirty- 
 three well-studied “‘pure mitral’’ cases. In one of the cases there was 
 also sharp pain in the right side of the chest at a point corresponding 
 
7O FACTS ON THE HEART 
 
 with the position of the infarct. In the other twenty-four the 
 infarcts were not and probably could not have been recognized. 
 
 Infarct of the kidney was known to be associated in one case out of 
 thirty-nine with a sharp pain in the right hypochondrium, which led 
 to a guess that infarction had occurred. ‘The urinary findings in the 
 cases Showing infarction post-mortem were in no way characteristic 
 or suggestive. Four cases showed only the “slightest possible 
 trace”? of albumin, four others a “slight trace”? with casts, one a 
 “large trace” alone, and one a large trace with casts, but this latter 
 case had also a general peritonitis. It is entirely reasonable that the 
 urinary findings should not be characteristic, for the infarcts found 
 post-mortem were of all ages. Only a fresh infarct could be expected 
 to produce hematuria and that for a brief period alone. 
 
 Splenic infarct was suspected in two cases out of the 42 in which it 
 was found post-mortem. In one of these there occurred on three 
 occasions a sharp sudden pain in the splenic region without any other 
 assignable cause. In the presence of decompensated valvular disease 
 such pain might naturally suggest infarct. 
 
 TABLE 43.—EMBOLIC AND THROMBOTIC LESIONS AT NECROPSY IN 180 CASES 
 
 Embolism and Thrombosis in Mitral | M+A mite Total 
 comb. 
 1. Heart. 
 Left-auriculan appendage, swe. ne ae a5 4 2 ay 
 Both appendages: ances Fel cn ee f ° fe) 5 
 Ball thrombus, left auricle..... 4 ° ° 4 
 Other thrombi deit-sunclies ye ee. ee ae 2 I ° 3 
 Right auricular appendage... ....«:.<% 4. - 2 fe) 2 - 
 Place\not stated’ orem. tera” . ee 3 3 
 Left) ventricle; te clatter ee ° fe) fo) fe) 
 Total carhacthrombinn eaves. ane. ae, ye 28 5 8 41 
 2 PULINOUGTY BESSELS et eres tye a ee A 9 I ° 9 
 5.2 Ore DEEP AL CCS SCS enema Relies lo, 2, «ecu: 7 2 fe) 9 
 A Cerebral pessels 2 oir intern. Whe ote! ise eee I 2 I 4 
 5. Kidney vessels....... I I fe) 2 
 ON SD PlCeh MOSSES), Wee Thee Cea eae taste is ae I I fe) Rie 
 7. J LVUCT VESSELS ci Gk Re EE Oe tis eRe fo) I ° I 
 SS (nsestinal: Bessclse aw es es ee Os ahah See I fe) fe) I 
 O.-Lnnaminale very oe pete arte. ade. ee I 
 
 | 
 | 
 | 
 | 
 
 Total lesions 733 ste ea et ae 
 
 ft 
 \O 
 — 
 i) 
 Ke) 
 Ov 
 \O 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 71 
 
 In a third case, a spleen which turned out to contain an infarct was 
 palpable during life, but no suspicion of the infarct was aroused, nor 
 should it have been suspected, since infarcts often do not enlarge the 
 spleen and other causes of splenic enlargement could not here be 
 excluded. But it has been my experience with necropsied cases not 
 included in this series that when a spleen has been observed during life 
 to grow notably larger within a few days, the diagnosis post-mortem is 
 always infarct. Leukemic and “infectious” spleens grow more 
 slowly. 
 
 Comment.—The well known tendency for thrombi to form in the 
 left auricle when its outlet is blocked by mitral stenosis and its current _ 
 is slowed by auricular fibrillation, receives abundant illustration in 
 these necropsies. In the presence of an advanced case of mitral stenosis 
 with fibrillation, we must realize that the chances of intracardiac 
 thrombosis are one in four and that in over go% of these cases this 
 thrombus will be in the left auricle. The danger of detaching this 
 clot when we stir up the previously passive and fibrillating auricle 
 with quinidine has been recently emphasized by Paul D. White and 
 others. Cerebral embolism and death have been thus produced. 
 
 Next to the heart, the lungs, the brain and the peripheral vessels 
 are oftenest involved. 
 
 Clinical Evidences of Embolism or Thrombosis.—1. Cerebral 
 (13 cases).* In eleven of the 104 “pure mitral” cases, and in two of 
 the “‘mitral and aortic” cases there were signs and symptoms point- 
 ing to a focal brain lesion. 
 
 In ten of these 13 cases a sudden hemiplegia was the central fact. 
 This affected the right side of the body in six cases, the left in two 
 cases, while in one case the right arm and the left side of the face are 
 recorded as paralyzed. In the tenth case the side is not stated in 
 the record. Four cases showed signs of “‘apoplexy”’ or cerebral 
 hemorrhage, but without hemiplegia. 
 
 These cases do not bring out the clinically familiar fact that the 
 embolic hemiplegias of mitral stenosis give a relatively good progno- 
 sis when compared with hemiplegias associated with hypertension 
 and arteriosclerosis. But neither do they contradict it. 
 
 2. Pulmonary.—The recognizable cases have already been referred 
 to with pulmonary infarct. 
 
 3. Peripheral—(See Table 50.) 
 
 * This does not contradict Table 43 where only 4 cases are listed as showing cerebral 
 lesions at necropsy. Permission to examine the brain is often, indeed usually, refused in 
 our cases. 
 
72 FACTS ON THE HEART 
 
 Auricular Thrombi and Arrhythmia.—In 23 cases out of thirty- 
 seven, clots in the left or right auricles were associated with an 
 extreme irregularity of the pulse so described (in most cases) as to 
 warrant the inference that auricular fibrillation was present. In 
 three cases similar clots occurred apparently without any fibrillation 
 during the period of observation. Fibrillation without clots occurred 
 in only four cases. In two other cases the records were not clear. 
 
 From these figures it appears that intracardiac clots are usually 
 preceded by fibrillation. 
 
 TABLE 44.—INFECTIOUS PULMONARY COMPLICATIONS FoUND AT NECROPSY 
 
 Pulmonary lesion Mitral | M-+A One Total 
 comb. 
 
 Lobar pneumonia 
 Bronchopneumonia 
 
 Organizing. pheumonia. omc a oer aie 2 tne 
 Résolyingopm euinonia yee snes tie at tant. 
 Pulmonary abscess 
 
 Comment.—1. Twenty-seven in 180 cases, or about one-seventh 
 of the whole ‘“‘rheumatic”’ group showed a definite pulmonary disease 
 other than passive congestion, edema, hydrothorax, or “‘hypostatic 
 pneumonia.” ‘These twenty-seven cases were all of pneumonia or 
 its results. 
 
 2. There were 4 pulmonary abscesses 3 of which occurred in cases 
 showing a partially organized pneumonia. Abscess and organization 
 were doubtless aspects of the same process. 
 
 3. From the frequency of these complicating pneumonias we may 
 suppose, therefore, that the pulmonary congestion due to mitral 
 disease favors inflammation of the lung though it certainly does not 
 favor tuberculosis. 
 
 The Occurrence of Nephritis and Other Renal Complications in 
 Mitral Disease.— Nephritis, acute or chronic, was found post-mortem 
 in 18 of 107 mitral cases (17%), in 12 out of 40 mitral-and-aortic 
 cases (30%), and in 4 of the 33 “‘other combinations.”’ Whether 
 there is any significance in the fact that nephritis was twice as com- 
 mon in the mitral-and-aortic as in the simple mitral cases I cannot 
 say. The outstanding fact is that late in the course of mitral disease 
 we may expect the presence of glomerulonephritis in one-fifth of all 
 
 EEE eS 
 
PHYSICAL SIGNS OF MITRAL STENOSIS fee 
 
 cases (35 in 180). Doubtless a similar nephritis occurs and heals in 
 the earlier stages of many more cases. 
 
 Only six of these 35 cases of glomerulonephritis were suspected in 
 life. Here suspicion was aroused usually by the condition of the 
 urine, sometimes by high blood pressure, edema, or uremic symptoms 
 in addition to the urinary abnormalities. In the remaining 29 cases 
 the urine showed nothing suspicious. 
 
 Of the 16 cases of acute glomerulonephritis proved post-mortem, 
 one showed a normal urine; one showed a slight trace of albumin and 
 many casts; one showed a trace of albumin, many casts, blood and 
 pus. In the rest there was nothing pointing to nephritis. 
 
 Of 7 cases of subacute glomerulonephritis, four were recognized 
 by the presence of albumin in considerable quantities wae many 
 casts and other clinical manifestations. 
 
 One case of chronic glomerulonephritis showed only a slight trace 
 of albumin and many casts. 
 
 TABLE 45.—NEPHRITIS WITH VALVE LESIONS 
 
 Com- 
 Mitral | M+ <A! bined 
 lesions 
 
 e 
 
 Acute glomerulo nephritis 
 
 Subacute glomerulo nephritis 
 
 Acute and chronic nephritis........ 
 Chronic nephritis 
 
 Mmvyioid. degeneration. ....:......-. 
 No nephritis 
 
 No record.... 
 
 [" or 25% 
 
 to 
 
 (Re ae tos egy eee 
 H 
 
 He Ww 
 
 Now HO FN AY 
 
 | 
 
 aS 
 re) 
 e 
 oe) 
 @) 
 
 Anginoid Attacks.—In necropsies 600, 810, 1098 and 3040 there 
 were attacks simulating angina. One of these has already been 
 analyzed (see p. 49). Another occurring in connection with abor- 
 tion in a woman of twenty-three, lasted six days as ‘“‘pain”’ over the 
 heart,—apparently the first attack and leading immediately to death. 
 No cause was discoverable post-mortem. I do not consider this 
 angina pectoris. 
 
 Another case occurred in a man of twenty-seven with a well- 
 marked history of syphilis (hard chancre, headache, alopecia, sore 
 throat, treatment by mercury pills). He had had substernal pain 
 on exertion for two years. Necropsy showed lesions probably to be 
 interpreted as syphilitic aortitis. “The mouths of the coronary art- 
 
74 FACTS ON THE HEART 
 
 eries were not occluded and the aorta and coronaries were otherwise 
 
 negative. ‘This is the only case in our 180 showing the association 
 
 of a syphilitic and a rheumatic lesion in the same heart, exemplifying 
 
 once more the queer fact of an association between syphilis and 
 
 angina pectoris even when the aorta is not diseased. | 
 TABLE 46.—CASES SHOWING PosITIVE (POST-MORTEM) CULTURES 
 
 Organism | Source Type of endocarditis Complications 
 
 Mitral | Streptococcus Blood 14 | Acute 3 | General Peritonitis 2 
 Spleen “1 | Chronic to | Local Peritonitis 
 Liver x | Acute & Chronic 4 | Erysipelas 
 Liver and 
 Spleen I Cancer of the liver 
 
 Pneumococcus Blood 3 | Chronic Lobar Pneumonia 
 Liver I 
 
 Pseudo Pneumococ- 
 cus t | Blood Acute & Chronic Lobar Pneumonia 
 
 B. muc. capsul. | ; Blood Chronic Bronchitis and Ulcera- 
 B. Coli f tive Colitis 
 
 B. Coli Chronic Local Peritonitis 
 Diplococcus Acute & Chronic 
 
 Streptococcus Not Stated | Chronic Appendicitis 
 Acute & Chronic Malignant Endoc. 
 Nephritis 
 General Peritonitis 
 
 Pneumococcus Not Stated | Chronic Pneumonia, lobar 2 
 Acute & Chronic Pneumonia, focal I 
 Pneumonia, organizing I 
 
 Staphylococcus Not Stated | Acute & Chronic 
 
 Streptococcus Acute & Chronic Pneumonia & Bronchiec- 
 lesions tasis 
 Chronic Erysipelas 
 Meningitis 
 
 Pneumococcus I Acute & Chronic Pneumonia 
 
 Pseudo pneumococ- 
 cus Pneumonia 
 
 Total Streptococcus Positive cultures 
 Pneumococcus Negative cultures 
 Staphylococcus No record 
 Pseudo-Pneumococcus 
 BrmtcyCapsulatisic BeGolw aay say 
 Diplococcus 
 
PHYSICAL SIGNS OF MITRAL STENOSIS 75 
 
 Blood Cultures.—Very few attempts were made during the life 
 of these 180 patients to isolate any organism from the circulating 
 blood, and only one urinary culture is recorded, No. 3566: staphy- 
 lococci. Out of 11 cases tested in life the blood in eight was negative, 
 3 positive,—streptococcus in all cases. 
 
 Post-mortem cultures were made in 143 cases. Of these forty-four 
 were positive (24%) and ninety-nine negative. In the forty-four posi- 
 tive cases one showed only bacillus coli which was very possibly 
 due to a complicating local peritonitis; one showed staphylococcus 
 albus (presumably contamination); two showed staphylococcus 
 aureus; /wenty-seven cases showed a streptococcus; ten cases a pneumo- 
 coccus; two a pseudopneumococcus, one bacillus mucosus capsul- 
 atus, one a few diplococci. The pseudopneumococci and eight of 
 the ten positive pneumococcus cultures came from cases complicated 
 by pneumonia. 
 
 In the twenty-seven streptococcus cases acute endocarditis was 
 present post-mortem fifteen times. Two of these were of the ulcerat- 
 ing type; the rest showed minute vegetations only. In one of the 
 others, showing only chronic endocarditis, there was a terminal erysip- 
 elas; in two others general peritonitis had supervened, upon hysterec- 
 tomy and upon appendectomy respectively. General peritonitis 
 was also present in connection with two of the cases of acute endo- 
 carditis with positive streptococcus cultures. 
 
 From these cultures I can draw no conclusions of significance. 
 Streptococcus cultures post-mortem occur only in 15% of our 
 necropsied cases. Nevertheless in non-cardiac cases of this chronic 
 exhaustive type the percentage is not far different. 
 
 The only point of interest is the absence of the influenza bacillus 
 and of the gonococcus, organisms not infrequently mentioned in the 
 literature of endocarditis and both of them organisms which our 
 pathologists have been especially interested to search for. 
 
 The two staphylococcus cases showed curiously enough no local 
 abscesses at necropsy. One showed endocarditis of the acute poly- 
 pous (as well as chronic) type; in the other the lesions were purely 
 chronic. 
 
 Has the Size of the Mitral Orifice Any Relation to Its Clinical 
 Manifestations?—Nothing of significance could be learned on this 
 topic from the study of the present series. Some of the cases with 
 extreme narrowing seemed to be rather more subject to repeated 
 attacks of decompensation closely following one another. For 
 instance: 
 
76 
 
 Necropsy 2748: 
 Necropsy 2226: 
 Necropsy 2091: 
 Necropsy 1806: 
 
 FACTS ON THE HEART 
 
 mitral 1 
 
 mitral 1. 
 
 But in contrast: 
 
 Necropsy 2960: 
 Necropsy 2635: 
 Necropsy 1675: 
 Necropsy 973: 
 
 mitral 1.2 cm. 
 mitral 1.5 cm. 
 mitral 1.8 cm. 
 mitral 1.5 cm. 
 
 cm, 
 mitral 2.5 cm. 
 mitral 1.5 cm. 
 cm. 
 
 no acute endocarditis. 
 no acute endocarditis. 
 no acute endocarditis. 
 no acute endocarditis. 
 
 2 decompensations in 1 year: 
 2 decompensations in I year: 
 2 decompensations in I year: 
 2 decompensations in 1 year: 
 
 Nothing characteristic in course. 
 Nothing characteristic in course. 
 Nothing characteristic in course. 
 
 Nothing characteristic in course. Died of pneumonia. 
 
 On the whole it does not appear that the size of the stenosed 
 mitral orifice is in itself a recognizable factor in determining what or 
 how much the individual shall suffer (see Table 47). 
 
 TABLE 47.—DIMENSION OF THE MITRAL VALVE 
 
 Q. 
 8. 
 8. 
 7% 
 vk 
 6. 
 6. 
 ne 
 5. 
 4. 
 4. 
 or 
 ay 
 2 
 2. 
 iy 
 i 
 
 Size of orifice 
 
 Other 
 
 Mi 
 fitral aie 
 
 M+A Total 
 
 bs Gr tOn NS oS © Oye Or 01, OOS il Sy ee Ory O° Oy Ot 
 On Ol Oe sO Oe sO2 Rieti) at = COnGTEO, 
 OH HH NW HH O FH NH NH HWW DbD O O 
 
 ‘“‘Fish-mouth” 
 
 “Buttonhole” 
 
 ““Very small” 
 
 ““Not very small” 
 
 Admits forefinger tip 
 
 Admits middlefinger tip 
 
 Admits littlefinger tip 
 
 Admits closed blades of scissors............. 
 Admits two finger tips.. ve vee 
 Admits three finger tips en shies 
 
 On FEsOMeO Oo Os Or Oe 
 ONO. Oot Os TH. O60 
 
 RTH? 
 
MODE OF DEATH 77 
 
 Comment.—55% of the mitral cases, 28% of the mitral-and-aortic 
 cases, and 55% of the ‘“‘other combinations” showed a mitral ring 
 measuring 7 cm. or less instead of ten cm.,—the average for adults. 
 It would seem that the “pure mitral”’ cases tend to a greater degree of 
 narrowing than the ‘“‘mitral and aortic” cases. Possibly this may 
 help to account for the fact that passive congestion is as often marked 
 at necropsy in the “‘pure mitral” cases as it is in the “‘mitral-and- 
 aortic.’ A very narrow mitral perhaps does as much harm as a 
 fairly narrow mitral plus some aortic stenosis. 
 
 MODE OF DEATH 
 
 TaBLE 48.—MopE OF TERMINATION IN 106 CASES OF MITRAL STENOSIS 
 
 i EEC Tn ee dace le AS elie is A Cas gh 49 
 imen-cardiac disease (cancer, nephritis, €tc.).........0...6..0.68 0. 33 
 EVOMSI I aga.) ae es 8 Re cate Par Pen, oem sen iolhi te. aks 12 
 MSN Fe PS rete NO oe ngs Bical oe eye see Xn, vey e git 6 « Ke) 
 RIM ETC RO LANICO se ig wrk buat kt gle dos ato ww oo oenasazane logit a vs 2 
 
 106 
 
 1. Deaths from Chronic Passive Congestion.—Only forty-nine out 
 of our 106 cases of “‘pure”’ mitral disease died a “‘congestive death.” 
 In these forty-nine the symptoms and signs before death and the 
 findings after death were predominantly those of passive congestion, 
 though in thirteen cases there was also a slight acute endocarditis,— 
 believed to be of the terminal type and not the main cause of death. 
 
 Of these forty-nine cases with ‘‘congestive death,” thirty had a 
 typical rheumatic or choreic history, and nineteen did not. These 
 nineteen cases were on the average older than the thirty rheumatics, 
 averaging forty-five years and having complained of dyspnea and 
 other cardiac symptoms for seven and a half years. In three of 
 these (fifty, sixty-three, and sixty-five years of age) the symptoms 
 had been noticed “for years.” 
 
 2. Deaths from Other Diseases with Latent Mitral Stenosis —There 
 were thirty-three cases of this type—nearly one-third of the whole. 
 The main causes of death are shown in the following table. 
 
 TABLE 49.—CAUSES OF DEATH IN LATENT CASES OF MITRAL DISEASE 
 
 Infections (Pneumonias 5, General Peritonitis 3).................+. I4 
 MOMS lad RS Ca) edn Pee hee eh Ua Rh eee eh 6 
 Benen BETO AOT Acca: e, Sit, FE PIA Site ha dik. Mens ws Wank De SESE 4 
 RIES Et ante DANSTION Ao ak seein Bee em ee we edie ae Sos [- 
 Ne NIE, SEC eee NENG, ee A ele Na ee ek Leis 0B 2 
 ee Ck eee ne ae are ee ede EN ae I 
 ee RRS CUI ILI DEC-SOLE ry eave at Cle eek Ghd pea ce ees Be I 
 
78 FACTS ON THE HEART 
 
 Passive congestion was absent at necropsy in these cases. 
 3. Embolic Deaths —In twelve patients embolism was the only 
 or the chief cause of death. The site of the emboli was as follows: 
 
 TABLE 50.—SITE OF EMBOLI CAUSING DEATH IN MITRAL STENOSIS 
 
 Peripheral (one or both legs)... .. 2.4. ..50%... Se en i 
 Peripheral and ‘cerebralis 20% 00-5 6 oes es nes © a tendorae ety ee I 
 Cerebral.'i0), gis oie ae cap nae th ® eee tleps 0a Pkg Oe I 
 Mesentericsatico.b6 aad co Ph eh ces. 0 Gh eee ee I 
 Pulmonaty artery. i505 6s Se. ons as 0s ceed occ ae ner 2 
 Pulmonary and renal arteries... 02... ov 25 owe ors, 7 cee aie ee I 
 Abdominal aorta, iliac-and left renal;. .....% 2. <6 wi) ee I 
 
 I2 
 
 4. Acute Septic Deaths——An accompanying acute endocarditis, 
 with the general septicemia resulting, seemed the chief cause of 
 death in ten cases. These have also been counted among the 
 
 cases of Acute Endocarditis in Chapter VII but are included here © 
 
 because the mitral valve was definitely stenosed. 
 
 5. Sudden Death Unexplained—Two patients died suddenly and 
 without any notable symptoms or signs until the coma abruptly 
 appeared. ‘These cases are of sufficient rarity and interest to deserve 
 description in detail. 
 
 Necropsy 1621 was performed on the body of a white American 
 woman of thirty-five who had had chorea in childhood but no 
 rheumatism. She was brought to the hospital in collapse March 1, 
 1906, and died on March 5th. There was a vague history of similar 
 attacks in 1903 and 1905, but as she had had many epileptiform 
 attacks (the nature of which is not clear) we cannot be sure that the 
 seizures of 1903 and 1905 were due to the cardiac disease. She had 
 not been known to be ill and had been found in coma by her brother 
 who brought her to the hospital. Though she was but thirty-five 
 there was well-marked arteriosclerosis of the pulmonary artery and of 
 the aorta. There was a mitral stenosis (orifice three cm.) and a 
 moderate hydropericardium but no other dropsical effusions. 
 
 Necropsy 1981 concerned a man of forty who was brought in 
 unconscious and died the same day. He had worked till the day 
 before entrance, and had not been known to be ill. 
 
 Necropsy showed a mitral orifice of 4.5 cm., a non-deforming 
 chronic endocarditis of one aortic cusp, chronic passive congestion 
 with hydropericardium, and hydrothorax. There was also a general 
 arteriosclerosis and some unexplained cicatrices in the liver—not 
 definitely syphilitic. 
 
 io 
 
DIAGNOSTIC ERRORS 79 
 
 TABLE 51.—ERRORS IN DIAGNOSIS 
 
 Other 
 
 Mitral M+A 4 
 lesions 
 
 See below 
 
 Recognized ante-mortem p. 160 
 
 Unrecognized ante-mortem p. 160 
 
 Doubtful . p. 160 
 
 DIAGNOSTIC ERRORS 
 
 I have disregarded the clinical diagnoses written on the records 
 because in many instances these diagnoses have shown strong 
 internal evidence of having been copied from the necropsy record. 
 I have considered the cases as rightly diagnosed during life whenever 
 a presystolic or diastolic murmur was recorded or heard at or near 
 the cardiac apex and not otherwise explained. When systolic 
 murmurs only were heard, or no murmur at all, I have considered | 
 the case as not diagnosed in life, because 7m the absence of other signs 
 pointing to mitral stenosis I know no way in which a systolic murmur 
 alone can be held to justify such a diagnosis. 
 
 Reasons for Failure to Recognize Pure Mitral Stenosis.—(z) 
 The absence of a history of cardiac symptoms and the obvious presence 
 of some other disease. ‘This was the case in 35 of 54 of our failures. 
 Under these conditions cardiac examination is often superficially 
 made, especially in surgical wards where 35 of these patients were 
 treated. 
 
 (2) A very short period of observation and a moribund patient. 
 This condition obtained in 6 cases. 
 
 (3) Failure to recognize any murmur but a systolic at the apex: 
 18 cases. 
 
 (4) No murmur whatever recognized: 21 cases. 
 
 (5) Lack of realization of the fact that there are certain reasons 
 for expecting mitral stenosis and so for searching for evidence of it 
 with particular attention. Such reasons apparently ignored in this 
 series are: 
 
 (a) The presence of arterial embolism or thrombosis (hemiplegia, 
 peripheral gangrene, in relatively young patients (e.g. embolic gangrene 
 of right foot at 29, cerebral embolism with hemiplegia at 35, gangrene 
 of both feet at 44). 
 
80 FACTS ON THE HEART 
 
 (b) The presence of decompensation with a rheumatic or choreic 
 history and without hypertension or syphilis. Knowing that under 
 these conditions mitral stenosis (with or without aortic disease) 
 is present in almost 80% of all cases, one would look for it harder 
 and more successfully than is the case in this series. 
 
 (c) Suggestive cardiac signs other than a murmur, e.g. in Necropsy 
 1926 the heart was greatly enlarged (7th interspace, 20 cm. from 
 midsternal line), the apex rst sound was short and sharp, the pulmonic 
 2d accentuated, and the aortic 2d barely audible. These signs in a 
 woman of thirty-five, who had had decompensation almost without 
 intermission for a year and who had no hypertension, no nephritis, 
 and no evidence of syphilis, should make us assume, even if no 
 murmur is present, that mitral stenosis is present. (We might well 
 expect also adherent pericardium or tricuspid stenosis, neither of 
 which was in fact present here.) 
 
 (d) An apical systolic murmur alone with rheumatic or choreic 
 history, arrhythmia or decompensation in a person under 45 should 
 always make us suspect that repeated and careful search with 
 the patient in various positions at rest or after exercise will discover 
 a diastolic or presystolic murmur not audible at all times. In decom- 
 pensated cases we cannot rightly stimulate by exertion that increased 
 cardiac vigor which often “brings out”’ diastolic or presystolic mur- 
 murs in addition to the obvious systolic which is almost invariably 
 present. But a whiff of amyl nitrate will serve the same purpose 
 without harming the patient. 
 
 (e) With signs of acute (ulcerative, malignant) endocarditis one 
 should remember that in 56% of such cases discoverable in life 
 a chronic deforming endocarditis is also present and therefore to be 
 searched for or at least suspected. 
 
 MITRAL STENOSIS. ILLUSTRATIVE CASES 
 
 . Latent. 
 
 . Latent with cirrhotic liver. 
 
 . With recurrens paralysis. 
 
 . With acute endocarditis. 
 
 . With embolic gangrene of legs. 
 
 a1 & G©® Nb # 
 
 Necropsy 4292 
 
 An American dentist of thirty-eight entered January 14, 1922. 
 His mother died of valvular heart disease. One uncle died insane. 
 He had the minor diseases of childhood. At ten years of age he 
 was in bed for two months with “rheumatic fever,” all the joints 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 8I 
 
 being swollen, red, hot and very painful on motion, and at eighteen 
 he was in bed for a month with a second attack. Since then he had 
 at various times had one or two joints painful for a day or two. 
 At twelve he had tonsillitis. In general his health had been very 
 good. Occasionally he had had some epigastric distress and belch- 
 ing of gas after meals when he was very tired and worried. He 
 urinated once at night, chiefly because he awoke in the night and 
 went from habit. At twenty-six he had gonorrhea for a month. 
 He denied syphilis. His best and usual weight was 137 pounds, his 
 present weight 135. 
 
 Before the present illness he was a heavy smoker. He denied 
 the use of alcohol. 
 
 Three and a half years before admission after an especially hard 
 day’s work he was awakened suddenly in the night with.severe pal- 
 pitation, orthopnea, coughing and wheezing with about a half a cup- 
 ful of bloody frothy sputum. The attack lasted most of the night 
 but gradually passed off by morning, as did his rapid heart action. 
 Six months later he had a similar attack followed by a little cough 
 which lasted a week. From this time his symptoms had gradually 
 increased. He began to tire easily. Any unusual exertion caused 
 a feeling of epigastric distress with some dyspnea, which had been 
 steadily increasing. From time to time he had mild attacks like the 
 ones described. ‘Two years before admission he had a third very bad 
 attack similar to the first but lasting longer. At this time he was 
 particularly tired and nervous, having been worried a great deal 
 about his condition and his business. He continued to work hard 
 however for the next six. months. Then his gradually increasing 
 distress and dyspnea on exertion became very severe. His heart 
 action was also quite irregular, and had continued to be so. He 
 stayed two months in a hospital with much improvement. Five 
 days after leaving it he was forced to return for another month. 
 He gradually got back to his work and did well for six months. Then 
 his old symptoms of fatigue, palpitation, dyspnea, nervousness and 
 sleeplessness began to come back. Six months before admission his 
 ankles became swollen. He was having considerable cough with 
 frequent hemoptysis, never more than an ounce. He stayed in the 
 hospital again for two months with much improvement. Three 
 months before admission he went back to work and did well for a 
 short time before his symptoms began to return. Three weeks 
 before admission both knees and ankles became swollen, red, hot and 
 
 very painful on motion. This was soon followed by some pain in his 
 6 
 
$2 FACTS ON THE HEART 
 
 elbows and wrists. A week later he developed a red purpuric rash 
 on both legs. His dyspnea became much worse. He had been in 
 bed most of the time since, although he had improved. For a year 
 and a half he had taken digitalis from time to time with good effect. 
 For a week he had not taken any. 
 
 S$ 
 Nipple 
 
 3.cm |4 8 Cm? ae 3 cm 
 
 Fic. 1.—Cardiac measurements by percussion. 
 
 Physical examination. Well nourished. Weight 132 pounds. 
 Skin dry. Faint macular rash on the chest. Slight acne on the 
 back. The tonsils showed crypts on the left. Lungs negative. 
 Heart. Apex impulse not seen or felt. Measurements as shown in 
 
 2-1 eee 
 ol FBS 0 A 
 soa ere [vf i7 [1]19 [eelz [aa] zsfaelan|aelar ae 7|eo[o7| 7 
 ER SRR RRRRRBBRMe Es 
 
 aa6le tio nt Pd ed to Ts | a 
 Sle liar he et meg ted Med Onl Fe [ot ae as 
 200° ae NE eee 
 Sool boot PNT TAT STs [Nese he 
 oof Asta hot hE Ate ble ba At Bo 
 gol leet ieee Wei 
 ese pate 
 
 aelaiee | | WV A 
 
 BLOOD PRESSURE 
 
 (inven OF 
 
 the diagram. Action absolutely irregular, not rapid. Sounds of 
 good quality. P: equal to Ay. Systolic murmur heard during the 
 longer systoles. Pulses low volume and tension. Arteries normal. 
 Blood pressure 120/90-95/70. Abdomen and genitals negative 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 83 
 
 except for a reducible left inguinal hernia 2.5 cm. in diameter and 
 a very slight right inguinal hernia. Rectal examination. A few 
 external tabs. Extremities negative. Pupils equal, regular, reacted 
 poorly to light and distance. Reflexes normal. 
 
 Temperature and pulse as shown in the chart. Respirations 
 19-35 until January 30, then 37-50. Urine § 16-52 in 24 hours. 
 Sp. gr. 1013-1034. Acid at all four examinations. A slight trace 
 to a very slight trace of albumin at the last two, leucocytes at three. 
 No sugar. Renal function 50%. Blood: Hgb. 75%-80%. Leu- 
 cocytes 8600-52,000. ° Polynuclears 73%. Reds and _ platelets 
 normal. Wassermann negative. LElectrocardiograms, January 15, 
 auricular fibrillation, coarse. Rate 85. Flat T wave. On ten days, 
 Janunary 17-28, auricular flutter. See table. X-ray. See Fig. 
 3. Chest 25.5 cm. transverse inside diameter. 
 
 Auricular | Ventricular 
 
 Block 
 rate rate 
 ie ge aE ae 265 130 Varies; usually 2:1 
 Oa rae a 255 130 
 oe Sl ae a 255 130 
 MEERA Sf 20520 ieee 8 oe. 285 120 Varies. 
 RN oe ie. chy apne SR 325 162 act 
 IE loi Pan, +) 5 age Sas 320 160 ee 
 oo a) el er ge 340 170 O27 
 RM re so PU sean ck Goce oes 330 165 Zein SOmetIMes 3.7 
 ot li? Ae aa eae 320 160 bad 
 DMM oh. a Sas Se dy ae 280 140 Ta 
 
 Dr. Paul D. White noted January 25, ‘‘ Under quinidine sulphate 
 auricular flutter was induced. When the quinidine was stopped and 
 digitalis given to saturation the rate of the flutter circus movement 
 increased from 255 to 340, but neither normal rhythm nor auricular 
 fibrillation has ensued. Coincident with the progress of the flutter 
 there has been an acute infection (fever, leucocytosis) responsible for 
 at least a part of his symptoms of discomfort. The infection, prob- 
 ably respiratory, apparently subsiding now.” The night of Jan- 
 uary 27 the flutter showed signs of breaking. Every five or ten beats 
 there occurred several ventricular escapes. January 29 the heart 
 was still in flutter, but the ventricular rate was slower. He was 
 very restless and nervous. January 31 the heart action was still 
 regular and rapid. There were rales at the bases, more on the left. 
 
84 FACTS ON THE HEART 
 
 The patient was cyanotic and looked veryill. He grew rapidly worse. 
 The chest was filled with rales with fluid at the bases. February 2 
 the patient died. 
 
 Dr. White adds, ‘“‘The action of quinidine was unfavorable in 
 this case.”’ 
 
 Clinical Diagnosis—Chronic valvular heart disease (mitral 
 stenosis). 
 
 Myocardial insufficiency. 
 
 Auricular flutter. 
 
 Fic. 3.—Necropsy 4292. Mitral stenosis. Mural thrombi of the auricular appen- 
 dices. Embolic thrombosis of branches of the pulmonary artery. X-ray shows gen- 
 eral enlargement of the heart shadow, the greatest prominence in the region of the 
 
 auricles, particularly the left. (Roentgenological Department, Massachusetts General 
 Hospital.) 
 
 ‘ 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis of the 
 mitral valve with stenosis. 
 
 Acute endocarditis? 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Infarcts. . 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral valve 
 (stenosis). , 
 
 Hypertrophy and dilatation of the heart. 
 
 Mural thrombi of the auricular appendices. 
 
MITRAL STENOSIS. ILLUSTRATIVE GASES 85 
 
 Embolic thrombosis of branches of the pulmonary artery. 
 
 Infarcts of the lungs. 
 
 Chronic passive congestion, general. 
 
 Acute serofibrinous pericarditis. 
 
 Acute serofibrinous pleuritis, left. 
 
 Chronic pleuritis, right. 
 
 Dr. OscAR RICHARDSON: The head was not examined. The face 
 was dusky and the lips purplish. The skin elsewhere was smooth and 
 pale. There were no signs of purpura at this time. The feet 
 and ankles were slightly swollen and pitted slightly. The subcutane- 
 ous tissues were a little wet. ‘The stomach and intestines showed 
 chronic passive congestion. The mesenteric and retroperitoneal 
 glands were negative. The liver at the time of necropsy was at the 
 costal border. 
 
 The pleural cavities: on the right 200 c.c. of thin brownish fluid, 
 clear; on the left 1500 c.c. of thin cloudy fluid and fibrin; and the 
 lower lobe of the lung on this side was coated with dirty reddish 
 fibrinous material. The trachea, bronchi and bronchial glands were 
 negative. The lungs showed chronic passive congestion, many 
 infarcts, and in places the branches of the pulmonary artery leading 
 to the areas of infarction showed occluding plugs. 
 
 The pericardium contained about 200 c.c. of thin cloudy fluid with 
 fibrin. The visceral and parietal surfaces were reddened and coated 
 with fibrin. The heart weighed 545 grams, considerably enlarged. 
 The myocardium was of good consistence, pale brown-red. There 
 was no evidence of myocarditis. The following measurements are 
 interesting because they picture mitral stenosis. The left ventricular 
 wall 1o mm., a little flabby; the right 6 mm., good consistence, the 
 columnae carneae a Jittle flat on the left, thickened on the right. The 
 cavities on the left side: the ventricle was full sized and showed 
 nothing remarkable; the left auricle was full sized and the wall was 
 thickened. In the left auricular appendix a short distance from the 
 tip, a mural thrombus,-—not uncommon in mitral stenosis. Theright 
 ventricle and right auricle showed considerable dilatation, and in the 
 right auricular appendix a few mural thrombi, bits of which had 
 passed over into the branches of the pulmonary artery, appearing 
 as the plugs mentioned. The aortic valve showed a little fibrous 
 thickening, nothing very definite, which faded out into the marked 
 thickening of the mitral valve. It is impossible definitely to say 
 -Whether there had ever been any infection on that valve or whether 
 it was a compensatory thickening. The only thing that makes one 
 
86 ’ FACTS ON THE HEART 
 
 think there may have been infection was that below the cusps on the 
 endocardium there was a small fibrous patch, which is abnormal; and 
 that possibly may have been a little patch of endocarditis x years ago. 
 It is of no great importance now, and of course had no relation to the 
 hypertrophy and dilatation of the heart. The mitral valve was in the 
 form of a flattened ovoid mass; and in the center of this mass was 
 the crescentic orifice of the valve, three and a half cm. long, with 
 the margins practically fused for one centimeter and closely approxi- 
 mated eleswhere. Theirsurfaces were very irregular, somewhat coral- 
 like in places, and altogether the valve showed marked deformity 
 and stenosis, with thickening and shortening of the chordae tendineae. 
 
 The coronaries showed a little scattered sclerosis. The aorta 
 and branches were out of the picture. The liver showed nutmeg 
 markings, that is chronic passive congestion. The gall-bladder, bile- 
 ducts, spleen, adrenals and kidneys were negative except that they 
 showed more or less congestion. The genito-urinary organs were 
 negative. 
 
 Necropsy 4605 
 
 An American railway clerk of twenty-six entered January 3, 1920, 
 complaining of dyspnea and weakness. His mother died of cancer of 
 the stomach. As a child the patient’s health was not good. He 
 easily took infections, and had pertussis, scarlet fever, mumps, 
 diphtheria, measles, and rare earache. At twelve he was laid up ina 
 hospital three months with “nervous prostration.” From the age 
 of seventeen to twenty-two he had malaria for several weeks every 
 summer. He had rare sore throats. A year before admission he 
 had influenza lasting ten days. With this he had bilious attacks 
 and vertigo. He occasionally urinated once at night. Several years 
 ago he weighed 125 pounds, his best weight. His usual and present 
 weight was 122. Until six months before admission he sometimes 
 drank large amounts of alcohol. 
 
 At seventeen, during a severe cold, he had with rather sudden onset 
 an attack of “‘congestion.’”’ He was put to bed and had dyspnea, 
 orthopnea, slight fever, persistent deep-seated cough with blood 
 streaked sputum, and frequent attacks of vomiting without nausea, 
 with small amounts of blood in the vomitus. He noted for the first 
 time palpitation and precordial pain, at times severe, preventing sleep. 
 For over a week he was confined to bed. Within three weeks he was 
 allowed to go back to his work. Except for general moderate asthe- 
 nia, dyspnea and palpitation on exertion there had been practically 
 no change in his condition until two years before admission. Then 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 87 
 
 he had a sudden chill in the afternoon. The next morning a moder- 
 ately severe dull pain in both lower quadrants gradually developed. 
 He was taken toa hospital. The next. day moderate fever developed. 
 The pain although continuous for two days was not severe enough to 
 prevent sleep. He was ina hospital a week, during the last four days 
 of which he was moderately jaundiced. The fever lasted only four 
 days and was never over 101°. Ten weeks before admission he had a 
 fleeting chill. The next day he observed swelling of the precordia 
 and sudden onset of dyspnea when walking slowly on a level. He 
 returned to work, but was dyspneic whenever not sitting absolutely 
 quiet. The precordial swelling increased. During the next five 
 weeks he had palpitation, tachycardia, dyspnea on walking even a 
 few steps, orthopnea, enlarged liverandswollenabdomen. Theankles 
 
 slightly dull 
 
 pull to 
 flat. 
 
 AVM) 
 
 Dull, with 
 
 moist rfles Diminished breath 
 
 NY 
 : Dull to flat. 
 SVAN 7 
 SAY 
 pistes Rales. 
 
 cy 
 
 Fic. 4. 
 
 and lower legs were edematous. After a week of complete rest in bed 
 with medication the orthopnea, dyspnea and palpitation disappeared 
 and the swelling of the abdomen, ankles and precordia markedly 
 diminished. During this period he had moderate cough. After 
 working for two weeks the symptoms gradually increased. An 
 increasing heavy sense of discomfort in the abdomen, although pain- 
 _less, tended to keep him awake at night. 
 
 Examination showed a fairly well developed and nourished man 
 with bright red lips and cheeks. The sclerae, throat and tonsils 
 were slightly injected. The jugulars were much distended. There 
 was slight general adenopathy. There was bulging of the precordia. 
 The lungs signs were as shown in Fig. 4. The diaphragm excursion 
 was slight. There was diffuse cardiac impulse over the whole 
 precordia and felt in the midaxillary line. Thesounds were absolutely 
 irregular in quality. There was a pulse deficit of 52. The first 
 
88 FACTS ON THE HEART 
 
 sound at the apex was loud and snapping. The pulmonic second 
 sound was accentuated. <A soft blowing systolic murmur was heard 
 over the precordia, loudest at the apex. There was a short middias- 
 tolic murmur, loudest at the apex. The pulses were of small volume 
 and tension. The beats varied in force. The blood pressure was 
 150/85 to 110/80. The abdomen was slightly distended, with shift- 
 ing dullness in the flanks. The liver dullness extended from the 
 fourth rib to ro cm. below the costal margin. The edge was felt 15 
 cm. below, slightly tender. The spleen was just felt. There was 
 moderate edema of the ankles. The pupils were dilated. The right 
 was greater than the left. The knee-jerks were sluggish. 
 
 Chest 26 
 Measurements by X-ray January 1 (92s. 
 Fic. 5. 
 
 The temperature was 96.1° to 99.9°, the pulse 28 to 84 (radial), 
 the respiration 12 to 26. The output of urine was 16 to go ounces, 
 the specific gravity 1.018 to 1.030. The urine was cloudy at three of 
 five examinations, alkaline at one, showed a slight trace to the very 
 slightest trace of albumin at two, rare leucocytes at three. The renal 
 function was 60%. The hemoglobin was 70%. The leucocytes were 
 6400 to 15,800, the polynuclears 70%. A Wassermann was negative. 
 X-ray January 7 showed the lower part of the right chest dull, the 
 costophrenic angle obliterated, perhaps because of an extensive high 
 diaphragm on this side, perhaps because of a little fluid at the right 
 base. Both lung roots were considerably thickened and the lung 
 markings prominent. There were some calcified glands. The heart 
 shadow was very much enlarged. There was marked prominence in 
 the region of the left auricle. January 21 the shape of the heart was 
 much the same as at the previous examination. There was marked 
 increase across the extreme upper part of the heartshadow. Although 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 89 
 
 there was general enlargement, the prominence was most marked in 
 the region of the left auricle. Electrocardiogram January 3 showed 
 auricular fibrillation, rapid ventricular rate, 120, right ventricular 
 preponderance. January 5 there was auricular fibrillation, ventricu- 
 lar rate about 55, right ventricular preponderance, bigeminal pulse 
 due to ectopic ventricular contractions (probably the result of 
 
 digitalis). 
 Under a single dose of digitalis the pulse dropped markedly and 
 _the irregularity and the deficit were less marked. ‘‘ The prognosis is 
 
 absolutely bad,—probably a matter of months at most.”” By Janu- 
 ary 10 there was no friction over the liver. Theascites was much less. 
 January 17 he was still digitalized on the initial dose of one gram. 
 January 29 he was discharged partially relieved. 
 
 December 14, 1923, nearly 4 years later he was again seen 
 unconscious and in extremis. His sister said that under treatment in 
 the Cardiac Clinic of the Out-Patient Department of this hospital he 
 had been in “good health” apparently, with no complaints. His 
 last visit to the Clinic was in August, four months before admission. 
 Since his father’s death the previous spring he had been somewhat 
 more introspective and worried about himself than previously. 
 The morning of admission he felt well and cheerful. He arrived at 
 his place of business without in any way over-exerting himself, and 
 sat down at his desk. A little while later his head was seen to drop 
 forward, he stiffened out, and then collapsed in his chair. He had 
 been unconscious from 7 a.m. to 1 p.m. A physician had given 
 stimulants, etc., without effect. 
 
 Examination showed him cyanotic, with pinkish frothy sputum 
 pouring out of the mouth and nose. There were bubbling rales 
 throughout both chests. The cardiac dullness was increased. 
 The pulse was not felt at the wrist. There was no edema. There 
 is no record of the chart, urine or blood. The pulse was slightly 
 irregular at first, later very irregular. The blood pressure was 100/-, 
 gradually dropping. 
 
 Caffein, adrenalin and atropin were injected intramuscularly, 
 digifolin intravenously and adrenalin, caffein and atropin intra- 
 cardiacally with only slight temporary effect. Venesection was 
 without effect, as the blood was so thick and black it barely dripped. 
 The patient stopped breathing, and in spite of cardiac massage and 
 artificial respiration died half an hour after admission. 
 
 Clinical Diagnosis (from Hospital Record)—Acute pulmonary 
 edema. 
 
go FACTS ON THE HEART 
 
 Mitral stenosis. 
 
 Dr. Richard C. Cabot’s Diagnosis—Acute pulmonary edema. 
 
 Chronic endocarditis of the mitral valve. Stenosis. 
 
 Ball thrombus? 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral valve. 
 Stenosis. | 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Slight edema piae. 
 
 Obsolete tuberculosis of a mesenteric lymphatic gland. 
 
 Slight chronic pleuritis, left. . 
 
 Dr. RICHARDSON: There was a small amount of thin pale fluid in 
 the peritoneal cavity. The esophagus and gastro-intestinal tract 
 showed some areas of ecchymosis and reddening, the reddening of 
 course that of passive congestion. One of the mesenteric glands 
 showed marked calcareous degeneration,—obsolete tuberculosis. 
 
 The liver was two and a half cm. below the costal border. The 
 diaphragm on each side was at the sixth rib. In each pleural cavity 
 there were a few c.c. of thin fluid slightly blood stained. There were 
 no adhesions on the right; on the left a few in the region of the upper 
 lobe. The trachea and bronchi contained much pinkish froth and 
 frothy fluid. As far as that goes it would indicate, of course, edema 
 of the lungs. The lungs showed passive congestion and also much 
 edema. 
 
 The heart weighed 560 grams. That is considerably enlarged. 
 The myocardium was pale brown-red, with a right ventricle wall of 
 five to eight mm., indicating of course at once some obstruction on 
 the left side or some obstruction in the pulmonary valve. The pul- 
 monary valve was negative. The tricuspid valve was increased in 
 circumference, but otherwise was negative. ‘There was no hyper- 
 trophy of the left ventricle wall. The cavity of the left ventricle 
 was full sized. The left auricle was considerably dilated and the wall 
 somewhat thickened. The right cavities showed much dilatation. 
 The auricular appendices were free. The foramen ovale was closed. 
 
 The mitral valve showed much deforming fibrosis with areas of 
 fibrocalcareous change. This deforming process formed a flat collar 
 about the orifice of the mitral and reduced the opening to a button- 
 hole-like cervice one and a half cm. by five mm. There was some 
 thickening and fusion of the chordae tendineae,—all told, a marked 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES OI 
 
 mitral stenosis. In places on the endocardium of the left auricle, 
 above the mitral valve, there were here and there small areas of 
 fibrous roughening, and in one or two places these were covered with 
 thin smooth calcareous shells, the end result, of course, of endocardi- 
 tis extending to the auricular surface. The aortic valve measured 
 6.5 cm. and was negative. The coronary arteries were free and nega- 
 tive. Altogether this was a typical picture of mitral stenosis, with 
 hypertrophy of the right side of the heart, some dilatation on the left, 
 more especially in the left auricle, and marked hypertrophy and 
 dilatation on the right. The aorta and great branches, the pulmon- 
 ary artery and veins, the venae cavae, the portal vein and radicles 
 were frankly negative. 
 
 The liver weighed 1325 grams (normally 1200-2400) and showed 
 chronic passive congestion. It was 2!4 cm. below the costal border. 
 
 The spleen weighed 354 grams (normally 80-180), was moderately 
 enlarged and showed chronic passive congestion, that is, dark brown- 
 ish-red elastic tissue. There are three accessory spleens. The 
 kidneys were rather small but showed chronic passive congestion. 
 
 Dr. Casot: Dr. Richardson, do you realize that this man went 
 to his job feeling perfectly well on the morning that he was brought 
 here, that he was brought here at one o’clock, and died in half an 
 hour,—went from good health to death in four and a half hours,—and 
 that nothing that you have read in any way explains that—does it? 
 
 Dr. RICHARDSON: Of course if one says edema of the lungs, you 
 ask me what that is due to; and then if I say the heart muscle gave 
 out, we are still in the same place. There was no medication in this 
 case, was there? 
 
 Dr. Cazsor: I do not believe that anything given him killed him. 
 He was under our care in the Out-Patient Department when last 
 heard from before the day of death. 
 
 Dr. RICHARDSON: I mention that on account of a case that stands 
 out very distinctly in my memory, a medico-legal case in which the 
 patient was being treated at the Out-Patient Department. At her 
 death, which was rather sudden, the case was made medico-legal. I 
 think I found as many as half a dozen bottles of all kinds of drugs for 
 heart disease which she had accumulated and kept under the pillow, 
 eating them as she saw fit. That is a remote possibility of course, 
 but it could happen. It was a perfectly clear-cut case so far as the 
 anatomy went. 
 
 Dr. Casot: The case seems then merely to give one more illus- 
 tration of how little we know about the immediate cause of death. It 
 
Q2 FACTS ON THE HEART 
 
 does not seem as if in medical literature our complete ignorance on 
 that matter has been stressed as much as it should be. We know 
 pretty well why he lived for four years; we do not know at all why 
 he died at the end of four years. I do not know any more striking 
 example of how little we know in these cases. 
 
 Dr. RICHARDSON: Associated with this comparatively sudden 
 exit did he do any lifting or anything unusual? 
 
 Dr. Casor: No, it is particularly stated that he did not. 
 
 AN INTERNE: He rode seven miles in an open car coming here 
 after this thing had started, and was very much worse after he got 
 here. He was riding against the wind. 
 
 Dr. Casor: But he collapsed at his desk before that. 
 
 Dr. RicHarDSON: These patients do that, don’t they—I do not 
 mean collapse to death necessarily, but collapse? 
 
 Dr. Cazsot: No, I do not think they do when in good compensa- 
 tion, as he was. 
 
 Dr. MEAns: Did the microscopic examination of the heart muscle 
 show anything definite that might throw any light on this? 
 
 Dr. RicHARDSON: No. The myocardium macroscopically and 
 microscopically was negative as regards chronic interstitial myocardi- 
 tis. There was of course the marked hypertrophy and dilatation of 
 the right heart, and the mitral orifice or crevice measured 1% cm. by 
 5 mm., as compared with the usual measurement of 10 cm. 
 in circumference. 
 
 Necropsy 4525 
 
 ~ A Lithuanian rubber factory operative of thirty-three was referred 
 November 27, 1922, from the Out-Patient Department, where he 
 came complaining of swelling of the face and legs. Examination in 
 the Industrial Clinic showed pallor, edema of the eyelids, pyorrhea, 
 black dots on the gums, and weak hand grip, both sides. His past 
 history was negative except for occasional headaches and nosebleeds. 
 He smoked twenty cigarettes a day and occasionally took alcohol. 
 Seven weeks before admission he began to have cough with a 
 little white frothy sputum, followed by a pain in the stomach. 
 November 20 his legs and ankles began to swell. Since this time he 
 had had frequent urination by day and two or three times at night, 
 and dyspnea, occasional vomiting, and a cough which disturbed his 
 sleep. The urine had been cloudy and his mouth had felt dry in the 
 morning. He felt very well. 
 Examination showed a well nourished man with puffy face and 
 eyelids and some orthopnea. There were many acne scars on the 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 93 
 
 back of the neck and head. The mucous membranes were pale. 
 There were a few bean-sized cervical and some small axillary glands. 
 The lungs were clear in front. The lungs showed rales in both 
 backs. The apex impulse of the heart was seen and felt in the fifth 
 space 14cm. to the left. The left border of dullness was 14 cm. to the 
 left of the midsternum, the right border 4 cm. to the right, the supra- 
 cardiac dullness 7cm. There wasa presystolic thrill. The pulmonic 
 second sound was markedly accentuated. A rumbling diastolic 
 murmur followed the first sound, which was largely replaced by a loud 
 systolic transmitted to the axilla. Both murmurs were best heard 
 over the apical region. The blood pressure was 160/85 to 140/95. 
 The abdomen was slightly prominent, with edema of the wall and 
 shifting dullness in the flanks. There was massive edema of the 
 feet and legs. The fingers and toes showed marked clubbing. 
 There were many purpuric spots over both lower legs. The knee- 
 jerks were unequal, the pupils normal. 
 
 The temperature was 97° to 100.6°, the pulse 62 to 110, the respi- 
 ration 20 to 31. The output of urine was 32 to 62 ounces, with one 
 drop to 16 ounces January 3. The specific gravity was 1.008 to 
 1.020. The urine was cloudy at nine of twelve examinations, 
 alkaline at four, and showed a very slight trace to a very large trace 
 of albumin at nine, red blood cells at all but one, 50 to 150 per high 
 power field at all but three, leucocytes at seven, an occasional 
 granular cast at the first three, hyaline casts at the last. The renal 
 function was 30 to 38%. The hemoglobin was 60 to 70%, the 
 leucocytes 4400 to 7000, the polynuclears 72 to 48.5%, the reds 3,392,- 
 000 to 4,976,000. December 22 there was 9.5% atypical mononu- 
 clears, some vacuolated cells, lymphocytes of all sizes and shapes, 
 many not typical, platelets apparently diminished, red cells slightly 
 achromic, a moderate number of small oval cells and some true 
 microcytes. A blood culture December 16 showed Gram-positive 
 diplococci; others December 19 and 22 were negative. The non- 
 protein nitrogen was 50.7 mgm. to 47.1 mgm. A Wassermann 
 Was negative. Examination of the fundi December 22 showed the 
 retinal vessels tortuous, the nerve heads somewhat blurred; possibly 
 smal] congenital hemorrhage of the left nerve head. A throat con- 
 sultant found the tonsils small, not infected. The nose showed a 
 tendency to atrophic retinitis. There wasno pus. ‘The sinuses were 
 clear. No focus of infection was found. X-ray November 29 
 showed the sinuses normal in density and outline. The right frontal 
 sinus was somewhat larger than the left. The teeth were negative. 
 
94 FACTS ON THE HEART 
 
 December 22 there were no changes as far as could be made out in 
 the feet. The fingers however showed distinct increase in the size 
 of the tips of the terminal phalanges. (See illustration.) 
 
 By December 2 the edema was going. There were still a good 
 many red cells and a trace of albumin in the urine with a little pus. 
 No foci of infection were discoverable. His industrial history was 
 gone into twice without proving much as to the possibility of lead 
 posioning. His work had nothing to do with mixing. His house was 
 piped with lead pipes. His gums showed a blue line, but with the 
 
 Flt nse ss iano i DANS EE an 
 
 Fic. 6.—The tips of the terminal phalanges show distinct increase. 
 
 magnifying glass it had not the characteristics of a lead line. Of 
 the classical symptoms he had had only constipation. Reéxam- 
 ination of an over-stained blood smear showed no stippling. The 
 platelets were increased. December 17 there were a few petechiae 
 on the feet. December 23 the visiting physician found the spleen 
 three inches below the costal margin. The red blood count tended 
 gradually downward. There were occasional new pin-point purpuric 
 spots on the feet. The spleen enlarged slowly but steadily. 
 
 January 20 he was discharged unrelieved. 
 
 After his discharge he felt much better for two months. March 
 12, 1923, records of the Out-Patient Department showed edema of 
 the extremities, purpuric spots, rales in the lungs, heart condition 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 95 
 
 about the same, blood pressure 140/98, hgb. 60%, reds 3,880,000, 
 smoky urine. Orders, digitalis gr. iss. About March 20 he began 
 having dyspnea on slight exertion and general weakness. Soon after 
 this he began having cough, at first unproductive, later with white 
 sputum. April 6 he began to have edema of the lower extremities 
 and Aprial 8 edema of the eyelids. April 6 he noticed also numerous 
 spots on the legs. Since his discharge he had slept with two pillows. 
 He had urinated twice at night until April 4, then four or five times. 
 He had stayed at home, and his greatest exertion had consisted in 
 daily walks. 
 
 April 10, 1923, he was readmitted to the wards. Examination 
 showed frequent cough, pyorrhea, shotty cervical and left axillary 
 glands, and engorged veins in the supraclavicular space on the right. 
 The chest expansion was limited. The right chest was full of coarse 
 
 Cearse musical 
 inepiratory and 
 expiratery 
 rales. 
 
 ATs 
 
 t 
 
 Coarse moist inspiratory 
 and expiratory ralés 
 
 p» 
 Ey 
 
 al 
 
 mt 
 y 
 
 NO 
 oe 
 
 e/ 
 
 NY 
 
 Fig: =9; 
 
 musical inspiratory and expiratory rales. There were a few coarse 
 rales at the left posterior apex. The heart was enlarged downward 
 and to the left. The impulse was heaving. At the apex, 14 cm. to 
 the left in the sixth space, was a short faint systolic murmur. A long 
 rough harsh diastolic was heard over the lower precordium. At the 
 base the pulmonic second sound was accentuated and greater than 
 the aortic second, with a blowing systolic and diastolic murmur. 
 There was a questionable thrill at the apex. The blood pressure was 
 120/85 to 150/90. The abdomen showed a large area of shifting 
 dullness. (Fig. 7.) The liver was four finger-breadths below the 
 costal margin, the spleen one or two finger-breadths below. ‘There 
 was marked edema of the sacrum and ankles. The finger tips were 
 clubbed, with an inflammatory zone around the nails. There were 
 red thickened areas the size of a dollar on the palms. 
 
 The temperature was 94.6° to 102.7° (rectal), the pulse 53 to 127, 
 the respiration 20 to 34. The output of urine was 32 to 80 ounces, 
 
96 FACTS ON THE HEART 
 
 the specific gravity 1.010 to 1.014. The urine was reddish and cloudy 
 at one of eight examinations, showed a slight trace to a large trace of 
 albumin, leucocytes, many red blood cells, and rare to many granular 
 casts at all, cellular at four. The renal function was 10 to 15% 
 (four tests). The hemoglobin was 60%, the leucocytes 9700 to 
 25,000, the polynuclears 64%, the reds 3,800,000 to 3,960,000, 
 with some variation in size and occasional oblong cells. The 
 platelets were descreased. Blood cultures April 21, 23 and 24 
 were negative. The non-protein nitrogen was 58.2 mgm. April 
 13, 64.5 mgm. April 18, 91 mgm. April 24, 110 mgm. May 2, 163.5 
 mgm. May 8. A Wassermann was negative. 
 
 It was difficult to restrain the patients fluid intake. By April 17 
 he was losing a little puffiness about his face. The temperature was 
 a little more steady and the pulse slightly lower. The administra- 
 tion of mercurochrome April 23 was followed by a chill, and the 
 patient felt very uncomfortable the rest of the day. 
 
 April 25 a hematoma appeared on the inside of the cheek as a 
 result of biting the cheek. Two days later the area was infected and 
 a crusted gray area showed. A smear showed many organisms of all 
 sorts, many spirochete forms, bacilli, cocci, streptococci, some 
 fusiform bacilli: April 28 Dr. C. Morton Smith noted considerable 
 numbers of the organisms of the Vincent’s angina group. ‘The cheek 
 was painted with diarsenol. By the 30th the ulcer was a sizable 
 slough. 
 
 The patient became increasingly edematous and -stuporous. 
 The leucocyte count and the non-protein nitrogen rose. May 8 
 the patient quietly died. 
 
 Clinical Diagnosis (from Hospital Record) —Rheumatic heart 
 disease. 
 
 Mitral stenosis. 
 
 Subacute bacterial endocarditis. 
 
 Acute nephritis. 
 
 Dr. Richard C. Cabot’s Diagnosis-—Chronic endocarditis of the 
 mitral valve. 
 
 Mitral stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Infarcts of the spleen and kidneys. 
 
 Terminal infection? 
 
 Anatomical Diagnosis—Chronic and subacute endocarditis of 
 the mitral valve. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 07 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, right. 
 
 Ascites. 
 
 Slight hydropericardium. 
 
 Anasarca. 
 
 Infarcts of the spleen and kidneys. 
 
 Chronic pleuritis, left. 
 
 Obsolete tuberculosis of a bronchial gland. 
 
 Chronic peritonitis. 
 
 Wet brain. 
 
 Dr. RicHARDSON: This man had pop-eyes. 
 
 A House OrFicer: That should have been noted in the record. 
 There was an appearance of exophthalmos, but not very marked. 
 
 ‘ Dr. Casot: That rather goes to support those who believe there 
 is nephritis in the case. That goes with nephritis. 
 
 Dr. RicHarpson: The pia showed marked edema, infiltration 
 with thin pale fluid, and there was considerable in the brain tissue. 
 The vessels of Willis, the sinuses, the pineal and pituitary glands were 
 negative. That leaves nothing but a wet brain. 
 
 The fingers and toes showed well marked clubbing. 
 
 Much frothy fluid ran from the mouth. 
 
 The feet and ankles were swollen and pitted on pressure, and 
 there was a little edema of the thighs. Scattered over the legs and 
 feet and on the skin of the trunk were those purplish areas spoken of 
 in the clinical picture. 
 
 The peritoneal cavity contained at least 200 c.c. of clear straw- 
 colored fluid. The serosa of the intestine showed scattered over it 
 here and there small hemorrhagic areas. 
 
 The gastro-intestinal tract on section showed chronic passive 
 congestion. 
 
 The anterior margin of the right lobe of the liver was twelve and 
 a half cm. below the costal border. The diaphragm on the right 
 was at the fifth rib, on the left at the sixth interspace. That is down 
 at least a rib’s width on each side. 
 
 The right pleural cavity contained about 1000 c.c. of fluid. On 
 the left there was no fluid, but the cavity was obliterated by old 
 adhesions. These adhesions were juicy, but there was no free 
 fluid. 
 
 There was much brownish-red frothy fluid in the trachea and 
 
 bronchi. The bronchial glands were slightly enlarged, brownish-red, 
 7 
 
98 FACTS ON THE HEART 
 
 juicy, congested; one of them was transformed into fibrocalcareous 
 material, obsolete tuberculosis. 
 
 Dr. Casort: That is all an old process? 
 
 Dr. RicHarpDson: Absolutely. The difference between the 
 right and the left lung is slightly important. We have much fluid on 
 the right, none on the left. But the left lung was much wetter than 
 the right one. The left of course was bound up in the adhesions. 
 
 The pericardium showed 100 c.c. of thin clear fluid,—no pericardi- 
 tis. The heart weighed 685 grams. For this man a heart of 350 
 grams would have been a fair size. In the text books they give tables 
 
 of heart weights, but every man’s heart must be considered in compari- 
 gnts, y p 
 
 son with the makeup and muscular development of the man. The 
 myocardium was of fair consistence and brown-red. I could not 
 make out any areas of myocarditis, meaning by myocarditis the 
 replacement of muscle tissue by fibrous tissue. The thicknesses 
 were four to five mm. on the right, ten on the left,—perhaps a little 
 thin on the left, and full thickness on the nght. The columnae 
 carneae were well marked. So that all told it was a muscular heart. 
 
 There was much dilatation on the left, moderate dilatation on the 
 right.. The valve circumferences were as follows: the mitral 1314 cm. 
 —usually ten; but in spite of that the mitral was the seat of chronic 
 endocarditis and some subacute endocarditis. That appeared on 
 the valve in this fashion. The curtain itself showed some diffuse 
 fibrous thickening rather generally and in two places was definitely 
 thickened. Rising from that was a fringe of small masses which at 
 the bases were perhaps a little firm, but as we went towards the tip 
 grew spongy and soft. So that we have some old endocarditis and 
 on top of it this subacute endocarditis. 
 
 Dr. CazotT: There is rather surprisingly little chronic endocarditis. 
 
 PTE es She spate 
 
 ~ 
 Mm 
 
 23 cata 
 
 Dr. RICHARDSON: At one end of that valve there was quite a large 7 
 
 patch extending up on the endocardium of the left auricle, occupying 
 an area at least three or four cm. across. 
 
 Dr. Casort: Is that the subacute process? 
 
 Dr. RICHARDSON: Yes, on its surface; but at the base it was a 
 little fibrous. Again, under the mitral curtain it curved around 
 on the under surface of the valve. 
 
 The aortic, tricuspid and pulmonary valves were out of the pic- 
 ture except for some increase of the circumference of the tricuspid. 
 
 Here we have a rather curious condition,—a valve which meas- — 
 ured laid open 1314 cm. and yet had masses of vegetations on it 
 which when the valve was shut one would think would decrease its — 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 99 
 
 circumference, a paradoxical condition. When those masses were 
 together I should say there was a little decrease. There was an 
 increase in the circumference when the valve was laid open, but when 
 that was brought together there probably would be a slight decrease 
 in the circumference. The blood would have a smaller space to go 
 through. 
 
 The coronaries were free and negative. That gives us a chronic 
 and subacute endocarditis with hypertrophy and dilatation; and 
 I could find nothing else as the basis for that hypertrophy and 
 dilatation. 
 
 The aorta and great branches, the pulmonary artery, veins and 
 vena cava were negative. In other words, the circulatory apparatus, 
 except that it had been the means of conveying from this mitral valve 
 smaller and larger bits to the spleen and kidneys, was out of the pic- 
 ture. It did convey to them the small bits of vegetation and it did 
 set up in them infarctions. 
 
 The liver, which was a little large, showed beginning congestion. 
 The spleen weighed 465 grams and was the seat of infarcts. The 
 adrenals were negative. 
 
 The kidneys were rather large, weighing 375 grams. They 
 showed the infarcts, and macroscopically I could make out no definite 
 nephritis. Of course there was passive congestion. There was 
 nothing the matter with the kidney vessels, no arteriosclerotic 
 changes in the renal branches; that is, none of the fibrosis which we | 
 see in the section surfaces and which is one of the landmarks of 
 arteriosclerotic nephritis. The only other thing in the kidneys was 
 that in each kidney there were infarcts. Some of these infarcts 
 seemed to be old, others more recent. That is in harmony with the 
 picture on the valve,—some of it old, organized, some of it softer 
 and more in the subacute stage. 
 
 Culture from the heart blood showed no growth. This case from 
 the anatomical side looked like one of those where the organism is of 
 the viridans group; and in those cases it is not unusual to get a cul- 
 ture and also not unusual to find none. Once in a while we get them 
 at necropsy, and in one case I have seen the blood stream was negative 
 and I found the organsim in an infarct of the spleen, which was soft 
 and broken down. But it all depends on whether the fish are running 
 in the stream and whether we know the hour when to fish. At 
 intervals the stream seems to clear up and the organisms all go into 
 their lairs. They come out again, and if we are there with the material 
 we can get them. - 
 
IOO FACTS ON THE HEART 
 
 In the region ofthe gall-bladder there were a few old adhesions. 
 
 Dr. Caspot: Was there any change in his fingers between the 
 first entry and the second? 
 
 A House OFFICER: Yes, sir. There was apparently a very rapid 
 development. There were no hemorrhages in the finger tips, although 
 they were present in other parts of the body. The clubbing even at 
 the firsty entry was very marked. 3 
 
 Dr. Capot: I think this is a very interesting case. Perhaps 
 the greatest interest is that he did not have nephritis. 
 
 A PxysIctAn: Will you review why you barred that? 
 
 Dr. Cazot: In the first place, he never had a high blood pressure. 
 
 A PuysicIAN: What do you call a high blood pressure—one 
 hundred and sixty? 
 
 Dr. Casot: I depend a good deal more on the diastolic than on 
 the systolic. He must have a diastolic of over one hundred and a 
 systolic of more than this—I won’t try to say how much more— 
 before I call it elevated. 
 
 It is only at the end that he had any high non-protein nitrogen, 
 only at the end that he got anything approaching fixation of gravity, 
 only at the end that his renal function by the red test was low at all. 
 He never had any uremia, or anything to approach a uremic state. 
 The clubbed fingers which he had from the start do not come from 
 nephritis. They come only when we have something other than 
 nephritis; he had that something from the beginning. He never, 
 even to the very end, had a low enough renal function by the red 
 test to make us sure of chronic nephritis. He never got below ten. 
 
 A PuysIciAn: Were the emboli septic emboli? 
 
 Dr. Casot: I suppose so. We have to say they were bacterial 
 emboli, but they were of low virulence. They never produced any 
 sepsis around the nails. 
 
 It seems to me very interesting to know that we can get a high 
 rising non-protein nitrogen from renal infarcts. I was banking a 
 good deal on the fact that I am confident that when a spleen grows 
 under observation it is infarcted. If we have splenic infarct, then 
 renal too. If infarcts are blocking the kidney that will account for 
 the loss of kidney function even though there is no nephritis. 
 
 The condition of the mitral valve seems very interesting too, 
 because on the whole we have to say le did have mitral stenosis 
 even though the circumference was increased, because the masses 
 on the valve narrowed the opening. | 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES IOT 
 
 Necropsy 4289 
 
 An American elevator man of forty-four was referred to the wards 
 from the Out-Patient Department January 25, 1921, where he had 
 come complaining of dyspnea of three weeks’ duration. He had 
 “rheumatism” at twenty-two in the soles and small joints of the feet; 
 no fever; at twenty-five or thirty “‘soft chancre’’ for a week. He 
 denied syphilis. At thirty he had a bubo, which “broke” and healed 
 in a week. He drank much beer until prohibition in 1920. He 
 rarely urinated at night. His best weight was 145 pounds, his 
 usual weight 135. 
 
 A year before admission he noticed palpitation on exertion, 
 brought on he believed by the strong winter winds. For three 
 months this persisted. One evening he had hemoptysis five or six 
 times, though he had no cough or edema. After this he was better, 
 though the palpitation on exertion persisted in less degree. Five 
 weeks ago the strong winter winds brought the dyspnea back. 
 Dull precordial pain always followed the dyspnea, at first for short 
 periods, later for longer. A week and a half later he got his feet 
 wet, ‘‘caught cold,’ and began to have attacks of coughing with 
 dyspnea once a night, the attacks increasing in length until they had 
 lasted all through the last three nights, with orthopnea and “‘asth- 
 matic’ coughing and white sputum, lately as much as a cupful, 
 mostly expectorated in the evening and early night. Three weeks 
 ago he began to have fairly sharp steady pain in the precordia and 
 left lower chest in the posterior axillary line when he opened the 
 elevator door. This seemed to be getting worse. 
 
 Examination showed a fairly well nourished man weighing 12014 
 pounds, with flushed cheeks. (Cyanosis of the nose and lips is 
 mentioned in the Out-Patient examination.) There were some cari- 
 ous teeth and pyorrhea. ‘The nasal septum deviated slightly to the 
 right. There was mucus in the nasopharynx. The lung signs were 
 as shown in Fig. to. The apex impulse of the heart was seen and 
 felt in the fifth space 8.5 cm. to the left. The measurements by 
 percussion and by X-ray are shown in Figs. 8 and 9. The action 
 was absolutely irregular. The sounds were of poor quality, the pul- 
 monic second sound greater than the aortic second. There was a 
 presystolic roll at the apex and a systolic murmur over the precordia. 
 No thrill was felt. The pulses were normal, the artery walls 
 palpable. The systolic blood pressure was 135, the diastolic 75. 
 Electrocardiogram showed auricular fibrillation, ectopic ventricular 
 contractions, rate 100, only moderately irregular. The liver dullness 
 
I02 FACTS ON THE HEART 
 
 began at the fifth space. The edge was felt 4 cm. below the costal 
 margin. The genitals, extremities, pupils and reflexes were normal.” 
 
 January 25 and 26 the temperature was 100.4° to 98°, the pulse 
 100 to 83, the respiration 32 to 20; afterwards the temperature was 
 not elevated (occasionally 97° or a little below), the respirations 
 were not remarkable, the radial pulse was 92 to 50; deficit 2 to 15 
 
 OS cn. 
 
 3.5 9 eae SH 
 Fic. 8.—Measurements by percussion. Fic. 9.—Measurements by X-ray. 
 
 The amount of urine was 15 to 80 ounces, the specific gravity 1.034 
 to 1.016. The urine was cloudy and alkaline at four of five exami- 
 nations; no albumin or sugar. The renal function was 50%. The 
 blood was normal. Two Wassermanns were negative. Fluoros- 
 copic examination showed the findings seen in Fig. 11, and also 
 
 showed the diaphragm very low, and forced respiratory excursion 
 limited on both sides. 
 
 Slignt dudiness} 
 both apices. 
 
 Coarse 
 moist 
 
 Scattered fine and 
 mediius woist rales, 
 a rare? coarse dry 
 rale. 
 
 —— 
 
 ———<s 
 7S 
 
 Fic. 10. 
 
 The orders were as follows. January 25 soft solids, codein gr. 
 14 by mouth at 7:30 p.m., repeat s.o.s. tonight; January 26 saturated 
 
 * (From the Out-Patient record.) Heart. Apex impulse heaving, slightly outside 
 the nipple line. Some enlargement to right and left. 442 | II First 
 sound at the apex very sharp, preceded by a crescendo murmur. A questionable thrill 
 at the apex. Abdomen negative throughout. - In the left inguinal region was a scar, 
 
 probably of old bubo. Otherwise genitals negative. Extremities cyanosed. No 
 edema. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 103 
 
 solution KI ten drops t.i.d., codein gr. 14 by mouth s.o.s.; February 7 
 fluid extract of convallaria 2 c.c. t.1.d.; February ro convallaria 5 c.c. 
 t.i.d.; February 11 convallaria to c.c. t.i.d.; February 12 convallaria 
 15 c.c. t.id.; February 13 discontinue convallaria; February 14 
 digitalis leaves gr. iil. t.i.d. 
 
 January 30 it was noted that the pulse was coming down and 
 the heart’s action was more regular. There were now a few extra- 
 systoles. February 3 the deficit was quite small. Convallaria was 
 
 Fic. 11.—The heart shadow is distinctly enlarged, but almost entirely in the region 
 of the auricles. There is marked prominence of the heart shadow in the region of the 
 left auricle. The appearance is characteristic of mitral stenosis with dilatation of the 
 auricles. The hilus shadows and lung markings are increased on both sides. The 
 tight upper chest is less radiable than the left. Extending across the right lung field 
 from the hilus to the chest wall is a dense linear shadow suggesting thickened interlobar 
 septum. The costophrenic angles are clear. 
 
 ‘found to have practically no effect. February 14 he was put upon 
 digitalis. February 15 there was improvement in the condition. 
 February 19 he was discharged, with instructions to take a small 
 dose of digitalis. 
 
 March 5, 1921, he returned to the Out-Patient Department com- 
 plaining of fatigue and dyspnea on very little exertion, frequent swell- 
 ing of the feet, and early morning cough. His Ue eats and sleep 
 were fair. He was taking no digitalis. 
 
I04 FACTS ON THE HEART 
 
 Examination showed a pulse deficit of 27 (apex 106, radial 79). 
 The heart showed absolute irregularity; a low rumbling diastolic 
 murmur at the apex with a blowing systolic just inside (tricuspid 
 area); the pulmonic second sound accentuated; the first sound at the 
 apex not much accentuated. The lungs were filled with sonorous 
 and crackling rales, groans and wheezes, most marked at the right 
 base behind. There was cyanosis of the lips, nose, cheeks and ears. 
 
 He was ordered digitalis leaves 0.1 gram t.i.d. for three days, then 
 once a day until March tro, when he was told to return to the Cardiac 
 Clinic. 
 
 March 10 he felt quite well, though he was still short of breath 
 on exertion. He had taken the digitalis as ordered. His weight was 
 found to be 13014 pounds. Examination showed the apex pulse 
 to be 58, the radial 56. He had the typical mitral facies. The 
 diastolic murmur was very marked, typical of mitral stenosis. He 
 was ordered to take a grain and a half of digitalis once or twice a day 
 and report again in four weeks. 
 
 April 7 he felt pretty well. He had taken one pill daily except 
 for three days when he took none. He was hoarse, and had been so 
 at times for two months. On examination he weighed 133 pounds. 
 The diastolic murmur was very marked. The left border was to cm. 
 from midsternum,—a straight left border suggestive of left auricular ~ 
 enlargement. He was ordered a grain and a half of digitalis once 
 a day; to report again in two months. 
 
 June 9 examination showed his weight to be 132 pounds. He 
 felt fairly well. Electrocardiogram showed auricular fibrillation, 
 right ventricular preponderance, a rate of 90. The murmur was as 
 before. He was hoarse. He was ordered a grain and a half of digi- 
 talis once or twice a day; to report again in two months. He was 
 referred to the Throat Department with a question as to laryngeal 
 paralysis. 
 
 August 4 he was feeling very well. The hoarseness continued. 
 He had been taking digitalis regularly twice a day for the first three 
 weeks, then oncea day. He was working regularly. On examination 
 the apex rate was 72, the radial 64. There was a mitral diastolic 
 murmur at the apex as before, and absolute arrythmia. He was told 
 to continue the digitalis as before and to report again in two months. 
 He now went to the Throat Room, where the only finding was dis- 
 eased tonsils which it was thought should be removed if the condition 
 would warrant operation. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 105 
 
 October 27 he reported that he had kept on with the digitalis 
 until it gave out the week before. He was getting very short of 
 breath again. 
 
 Examination showed his weight to be 13214 pounds. The sys- 
 tolic blood pressure was 130, the diastolic 80. The apex pulse was 82, 
 the radial 82. There was absolute arrythmia and a typical mitral 
 diastolic murmur. He was told to take digitalis as before and to 
 report again in three months. 
 
 Discussion by Dr. Paul D. White —It is obvious from the history 
 and physical examination that this patient had rheumatic heart 
 disease with mitral stenosis, auricular fibrillation, and a tendency 
 to failure of the congestive type. Although it is possible that there 
 has been a syphilitic history in the past there is no reason to believe 
 that it is in any way a factor in the causation of his present heart 
 condition. He has a typical mitral facies. The report of the physi- 
 cal examination made in the ward January 25, 1921, states that the 
 action of the heart was absolutely irregular, sounds of poor quality, 
 presystolic roll at the apex and a systolic murmur over the recordia. 
 A somewhat similar examination made in the Out-Patient Depart- 
 ment just prior to admission to the ward I feel is quite inaccurate. 
 My opinion is based on the findings made in the Cardiac Clinic in 
 March, where the absolute irregularity was still found, and a low 
 rumbling diastolic murmur at the apex without a presystolic accen- 
 tuation. This low rumbling diastolic murmur beginning at a short 
 interval after the second sound and heard best at the apex (in the 
 reclining position with a bell stethoscope) is typical of mitral stenosis 
 when auricular fibrillation is present. One does not find the presys- 
 tolic murmur of mitral stenosis in the presence of auricular fibrilla- 
 tion, except rarely when the heart is beating very fast. The much 
 more Important murmur is the mid-diastolic rumble which was the 
 only murmur in his case’ in diastole. His mitral stenosis must have 
 been of years’ duration. His auricular fibrillation quite probably 
 started at the time he first noticed palpitation a year ago. 
 
 One rarely finds auricular fibrillation in rheumatic’ heart disease 
 without mitral involvement, and very frequently the two conditions, 
 mitral stenosis and auricular fibrillation, go together. It is for this 
 reason that I insist on the absolute need of recognizing the mid-dia- 
 stolic murmur when these two conditions are present together. As 
 a matter of fact even when the rhythm is normal the mid-diastolic 
 murmur is still present if there is much mitral stenosis, but there is in 
 addition a presystolic accentuation which used to be regarded as the 
 
106 FACTS ON THE HEART 
 
 only important murmur in mitral stenosis. I am surprised to find 
 that the records even at the present time are still full of such inaccu- 
 racy as is found here in both the record made in the ward and the first 
 examination in the Out-Patient Department. It is high time that 
 the diastolic rumble of mitral stenosis in auricular fibrillation be 
 described as such and not falsely interpreted as a presystolic roll. 
 
 Electrocardiogram confirmed the diagnosis of auricular fibrilla- 
 tion, and also showed evidence of preponderance of the right ventricle 
 and occasional ectopic contractions. One of the ward notes, Jan-— 
 uary 30, states that there were a few extra systoles. It takes a clever 
 man to diagnose extra-systoles in the presence of auricular fibrilla- 
 tion unless they are coming in a bigeminal fashion. Therefore I 
 should feel doubtful about this statement. 
 
 Now as to treatment. In the ward he was put to bed and given 
 soft solids and codein. This sounds like common sense. Another 
 order appears for potassium iodide. Just why this is given I do not 
 know unless for its action as an expectorant, but we have no proof 
 that it would help the condition of fibrillation or rheumatic heart 
 disease. From February 7 he received fluid extract of convallaria, 
 and continued to receive it for six days in steadily increasing doses. 
 At this particular time investigation of the digitalis-like action of 
 convallaria and apocynum was being carried on in the wards. They 
 are said to belong to the digitalis group, but it was felt that they had 
 not been properly classified. ‘The dose of convallaria in the pharma- 
 copeia is stated to be 14 of 1 c.c. in fluid extract. Having already 
 determined that larger doses were necessary to produce any effect 
 at all in cases of auricular fibrillation we gave two c.c. three times a 
 day at the start of the therapy in this case. Three days later this 
 was increased to 5 c.c. three times a day, one day later to ro c.c. three 
 times a day, and still a day later 15 c.c. three times a day. About 
 twenty-four hours after this, since convallaria was having little or no 
 effect and since it was necessary to have a digitalis action in this case, 
 the convallaria was stopped and digitalis given at the dose of three 
 grains three times a day in the standardized leaf. This makes two- 
 tenths of a gram three timesa day. Quite rapidly there was improve- 
 ment from the digitalis, such as was hoped for, with the reduction of 
 apex rate and clearing up of some of the symptoms of failure. The 
 convallaria even in doses thirty times the dose recommended in the 
 pharmacopeia had failed to produce the desired effect. 
 
 When the patient was discharged he was given instructions to 
 take small doses of digitalis. I find no note indicating how much he 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 107 
 
 was told to take. However, it was obvious that he took too little, 
 for when he returned to the Out-Patient Department March 5 he 
 was feeling badly. He had some edema, cyanosis, his lungs showed 
 rales, he was very dyspneic, his apex rate was 106 and his radial 79, 
 making a deficit of 27. He was told to take 149 of a gram of digitalis 
 three times a day. He returned March 10 feeling very much better. 
 His apex rate had dropped to 58, his radial rate was 56, a deficit of 
 two. This observation is a very important one. It shows the need 
 of giving a proper amount of digitalis, and it shows the excellent 
 control obtained by studying the apex rate and the pulse deficit. 
 He was told to continue on 149 of a gram of digitalis leaf once or twice 
 a day as needed. ‘This he has done most of the time. Since the first 
 observation was made in the Cardiac Clinic he has been quite well. 
 He had been at work and has stated occasionally that he felt very 
 well. Investigation of his hoarseness revealed nothing, although it is 
 quite likely that there is some pressure on his left recurrent laryngeal 
 nerve from the markedly enlarged left auricle, which in turn through 
 the pulmonary artery presses against the aorta and constricts the 
 nerve. 3 
 
 The moral from this experience is as follows: If digitalis is needed, 
 as it is in auricular fibrillation, it should be given in proper doses. 
 The patient should be quickly saturated with the drug, and the satura- 
 tion would be complete in within 48 to 72 hours, the dose depending 
 on the weight of the individual. Here we found that 69 of a grama 
 day quickly saturated this patient in our first observations in the 
 Cardiac Clinic. From 49 to 249 of a gram is excreted daily by the 
 average patient. Enough additional digitalis should be given daily, 
 therefore, to make up for this amount excreted. By the maintenance 
 of saturation the apex rate is kept down within normal bounds,—it 
 usually should be between 55 and 75,—the heart contracts strongly 
 and has plenty of rest. For this particular purpose digitalis is prac- 
 tically a specific, and it is in fibrillation of course that it acts so 
 dramatically. 
 
 Another important lesson is that drugs of the type of convallaria, 
 —this should alsoinclude apocynum and squill,—may well be omitted. 
 Digitalis does much more in benefiting the heart than any of these 
 drugs. Any other reasons that we have been able to observe for 
 which they might be given are absent. The dosage is inaccurate, 
 and they are not primarily diuretics. I see no reason why they 
 should be given any more. Cactus is a drug which has been included 
 by some in their treatment of heart disease. It has been given in 
 
108 FACTS ON THE HEART 
 
 enormous quantities in experiment without effect. It is my feeling 
 that this drug should be omitted from cardiac therapy, at any rate 
 from treatment of heart disease with failure. 
 
 With regard to digitalis I feel that it is given far too often and 
 when it is given it is often given wrongly. Digitalis may be recom- 
 mended for any one of the following three conditions, first, auricular 
 fibrillation, second, auricular flutter, and third, heart failure, no 
 matter what the rhythm. As a prophylactic of heart failure or 
 auricular fibrillation in an acute infectious disease such as typhoid or 
 pneumonia without cardiac damage I feel that it has no place. In 
 fact it is possible to produce fibrillation by the drug alone. Digitalis 
 is an irritant to the heart and a drug for which we should have great 
 respect, using it only when we have a clear indication for its use. 
 This also applies to the preparation of patients for surgical operation, 
 or for emergency use in so-called surgical shock, where again it has 
 no place. (My experience is entirely like Dr. White’s R.C.C.) 
 
 This patient has just been admitted to the ward (Novy. 8) 
 specifically for the treatment of auricular fibrillation. This treat- 
 ment consists in the use of quinidine sulphate. Quinidine sulphate 
 has a drug action which is one of the most dramatic in the whole 
 field of functional therapy. It abolishes auricular fibrillation or 
 auricular flutter in at least two-thirds of all the cases in which it is 
 tried. It does not of course cure heart disease, but in many cases it 
 restores normal rhythm and relieves the patient of disturbing palpita- 
 tion and of the likelihood of failure. It is not a drug, however, to be 
 given indiscriminately. At the present time investigations of its 
 use are being carried on all over this country and elsewhere. It is my 
 present feeling that it is one of the most valuable steps in advance in 
 our cardiac treatments to be made since Withering introduced 
 digitalis over one hundred years ago. Its action is well described by 
 Sir Thomas Lewis in the British Medical Journal for October 1, 1921. 
 Lewis had previously shown that auricular fibrillation and auricular 
 flutter are due to a curious circus movement of a contraction wave 
 in the auricle. This movement continues until broken up in some 
 way. Ordinarily it persists throughout life in the human being. 
 Increase of the refractory period of the auricular muscle is needed to 
 break up this circus movement. Quinidine does this. The drug 
 itself was investigated and found to have a specific action in these 
 abnormal rhythms by Frey in Berlin during the great war. Lewis’s 
 investigations of the mechanism of the circus movement were going 
 on independently. When these two very important pieces of work 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES IOg 
 
 were codrdinated a marked advance in the treatment of heart disease 
 was effected. 
 
 At the present time out of thirty-five cases of auricular fibrilla- 
 tion and auricular flutter at the Massachusetts General Hospital we 
 have restored normal rhythm, at least temporarily, in twenty-three. 
 
 Diagnosis —Rheumatic heart disease with mitral stenosis. 
 
 Auricular fibrillation. 
 
 Failure of the congestive type. 
 
 History, Continued.—Aiter his discharge from the hospital he 
 did not go back to work for three weeks. He had been taking 
 two pills daily. He had no precordial pain, but became dyspneic on 
 climbing two or three flights of stairs. He still slept propped up with 
 pillows. At times he awoke at night and coughed up a mouthful of 
 white frothy sputum. He had rare cough during the day. He had 
 been able to work comfortably. 
 
 Examination was as before except for the points noted. His 
 cheeks were flushed. The lungs showed slight dullness at the right 
 apex and coarse moist rales at both bases. The apex impulse of the 
 heart was seen and felt in the fifth space 1o cm. to the left. The 
 action was irregular, slow. The pulmonic second sound was accen- 
 tuated, fibrillating. There was a long rumbling mid-diastolic mur- 
 mur. ‘The left border of percussion dullness was 10.5 to the left of 
 midsternum, 2.5 cm. outside the midclavicular line, the right border 
 4.5 to the right, the supracardiac dullness 4.5 cm. Rectal examina- 
 tion showed a slightly enlarged prostate. A Wassermann was néga- 
 tive. Electrocardiogram November 8 showed auricular fibrillation, 
 rate 75, upright IT’ wave; November g, auricular fibrillation, rate 70, 
 diphasic T wave. 
 
 This patient, the thirty-sixth of our quinidine series, received a 
 total of 13.8 grams of quinidine sulphate in five and a half days 
 without restoration to normal rhythm and also without any toxic 
 effects whatever. The dose varied from o.2 gram twice the first 
 day to 0.08 gram five times on the fifth day. He must be recorded 
 as one of our quinidine failures. The duration of his arrhythmia may 
 be one of the reasons for its continuance even under quinidine therapy. 
 He was discharged from the ward November 13, 1921, and will 
 continue to be followed in the Cardiac Clinic of the Out-Patient 
 Department, being kept constantly on digitalis. 
 
 The records of the Out-Patient Department Cardiac Clinic show 
 that January 25, 1922, the patient reported shortness of breath for 
 the past three weeks, hemoptysis five or six times one evening. 
 
IIo - FACTS ON THE HEART 
 
 When seen in the wards January 26 he was in respiratory distress 
 and found it difficult to talk. January 23 at the beginning of a cold 
 snap he began to have unusual dyspnea with palpitation and coughed 
 up considerable white sputum. He continued at work, but went 
 home with some difficulty. January 25 he had dyspnea and palpita- 
 tion on the slightest exertion and was unable to go to work. His 
 legs were swelled to the knees. 
 
 Examination showed no dullness in the lungs. ‘There were many 
 moist rales below the angles of both scapulae and from the third 
 to both sixth ribs in front. The apex impulse of the heart was seen 
 and felt in the fifth space 8 cm. to the left. The left border of percus- 
 sion dullness was g.5 cm. to the left of midsternum, the right border 
 4 cm. to the right, the supracardiac dullness 5 cm. The action was 
 irregular, probably slow fibrillation, but there was a slight tendency 
 to bigeminy. The first sound was loud and snapping, the pulmonic 
 second sound accentuated. <A presystolic murmur was heard over 
 the precordium, and a faint systolic murmur, difficult to make out 
 because of rales and grunting respiration. A thrill was palpable, 
 maximum in the third space. The pulses were of low volume and 
 tension. The blood pressure was 125/60. There was very marked 
 edema of the ankles. 
 
 The temperature was 100.6°, rising steadily to 104°, the pulse 
 70 to tor, the respirations 19 to 50. The amount of urine is not 
 recorded. The specific gravity was 1.019. ‘The urine was alkaline 
 and there was a trace of albumin. The hemoglobin was 80%. The 
 leucocytes were 8400 to 14,800, the polynuclears 88%. A Wasser- 
 mann was negative. Electrocardiogram showed auricular fibrilla- 
 tion, rate 100, ectopic ventricular contractions, flat T wave, small 
 complexes. 
 
 The morning of January 27 slight dullness was found at the right 
 apex and around the spine of the right scapula with groaning rales 
 throughout the right lung and moist rales at both bases. The dysp- 
 nea seemed out of proportion to the other symptoms. That evening 
 there was dullness at both bases with rise in temperature and respira- 
 tion. That night the patient died. 
 
 Clinical Diagnosis (from Hospital Record) —Chronic valvular 
 heart disease. 
 
 Mitral stenosis. 
 
 Auricular fibrillation. 
 
 Bronchopneumonia. 
 
 Pulmonary edema. 
 
 a 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES i 2 
 
 Dr. Paul D. White’s Diagnosis.—Rheumatic heart disease. 
 
 Mitral stenosis. 
 
 Cardiac enlargement. 
 
 Bronchopneumonia. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosits.—Chronic endocarditis of the mitral valve 
 (stenosis). me | 
 
 Thrombosis of left auricular appendix. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, right. 
 
 Slight anasarca. 
 
 Chronic pleuritis. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 In the peritoneal cavity there was about fifty c.c. of thin pale clear 
 fluid. The mucosa of the gastro-intestinal tract was reddened, vel- 
 vety, juicy, showing chronic passive congestion. The mesenteric 
 and retroperitoneal glands were negative. 
 
 The right pleural cavity contained 500 c.c. of thin pale clear fluid. 
 On the left side the cavity was obliterated by old adhesions, but the 
 adhesions were wet. The lungs showed a typical picture of chronic 
 passive congestion, with a few small areas of questionable broncho- 
 pneumonia, but the macroscopical examination shows only chronic 
 passive congestion in these places. 
 
 The pericardium contained twenty-five c.c. of thin pale clear 
 fluid; negative. The heart weighed 545. grams,—considerably 
 enlarged. If he had had a heart weighing 350 it would have been a 
 good sized heart for him. The myocardium was pale brown-red and 
 a little flabby, toneless. The wall of the left ventricle was eleven 
 mm. thick; it was a little thin if anything. The right was four to 
 six mm., which of course is about twice as thick as usual, indicating 
 some obstruction in the region of the mitral valve or something in 
 the pulmonary valve. We can dismiss the pulmonary valve at once 
 because it was negative, and it is a very unusual place to have lesions. 
 The columnae carneae are part of the musculature, and it is well to 
 note them. On the left they were negative; on the right side they were 
 thick. So that we found marked hypertrophy of the right side of the 
 heart, the wall generally thickened. The cavity of the left ventricle 
 was negative as usual in mitral stenosis where the lesion is pure mitral. 
 The left auricle was dilated, the wall slightly thickened, and in it 
 there was a very large frank adhering thrombus. The right auricu- 
 
iL? FACTS ON THE HEART 
 
 lar appendix was free. The cavities on the right side were dilated 
 and distended with blood clot. The valve measurements were: the 
 aortic seven, the tricuspid 1414, the pulmonary g; these valves were 
 out of the picture. The mitral showed marked stenosis. In the 
 situation of the valve was a flat ovoid fibrocalcareous mass in the 
 center of which was a very small crescentic opening. The chordae 
 tendineae showed marked shortening and thickening,—a typical 
 picture of mitral stenosis with a mural thrombus in the left auricular 
 appendix. 
 
 The coronaries were free and capacious and showed a few scattered 
 small fibrous plaques. The pulmonary artery and veins, the aorta 
 and great branches, and the venae cavae were negative. The liver, 
 pancreas, spleen, adrenals, kidneys, showed chronic passive 
 congestion. . 
 
 In the gall-bladder were 16 yellowish-brown crystalline stones. 
 The bile ducts and the duct of Wirsung were free and negative. 
 
 Necropsy 4046 
 
 An American leather-worker of forty-six entered May 14, 
 1908. He had scarlet fever, measles, mumps and pertussis in child- 
 hood, ‘“‘rheumatism”’ (swelling and tenderness in many joints) at 
 fourteen and again at forty-two, confining him to bed four weeks each 
 time, at twenty-eight a sore on the penis followed by a bubo, at 
 thirty-one gonorrhea. For years he had had frequent attacks of 
 ‘bronchitis’? every winter, with wheezing respiration, usually 
 worse at night, and cough often with a cupful of sputum at night. 
 At forty-two he had pneumonia. He formerly drank several glasses 
 of beer and whiskey daily and had an occasional spree. For two 
 years he had taken very little alcohol. 
 
 A year before admission he had a slight attack of dyspnea, cough 
 and palpitation similar to the present one lasting seven to ten days. 
 Two and a half months ago he began to have attacks of dyspnea, 
 palpitation and cough with mucoid sputum and on two occasions a 
 mouthful of blood. He was in bed two weeks. After this he felt 
 perfectly well and intended to go to work again. May 9g he had a 
 recurrence of the symptoms. In both attacks his legs swelled in the 
 evenings and often his eyes and face were puffy in the mornings. 
 His hands had occasionally been swollen. Ever since the onset he 
 had had more or less constant gnawing pain in the lower midabdomen 
 radiating to the right hypochondrium, not related to eating, increased, 
 by exercise. For three months his bowels had not moved without 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES DES 
 
 catharsis, and when straining at stool “the bowel sometimes turned 
 wrong side out.” He had had two or three attacks of dizziness since 
 the onset lasting only a few seconds. 
 
 Examination showed a well nourished man with many old faded 
 and pigmented macules and papules on the skin of the trunk and right 
 arm. ‘There was a small wen on the back of the neck. The mucosae 
 were of fair color, a little pale. The throat was generally reddened. 
 There were enlarged glands in both axillae and in the left groin below 
 Poupart’s. The costal borders flared. The apex impulse of the 
 heart was diffuse over the lower precordia and in the left epigastrium, 
 seen and felt in the sixth space 12 cm. from midline, 114 cm. outside 
 the nipple line, corresponding to the left border of dullness. The 
 right border was 4 cm. to the right. No supracardiac dullness was 
 made out. There was very slight systolic retraction in the region of 
 the apex. No definite thrill was felt. There was absolute arry- 
 thmia. The first sound was loud but not flapping. The pulmonic 
 second sound was greater than the aortic second. The second sound 
 was accented at the apex. A blowing systolic murmur was heard 
 at the apex transmitted to the axilla, a faint diastolic murmur in 
 the third and fourth spaces along the left sternal margin. The pulses 
 were normal, the artery walls tortuous and beaded. The blood 
 pressure was 165/95 to 140/80. Harsh breathing was heard through- 
 out the lungs, with many groans and wheezes, and fine rales in both 
 axillae. There was slight tenderness in the right upper quadrant. 
 The liver dullness extended from the fifth space to 3 cm. below the 
 costal margin, where an indefinite edge was felt. The right pupil 
 was larger than the left. Both were slightly irregular but reacted to 
 light and distance. The reflexes were normal. 
 
 The temperature was 97° to 99°, usually 98° or below. The pulse 
 was 112 to 8o, the respiration 30 to 25 to May 16. Both were after- 
 wards normal. The urine and blood were normal. A Wassermann 
 was negative. The sputum showed moderate numbers of bacteria, 
 mostly pneumococci; no tubercle or influenza bacilli. The X-ray 
 
 is shown in Fig. 12. 
 . The patient gained rapidly. Action was taken by the Social 
 Service to find him lighter work. At his discharge, May 27, the 
 heart was slightly irregular, the sounds much the same as at entrance. 
 
 In June, 1910, a polygram taken in the Out-Patient Department 
 showed auricular fibrillation. Examination showed a systolic and 
 a short diastolic at the apex. He was taking digifolin gr. iss as needed. 
 
 The pulse at the apex was 70, at the wrist 66. He was ordered to 
 8 
 
II4 FACTS ON THE HEART 
 
 continue digifolin. A diastolic murmur was heard first in February 
 of the previous year. In July X-ray showed no evidence of gall- 
 stones. The following January he felt badly and was slightly cyano- 
 tic. Examination in the Out-Patient Department showed rales at 
 both bases, the liver two fingers down; no edema. The heart rate 
 was 45; no deficit except for occasional premature beats. ‘The first 
 sound was replaced by a murmur. 
 
 January 30, 1917, he returned to the wards reporting several severe 
 attacks since the previous admission, the first three weeks after dis- 
 charge following very strenuous work. He rested at home until Aug- 
 
 pean 
 
 Fic. 12.—Necropsy 4046. Plate I. Mitral stenosis. X-ray six years before 
 death. (Not taken at seven feet.) Heart shadow enlarged. Great vessels not abnor- 
 mal. Dense mass at both lung roots, probably glands. Lung markings extending out 
 from lung roots thickened and mottled. Angle between heart and diaphragm indistinct. 
 
 gust, 1908, then took light work. A year before readmission and 
 again in the summer of 1916 he had attacks each lasting four or five 
 days, with bronchial trouble, dyspnea, palpitation and distressing 
 cough. Between the attacks he had been in good condition. Two 
 weeks before admission he was laid up by an attack more severe than 
 the former ones. He felt comfortable while staying quiet, but on 
 light exertion became very dyspneic and had palpitation and severe 
 cough. 
 
 Examination was as before except for the points noted. He 
 
 was fairly well nourished. The mucous membranes were slightly | 
 
 cyanotic. There was barrel chest. The lungs showed sibilant 
 
 ‘ _— 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES II5 
 
 rales in front, moist crackles at the base. The nipple line was 1014 
 cm. to the left of midsternum, the apex impulse 1o cm., the border 
 of dullness 1314 cm. to the left. The right border was 414 cm. to 
 the right. The supracardiac dullness was6cm. There was absolute 
 irregularity. The first sound at the apex was replaced by a loud 
 blowing systolic murmur transmitted to the axilla. There was a 
 softer blowing diastolic at the apex. The pulmonic second sound 
 was much accentuated. The pulses were absolutely irregular, of 
 fair volume and tension. All the apex beats came through. The 
 systolic blood pressure was 130 to 140. The liver dullness extended 
 from the sixth rib to 2 cm. below the costal margin. The edge was 
 not felt. The pupils were equal, regular. 
 
 The temperature was 95.7° to 98.8°, the pulse 38 to 70, the res- 
 pirations 17 to 32. The amount of urine was go to Io ounces, 
 cloudy, specific gravity 1.010, findings negative. The hemoglobin 
 was 80%, the leucocytes 8000 to 13,000, the polynuclears 64%, 
 eosinophils 10%. A Wassermannn was negative. The renal func- 
 tion was 40%. The blood nitrogen was 30 mgm. per 100 C.c. 
 
 The radial pulse continued to stay about 4o for the first four days, 
 it was supposed because of digitalis treatment before entrance. 
 There was no edema except slight moisture in the bases of the lungs. 
 By February 7 he was feeling very well. The pulse rate was between 
 50 and 60. The dull pain in the right upper quadrant which he had 
 previously, had cleared up. February 8 he was discharged relieved, 
 with advice to rest several weeks and to return to the Out-Patient 
 Department once a week. 
 
 July 2, 1918, he came to the Out-Patient Department. He 
 was better, slightly cyanotic. There was probably fibrillation, but 
 slow. He was working. October 23 he reported influenza three 
 weeks earlier. November to electrocardiogram showed auricular 
 fibrillation with inversion of T wave. The heart was working very 
 well. February 6, 1919, the heart measurements were as shown in 
 Fig. 13. February 20 he had had no digitalis for four weeks. There 
 was edema, dyspnea, ascites, hydrothorax. The apex pulse was 
 120, the radial go. 
 
 January 12, 1920, he entered for the third time. He had done 
 no steady work for three years. Since his stay in the hospital his 
 heart had been decompensated most of the time, with an occasional 
 period of a few days to a week when he felt well. During the 
 attacks of decompensation he had edema of the feet and lower legs. 
 He had dyspnea on slight exertion, palpitation, and a variable 
 
116 FACTS ON THE HEART 
 
 amount of cough. His bowels were constipated. He urinated at 
 night and had occasional burning micturition. He was troubled 
 by gas and sour stomach. There was almost constant gnawing but 
 not severe pain in the right upper quadrant varying with severity of 
 heart symptoms. He now used three or four pillows. He slept 
 poorly and had nightmares. 
 
 On examination his skin was dusky, with generalized punctate 
 . papules. His mucosae were slightly pale. There was very marked 
 pyorrhea. The left chest was dull to flat throughout the front, with 
 musical rales and prolonged expiration. There was dullness with 
 occasional crackling rales at the left apex behind. There was flat- 
 ness from the midscapula to the base with crepitant rales, bron- 
 chophony, and distant bronchial breathing. The apex impulse of the 
 heart was in the sixth space 8.5 cm. to the 
 left. The left border of dullness was 11.5 
 cm. to the left, the right border 3.5 cm. to the 
 right, the supracardiac dullness 7 cm. The 
 sounds were irregular, rapid, of good quality. 
 The heart was in fibrillation. The pulmonic 
 second sound was accentuated. There was 
 
 155em@_ asoft systolic murmur at the apex transmitted 
 
 Fic. 13.—Heartmeasure- to the axilla. The pulses were normal, the 
 
 ares eegitr carte ae artery walls palpable. The systolic blood 
 
 pars pressure was 150, the diastolicgo. ‘There was 
 
 slight tenderness in the right upper quadrant. 
 
 The liver dullness extended from the fourth rib to 4 cm. below the 
 
 costal margin. The edge was felt. There was dullness over Traube’s 
 
 space. The fingers were clubbed. There was moderate edema oi 
 both legs and feet. The pupils were normal. 
 
 The temperature was 96.1° to 102°, the pulse 58 to 115, with tow 
 drops to 43-49, and a rise to 120 the day of death. The respirations 
 were 14 to 40. The amount of urine was 15 to 105 ounces. A 
 Schlayer test January 19 showed the specific gravity 1.008, 1.008, 
 I.O1O, I.O10, 1.014, 1.010; the slightest possible trace to a very slight 
 trace of albumin in all but one of six specimens; total chlorides 1.085— 
 2.214 gm.; four specimens cloudy, two alkaline. In six other exam- 
 inations the specific gravity was 1.026-1.037; there was a slight 
 trace to a very large trace of albumin at all, cloudiness at one, bile 
 at one, hyalin casts at five, leucocytes at five, red blood corpuscles 
 at three. The renal function was 20 to 30%. The hemoglobin was 
 70%, the leucocytes 7400 to 8400 the polynuclears 64%. The 
 
 ? Y 
 
 6 C72. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES Li 
 
 reds showed slight achromia, some anisocytosis and poikilocytosis. 
 The non-protein nitrogen was 45.7 mgm. The creatinin was 1 
 mgm. per 100 c.c. of blood. A Wassermann was negative. A chest 
 tap gave 1000 c.c. of clear blood-tinged fluid which showed 600 cells, 
 specific gravity 1.004, a negative culture, total chlorides 6.2 gm. 
 X-ray showed the heart shadow very much enlarged to the right and 
 the left. The outline of the various chambers was obliterated. 
 The diaphragm could not be made out on the left side. | 
 
 The chest tap gave some relief. The patient slept very restlessly, 
 and on some days looked very ashy. Diuretin gr. xv t.i.d. for five 
 days was followed by good diuresis, but the urinary output soon fell 
 again. He continued to have pulse deficit. Without diuretin the 
 chest began to fill up again with fluid. He responded poorly to 
 digitalis. He was drowsy most of the time. January 30, after an 
 interval of ten days, the diuretin was begun again. February 13 the 
 temperature rose to 102°, and each of the following days reached that 
 point. The edema increased markedly. February 15 he died. 
 
 Clinical Diagnosis (from Hospital Record) —Chronic endocarditis, 
 mitral valve. 
 
 Myocardial insufficiency. 
 
 Arteriosclerosis. 
 
 Bronchopneumonia. 
 
 Auricular fibrillation. 
 
 Possible adherent pericardium. 
 
 Dr. Wiliam H. Smith’s Diagnosis —Mitral stenosis and regurgi- 
 tation. 
 
 Possible adhesive pericarditis. 
 
 Arteriosclerosis. 
 
 Bronchiectasis. 
 
 Chronic passive congestion of liver and kidney. 
 
 Probable terminal infection. 
 
 Anatomical Diagnosis——Chronic endocarditis of mitral valve, 
 stenosis. 
 
 Thrombus in left auricle. 
 
 Slight chronic endocarditis of the aortic valve. 
 
 Hypertrophy and dilatation of the heart.. 
 
 Chronic passive congestion, general. 
 
 Hydropericardium. 
 
 Hydrothorax. 
 
 Ascites. 
 
 Anasarca. 
 
118 FACTS ON THE HEART 
 
 Infarcts of the lungs. 
 
 Chronic pleuritis. 
 
 Dr. RicHArpDsoN: This is a typical case of mitral stenosis. The 
 heart weighed 660 grams, was markedly enlarged, the right ventricle 
 wall seven mm., the left ventricle wall eight mm.,—that is, the right 
 ventricle wall markedly thickened, the left wall rather thin. There 
 was much dilatation of the left auricle and great dilatation of the right 
 ventricle and auricle. The mitral valve was the seat of a deforming 
 mass, reducing its curcumference to a crescent-shaped opening 
 about one and a half cm. in length, which is shown in the picture, 
 
 Fic. 14.—Mitral stenosis. Left auricle viewed from above. Large thrombus in the 
 left auricular appendage. 
 
 In the left auricular appendage there was a large adhering thrombus. 
 (See Fig. 14.) The aortic valve showed a few small areas of chronic 
 endocarditis, otherwise was negative. The other valves were 
 negative. 
 
 The kidneys showed chronic passive congestion. 
 
 The liver was large, 2300 grams, and was about a hand below the 
 costal margin. It showed typical nutmeg markings. The spleen 
 showed chronic passive congestion. 
 
 The gastro-intestinal tract showed a reddened, velvety, juicy 
 mucosa, that which accompanies chronic passive congestion. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES LI9 
 
 There was no growth from the heart blood. 
 The lungs showed chronic passive congestion, and there was a 
 slight amount of chronic pleuritis. 
 The anatomical diagnosis here is in logical sequence. It is a 
 typical case. 
 Necropsy 3768 
 
 A Swedish housewife of thirty-one entered August 16. The 
 history was obtained with difficulty from her husband. He did not 
 _ know whether she had had rheumatic fever, tonsillitis, etc. She had 
 a fever many years ago in which she lost her hair. She often had 
 headaches, and had had some trouble with her vision; at times she 
 had seen double. She had sore throat two or three times a winter. 
 Three years before admission she had some urgency and frequency. 
 During the past three years she had lost a good deal of weight. For 
 two years she had had intermittent slight cough with a small amount 
 of white sputum. She had had night sweats. Her bowels were 
 constipated. She had had eructations of gas and pyrosis. She had 
 been married four years, and had never been pregnant. 
 
 Two years before admission dyspnea, weakness, and dizziness 
 gradually developed. Three months before admission she was in a 
 hospital for ten weeks. After six weeks more in a convalescent home 
 she was discharged four weeks ago feeling very well. August 6 she 
 had pain in the left hypochondrium, increased by straightening up 
 and taking deep breath, accompanied by cough, and keeping her 
 awake. August 8 she began to cough up white sputum. August ro 
 the pain left the side and developed in the right flank and hypochon- 
 drium, becoming so severe that she screamed when touched. Next 
 day she was better. August 13 she began to vomit everything she 
 took. Her physician said he had given her too strong medicine. 
 The night before admission the vomiting ceased. She could not lie 
 on her left side, and had to be lifted to change position. For three 
 days she had had constant severe pain on one or both sides, and had 
 seemed to grow Weaker. The day of admission for the first time she 
 coughed up a little bloody sputum. ; 
 
 Examination showed a fairly well developed and poorly nourished 
 woman, cyanotic and very dyspneic. The mucous membranes were 
 pale. The teeth were poor. There wassome pyorrhea. The throat 
 and tonsils were reddened. The apex impulse of the heart was in 
 the fifth space. There was no enlargement to percussion. The 
 aortic second sound was greater than the pulmonic second. There 
 was a presystolic roll followed by a loud and sudden first sound. 
 
120 FACTS ON THE HEART 
 
 A slight thrill was felt. The artery walls were not palpable. The 
 blood pressure was 75/60. The lung signs were as shown in Fig. 15. 
 The pupils were regular. The left was greater than the right. 
 The right reacted slightly; the left was stiff and dilated. The rest 
 of the examination was not made because of the patient’s poor 
 condition. 
 
 The temperature was normal, the pulse 100 to 110, the respiration 
 48 to 30. The urine is not recorded. The hemoglobin was 80%, 
 the leucocytes 27,000 the polynuclears 89%. A Wassermann and a 
 stool examination were negative. 
 
 The patient became very cyanotic and dyspneic. Coarse rales 
 developed throughout the chest. The night of entrance she had a 
 profuse cold sweat. August 17 she died. 
 
 Occasional rales 
 
 Consonating and 
 sibilant rales. 
 Pleurisy 
 
 Pleurisy rub felt rub. 
 and heard. Many 
 dry clicks. 
 
 FIG. 15. 
 
 Clinical Diagnosis (from Hospital Record)—Mitral stenosis. 
 Myocardial weakness. 
 
 Dry pleurisy. 
 
 Pulmonary tuberculosis? (Miliary?) 
 
 Dr. William H. Smith's Diagnosis —Mitral stenosis. _ 
 
 Emboli in the lungs. 
 
 Auricular thrombosis. 
 
 Acute endocarditis? 
 
 Anatomical Diagnosis —Chronic endocarditis. (Mitral stenosis.) 
 Acute endocarditis. 
 
 Ball thrombi in the auricles. 
 
 Hypertrophy and dilatation of the heart. 
 
 Infarcts of the lungs, spleen, and kidneys. 
 
 Ecchymoses on the epicardium and peritoneum. 
 
 Acute pleuritis. 
 
 Chronic passive congestion. 
 
 Ascites. 
 
 Slight chronic pleuritis, right. 
 
 re 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES iZzt 
 
 Dr. RIcHARDSON: The circumference of the mitral valve was only 
 3cm. There were ball thrombi in each auricle, a combination which 
 we have never found before. 
 
 With a lesion in the mitral valve, stenosis, we should expect to find 
 hypertrophy of the right ventricular wall. That is precisely what we 
 did find. The heart weighed 337 grams, showing a hypertrophy of 
 roo grams for a woman of her size. The aortic, tricuspid, and pul- 
 monary valves were negative. The wall of the left ventricle was 8 
 mm. thick (normally 12 mm.); being in front of the obstruction it 
 had no work todo. The wall of the right ventricle measured 5 mm.; 
 having work to do, it hypertrophied. The coronary arteries were 
 negative. The heart muscle was good, and there was a good blood 
 supply. In typical cases of mitral stenosis the changes come back of 
 the obstruction; the left auricle, the right ventricle, the right auricle, 
 show marked dilatation. The left ventricle is out of the question 
 altogether; in a way it does not have so much to do, as the blood gets 
 through the valve in much smaller amounts than it does normally. 
 
 There were several small ball thrombi in each auricle. The 
 infarcts went.on the right to the lungs, on the left to the spleen and 
 kidneys. | 
 
 The culture was negative. Ispeak of that because it is the clinch- 
 ing fact in these cases of infection. If we get three or four things 
 that mean infection, but do not get the other one, in all probability it 
 means infection. In this case we had acute endocarditis, acute 
 pleuritis, and on the epicardium small areas of ecchymosis. From 
 the microscopical examination we add to that as evidence of the 
 presence of infection the acute degeneration of the epithelium of 
 the renal tubules. Though we did not get a growth in the blood 
 stream, the case stands as though there was an acute infection 
 present. 
 
 The lungs showed infarcts. Minute dissection of the organs was 
 not done, however, for we sent them to a medical college for teaching 
 purposes. The chronic passive congestion, of course, was the end 
 result of the obstruction at the mitral valve. 
 
 We usually find ball thrombi in the left auricle where behind a 
 mitral stenosis the stasis in the blood stream is great, especially in 
 the auricular appendix and where the blood supply to the auricular 
 wall may be poor. The thrombus becomes established on the wall 
 of the appendix, gradually increases in size, and pushes out into the 
 auricular cavity. As the thrombus increases in size its pedicle of 
 attachment to the auricular wall becomes more and more attenuated, 
 
I22 FACTS ON THE HEART 
 
 until finally the thrombotic mass is freed from its attachment and 
 becomes what we call a ball thrombus. If this floats down over and 
 closes a buttonhole mitral then sudden death occurs. In this case 
 particles from the left auricular thrombus may have gone up, into 
 the cerebral vessels and caused the disturbances mentioned in the 
 clinical record. This was a typical case showing thrombi in the auri- 
 cles and what they can do. 
 
 Necropsy 1410 
 
 An Irish housewife of twenty-seven entered May 26. She gave a 
 history of measles and pneumonia as a child, pleurisy at twenty-one. 
 Five weeks before admission her left shoulder and knee became pain- 
 ful, without redness or swelling. After two days the condition 
 extended to the right elbow, then to the ankles. Occasionally the 
 pain returned to the left shoulder. The day before admission there 
 was slight pain in the right wrist. At entrance both knees were 
 painful. 
 
 Examination showed a well nourished woman with pale skin and 
 mucous membranes. The tongue showed a heavy white coat. The 
 throat was slightly reddened. There was no enlargement of the 
 heart to percussion. The action was regular. A presystolic thrill 
 was felt at the apex. A loud presystolic murmur was heard at the 
 mitral area, but loudest at the apex, transmitted toward the axilla 
 and ending in a sharp first sound. The second sound at the apex 
 
 was scarcely audible. The pulmonic second sound was greater than 
 
 the aortic. The pulses were of fair tension, otherwise normal. 
 Over the left back there was slight dullness on percussion, with slightly 
 diminished vocal and tactile fremitus. The abdomen was normal. 
 Both knees were somewhat puffy and painful on motion. The left 
 pupil was greater than the right. Both reacted normally. The 
 abdominal reflexes and the knee-jerks were not obtained. 
 
 The temperature was 101.1° to 98.1° the pulse 115 to 80, the 
 respiration 19 to 29. The output of urine was 11 to 55 ounces, the 
 specific gravity 1.014 to 1.026. There was a very slight trace of 
 albumin to none, rare hyaline casts at four of five examinations, 
 granular casts at the last, very rare blood cells at two. The hemo- 
 globin was 85%. There were 10,300 leucocytes. | 
 
 May 28 the temperature had dropped to nearly normal and the 
 patient was practically free from pain. By the thirty-first there was 
 only occasional slight pain or stiffness. She continued alternately 
 very comfortable and troubled with pain, chiefly in the knees. The 
 
 | 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES I23 
 
 heart condition remained unchanged: After June 20 the tempera- 
 ture was 100° to 1o1° every afternoon. June 29 numerous moist 
 rales were heard in both lungs, with a few dry crackling rales just 
 below the left clavicle. The breathing was of the bronchovesicular 
 type. Ten grains of potassium iodid was given three times a day. 
 She looked pale and weak, but had no complaints, and except for the 
 fever would have been up. The night of June 30 she vomited half a 
 cupful of greenish material three times. The pulse was strong, and 
 she felt better after each attack. Three-quarters of an hour after 
 the last one she died. 
 
 Fic. 16.—Necropsy 1410. Ball thrombi in left auricle. Fine cockscomb vege- 
 tations on edge of stenosed mitral valve. The large thrombus occludes the mitral 
 orifice. (From a drawing by H. F. Aitken. Dr. Oscar Richardson.) 
 
 Clinical Diagnosis (from Hospital Record).—Acute articular 
 rheumatism. 
 
 Mitral stenosis. 
 
 Dr. William H. Smith’s Diagnosis ——Chronic endocarditis. 
 
 Acute endocarditis? 
 
 Acute or subacute glomerulo-nephritis ? 
 
 Anatomical Diagnosis ——Chronic and acute endocarditis of the 
 mitral and tricuspid valves. Mitral stenosis. 
 
 Thrombi in the left auricular appendix. 
 
 Ball thrombus in the left auricle. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hemorrhagic infarctions of the lungs. 
 
124 FACTS ON .THE HEART 
 
 Thrombosis of a branch of the pulmonary artery in the lower lobe 
 of the right lung. 
 
 Ecchymoses in the visceral pericardium. 
 
 Infarcts of the skin. 
 
 Anasarca. : 
 
 Dr. STEELE: The heart weighed 430 grams. The mitral valve 
 was stenosed, its circumference being 314 cm. (normally 10 cm.). 
 Resting over this valve and occluding it was a ball thrombus 614 
 xX 516 X 1144 cm., which occupied a great part of the left auricle. 
 The mitral and tricuspid valves showed granulations such as are 
 found in streptococcic endocarditis. There was also thrombosis 
 of a branch of the right pulmonary artery, and hemorrhagic infarcts 
 in several places in the lungs. 
 
 There was no macroscopic evidence of glomerulo-nephritis. 
 
 No culture from the heart was made, owing to the incision restric- 
 tion, but a culture made from the liver showed the presence of a 
 streptococcus. 
 
 Dr. RICHARDSON: Thrombi are usually found in the left auricle 
 and are commonly associated with mitral stenosis. In this case the 
 stasis of the blood stream in the left auricle due to the stenosis, 
 associated with the character of the blood and the streptococcus 
 infection, are the sources of the thrombus formation. These ball 
 thrombi, judging from the cases we have seen, arise in all probability 
 in the following manner. The conditions favorable to the erection 
 of thrombi are, of course, more favorable in the conical sac-like por- 
 tion of the auricle known as the auricular appendix, and thrombi 
 in the auricle are usually found in the region of the appendix. It was 
 so in this case. 
 
 The picture of the heart of this patient shows remarkably well 
 this evolution of the ball thrombus. The so-called wave markings 
 on the thrombus are well brought out, and the cox-comb-like granula- 
 tions (M, M) on the free margin of the stenosed mitral valve are well 
 indicated. 
 
 Necropsy 2960 
 
 Un unmarried Irish housemaid of thirty-five entered October 20. 
 Her mother died at thirty-five of ‘“dropsy.” The patient had — 
 scarlet fever and measles in childhood. At twenty-nine she had 
 “rheumatism”’ for four or five weeks affecting many joints. Since 
 this attack she had had twinges in damp weather. Her catamenia 
 were often irregular, with much backache. She had one child living 
 and well. The perineum was repaired seven years ago. She had had 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES I25 
 
 slight whitish vaginal discharge and attacks of headache and dragging 
 pain for six years. Since the attack of rheumatism she had noticed 
 steadily but very gradually increasing dyspnea on exertion. For the 
 past year this had bothered her a good deal while at work. For three 
 weeks she had felt tired all the time, and the dyspnea had markedly 
 increased. She had also had much distension and belching of gas 
 after meals. For two weeks she had had some urinary frequency, 
 with burning. A week ago she began to vomit after meals. Her 
 stomach retained only liquid food. She had little nausea, but much 
 stomach heaviness. For five days she had had slight soft swelling of 
 the ankles and occasional pains in the ankles and knees. She had 
 also had frequent chilly sensations and dull frontal headache. She 
 had slept poorly because of hacking cough and smothering sensations 
 in the lower chest followed by attacks of dyspnea. She had been 
 orthopneic. She had done a little work every day. Her bowels had 
 been very constipated for years. 
 
 Examination showed a pale, cyanotic and dyspneic woman five 
 feet and a half inches in height, weighing 10414 pounds. The apex 
 impulse of the heart was in the fifth space 4 cm. outside the nipple 
 line. The right border was 4 cm. to the right of midsternum. The 
 action was tumultuous. The sounds were of poor quality. At times 
 a rolling presystolic was clearly heard, ending in a sharp first sound 
 and followed by a systolic murmur. There was a loud systolic in the 
 second right space. The jugular seemed to fill, though slowly, from 
 below. An occasional presystolic thrill was felt. The pulmonic 
 second sound was weaker than the aortic second. ‘The blood pressure 
 115/85-125/85. The lungs showed flatness and diminished fremitus 
 in the right lower chest below the angle of the scapula. Just at the 
 angle there was egophony and bronchial breathing. The abdomen 
 was full, with shifting dullness in the flanks. The liver dullness 
 extended from the sixth rib to a hand’s breadth below the costal 
 margin, where a tender edge was felt. There was moderate soft 
 edema of the legs. The pupils and knee-jerks were normal. 
 
 The temperature was 98.2° to 95.1°, (usually 96°-97°.) The 
 pulse was 60 to go. ‘The respirations were normal. The output of 
 urine was occasionally 15 ounces oy less. The specific gravity was 
 1.025 to 1.020. There was a very slight trace of albumin and a 
 moderate number of granular casts at all of four examinations. The 
 renal function was 10%. Thehemoglobin was 80%. There was 15,000 
 to 23,000 leucocytes, 79% polynuclears. ‘The reds were normal. A 
 blood culture October 20 showed no growth. The fundi were normal. 
 
126 FACTS ON THE HEART 
 
 Until the 27th vomiting was the most prominent symptom. Digi- 
 puratum, digitalis, salts and elaterium were all vomited. Still she 
 passed a fair amount of urine. Hot air baths gave marked relief. 
 The jugulars were distended. There was marked lessening of the 
 ascites. November 8 caffein sodium benzoate gr. v 4 1.d. was given 
 
 and well retained, but no diuresis followed. November 13 she ~ 
 
 began to spit blood. November 11 diuretin suppositories gr. xv 4 1.d. 
 were given. The vomiting became more severe, and theocin gr. iii 
 every four hours in capsules was substituted. November 16 Seidlitz 
 powders were given one every hour during the day. The patient 
 failed rapidly and died the next morning. 
 
 Clinical Diagnosis (from Hosbital Record) —Double mitral lesion. 
 
 Myocardial failure. 
 
 Dr. Richard C. Cabol’s Diagnosis —Acute and chronic endocarditis 
 of the mitral valve, stenosis, with probably a stretching of the 
 tricuspid. 
 
 Predominant hypertrophy of the right ventricle. 
 
 Very possibly a thrombus in the left auricular appendage. 
 
 Hydrothorax, right. 
 
 Passive congestion of all the organs. 
 
 Probably no nephritis; if any, acute or subacute. 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral valve, 
 stenosis. 
 
 Thrombosis of the left auricular appendix. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Hydrothorax, left. 
 
 Ascites. 
 
 Edema of the lower extremities. 
 
 Obsolete tuberculosis of tracheal lymphatic glands. 
 
 Chronic pleuritis. 
 
 Chronic interstitial pneumonitis of the right lung, bony plates in 
 the pleura. 
 
 Chronic perihepatitis. 
 
 Chronic pelvic peritonitis. 
 
 Slight arteriosclerotic degeneration of the kidneys. 
 
 The heart weighed 337 grams. The left ventricle wall measured 
 8 mm.—very thin; the right 4 or 5 mm.,—thick. The mitral valve 
 was of the button-hole type, and measured 12 mm. Normally it 
 should be 1o cm. The tricuspid showed a slight amount of fibrosis, 
 but measured 13.5 cm., normal size. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES I27 
 
 The liver weighed 925 grams,—small and nutmeg. 
 
 The kidneys showed scarcely any change, certainly no cause for 
 uremia. 
 
 The stomach showed nothing so far as could be made out. The 
 autopsy was, however, done 346 hours after death. 
 
 Necropsy 3746 
 
 An Irish-American housewife of forty-eight entered June 12. 
 Since childhood she had had occasional slight attacks of tonsillitis. 
 At thirty-six she began to have rheumatism. At forty-one she came 
 to the Out-Patient Department of this hospital for relief of pain in 
 the ankles and the left arm, giving a history of swollen ankles for the 
 past two years, dyspnea on exertion, and very profuse flowing. Her 
 catamenia had always been irregular, with some dysmenorrhea. 
 For the past four or five years she had had flowing most of the time. 
 She urinated three or four times by day and six or seven time at 
 night. Her best weight was 165 pounds, her usual weight 145 pounds. 
 She thought she had lost a good deal in the last two or three years. 
 
 Seven years before admission she began to get out of breath on 
 slight exertion. Her ankles swelled during the day but went down 
 during the night. At the Out-Patient Department a harsh systolic 
 murmur was heard all over the precordia and in the axilla. The 
 specific gravity of the urine was 1.006. There was the slightest 
 possible trace of albumin and a few granular casts. She was advised 
 to enter the hospital, but did not. Since this time her ankles had 
 _ continued to swell and the dyspnea had increased. She had become 
 less able to work. Three weeks ago she was obliged to go to bed, 
 mainly on account of dyspnea. About the same time she noticed 
 that her abdomen was getting larger. She developed a cough, rais- 
 ing large amounts of thick yellowsputum. Her dyspnea had increased 
 to orthopnea. She often waked at night with an oppressed feeling 
 and had to sit up and gasp. 
 
 Examination showed a fairly well developed and nourished woman 
 with yellow skin and sclerae and pale mucosae. The apex impulse of 
 the heart was in the fifth space 1o cm. to the left of the midsternum. 
 The left border of dullness was 13 cm. to the left; the right border 
 was not found. The supracardiac dullness was 6.5 cm. There was 
 absolute irregularity of action. The sounds were of poor quality. 
 The first sound at the base was replaced by a blowing systolic murmur. 
 _ There was a soft systolic at the aortic area. The pulmonic second 
 sound was accentuated. The pulses were of poor volume and ten- 
 
128 FACTS ON THE HEART 
 
 sion. The blood pressure is not recorded. The artery walls were 
 palpable. The right breast was edematous. The right lung was dull 
 to flat from the midscapular region to the base posteriorly and from 
 the third to the seventh rib anteriorly, with diminished breath, voice 
 and fremitus, and with moist rales above. The left lung showed 
 moist rales to the level of the sixth rib in front and to the inferior 
 angle of the scapula behind. The abdomen was distended, the 
 edema extending to the back. The umbilicus was level. The 
 liver dullness was not made out. The extremities showed much 
 edema of the feet and legs, some of the hands and arms. Rectal and 
 pelvic examinations were not done. ‘The pupils and reflexes were 
 normal. 
 
 The temperature and respirations were not remarkable. The 
 pulse was 80 to 112. The amount and specific gravity of the urine 
 are not recorded. There was the slightest possible trace of albumin, 
 bile, diacetic acid, hyalin and granular casts, and leucocytes. The 
 hemoglobin was 40%. (?), the leucocytes 14,400, the polynu- 
 clears 87%. The reds were 2,046,000, with slight variation in size 
 and shape, much achromia and some polychromatophilia; no blasts 
 or stippling. The plates were somewhat reduced. A Wassermann 
 was negative. The urea nitrogen* was 24 mgm. per too c. c. of blood. 
 An abdominal tap gave 8 ounces of straw-colored fluid, the specific 
 gravity 1.010, 170 cells, all lymphocytes. 
 
 The patient became comatose six hours after entrance. The day 
 after entrance the visiting physician was able to hear no second sound. 
 There was marked edema of the walls of the chest and the abdomen 
 and brawny edema of the back, thighs, and legs. He found no 
 evidence of malignancy on rectal examination, and felt no definite 
 tumor anywhere. The uterus was not felt. The cervix was not 
 nodular. Two lumbar punctures gave a negative fluid under great 
 pressure. Slight improvement followed the tap. June 14 the 
 patient died. 
 
 Clinical Diagnosis (from Hospital Record) —Cardio-renal disease. 
 
 Severe anemia. Primary? 
 
 Cerebral edema. 
 
 Chronic nephritis. 
 
 Dr. William H. Smith's Diagnosis.—Mitral disease. 
 
 Anemia, primary? secondary? 
 
 Anatomical Diagnosis.—Chronic interstitial hepatitis with slight 
 fatty metamorphosis. 
 
 *The normal urea nitrogen is 12 to 15 mgm. per roo c.c. of blood. 
 
 ee ee ee ee 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 129 
 
 Chronic endocarditis of the mitral valve. 
 
 Submucous myoma of the uterus. 
 
 Anemia. 
 
 Hyperplasia ofethe bone marrow of the right femur. 
 
 Arteriosclerotic degeneration of the kidneys. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax. 
 
 Anasarca. 
 
 Cholelithiasis. 
 
 Chronic pleuritis, right. 
 
 Dr. RicHARDSON: There was a slight amount of fibrous sclerosis 
 in the aorta and the great branches, but nothing unusual. 
 
 The liver weighed 930 grams and was small. The organ showed 
 some thickening of the capsule, whieh was smooth and glassy. In 
 some few places this capsule rounded over small masses of liver sub- 
 stance, giving in those regions a slightly granular aspect to the sur- 
 face. In other places slender prolongations of the capsule extended 
 into the liver substance. The liver tissue itself was rather homogene- 
 ous, and, although not typical of an extreme case of cirrhosis, showed 
 enough to reduce the weight to 930 grams. There were some fatty 
 changes in the remaining liver cells. The interstitial increase was 
 mainly along the lines of the vortal vessels, appearing as a network of 
 grayish lines. 
 
 In the gall-bladder there were two stones which seemed to have 
 produced no result. 
 
 The spleen weighed 420 grams (normally 80-180). The hyper- 
 trophy was probably due to chronic passive congestion. 
 
 The kidneys weighed 300 grams (normally 200-400) and showed 
 a slight amount of arteriosclerotic nephritis. That means that in 
 areas scattered here and there over the tissue there were collections 
 of fibrous tissue and some sclerosis of the arteries. | 
 
 The heart weighed 570 grams, a weight which, with the lesions I 
 have mentioned, seems to be excessive. The right ventricle was 4-5 
 mm., the left ventricle 11 mm. ‘The cavities were considerably 
 dilated on the right side; not so much on the left. AJl this goes with 
 the fact that the only change in any of the valves was in the mitral, 
 which was somewhat shortened, and presented a thickened irregular 
 fibrous ridge along the free margin, dotted over in places with small 
 fibrocalcareous areas. The chordae tendineae reaching to those 
 
 areas were also shortened and thickened. We call that chronic 
 9 
 
130 FACTS ON THE HEART 
 
 endocarditis. The other valves were negative. The enlargment of 
 the heart is to be attributed partly to the mitral valve, partly to the 
 arteriosclerosis of the aorta and the great vessels, partly to the arte- 
 riosclerotic degeneration of the kidneys, and partly to the anemia, 
 plus, of course, the wear and tear of life, which is always a factor. 
 The right side was more hypertrophied than the left. The myo- 
 cardium showed in places what were probably a few areas of fatty 
 degeneration, but other than that was negative. 
 
 The bone marrow of the right femur looked, grossly, like the bone 
 marrow in pernicious anemia. It was of a rather dark red color and 
 cut out easily, but was a little mushier than it is in typical cases of 
 pernicious anemia. Still, if I were compelled to write the diagnosis 
 from the gross appearance I should not hesitate to say that it was 
 primary anemia. The microscopical examination, however, did not 
 quite bear out that opinion. It was not sufficiently typical to enable 
 us to write definitely the diagnosis of pernicious anemia. It was a 
 grave anemia, however. 
 
 If the anemia was not primary in this case, but secondary, what is 
 the explanation of its orgin? Within the uterine cavity there was a 
 polyp about three inches long, the surface of which was coated with 
 blood. Whether over a long period of time that polyp could bleed 
 enough to produce an anemia as grave as this is the question. I 
 should say that it could. The polyps may be of any size or shape. 
 On microscopical examination you will find that there is a network of 
 large thin-walled vessels running over the surface of the polyp. 
 For some reason, either because of a change in the pressure or some- 
 thing else, these thin-walled capillary vessels break, with the result 
 that there is a bleeding mass, the blood dripping from various points. 
 It is not uncommon to find in these cases a history of long bleeding. 
 That seems to have been the case here. 
 
 The anemia was a factor, I think, in her dyspnea. 
 
 A Puysician: How large was the uterus? 
 
 Dr. RicHarpson: It was considerably enlarged, enough to demon- 
 strate that when there is a mass in the uterine cavity the organ does 
 enough work in trying to get-rid of it to produce some hypertrophy. 
 
 If we did not have the polyp in the uterine cavity it would be 
 harder to prove that the case was not one of pernicious anemia. 
 
 Necropsy 3422 
 
 A housewife of forty entered January 5 for the relief of cough. 
 Her father, one brother, and one sister died of consumption. The 
 
 en ee 
 
 -— f= A. a 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 131 
 
 patient cared for all three during their illnesses. She had ‘“‘inflam- 
 matory rheumatism” at seventeen and off and on for the next ten 
 years, keeping her in bed four times for six weeks. She had had 
 chronic cough with yellowish sputum since she was seventeen. Her 
 bowels were always constipated. She had never been pregnant. 
 .Her best weight was 135 pounds, her present weight about roo. 
 
 For the past fifteen years she had tired very easily and had had 
 dyspnea on slight exertion. Nine months ago she found she could 
 not do as much work as usual. Her legs and ankles swelled. She 
 went to a hospital, from which the following report was sent. ‘The 
 patient was admitted May 20 last. The heart was somewhat 
 enlarged. The apex impulse was diffuse, best felt in the fifth space, 
 anterior axillary line. There was a possible presystolic thrill. The 
 heart action was irregular in force and rhythm. The first sound at 
 the apex was very sharp and accentuated and preceded by a rumbling 
 murmur. A systolic murmur was heard all over the precordia and 
 transmitted into the axilla. On entrance there was considerable 
 cyanosis and much edema of feet and ankles. She was discharged 
 June 30 feeling better than for years.’’ Since her discharge she had 
 been in bed more or less. Weakness and fatigue had been the char- 
 acteristics of her illness. Recently her cough had troubled her more. 
 During the past five days she had become hoarse, and now spoke in 
 a hoarse whisper. 
 
 Examination showed a poorly developed, fairly well nourished 
 woman with slightly cyanotic lips and mucosae and slight exophthal-_ 
 mos. ‘The apex impulse of the heart was seen and felt in the sixth 
 space. ‘The supracardiac dullness in the first space was 11.5 cm., 
 in the second space 9g cm. The other borders are not recorded, but 
 the visiting physician notes, ‘‘Heart enlarged and displaced to the 
 left.” The action was absolutely irregular. The pulmonic second 
 sound was greatly increased. At the apex was a sharp first sound. 
 A systolic blowing and a diastolic roll were heard at the apex, where a 
 thrill was felt. The blood pressure was 110/60. The lungs were 
 hyperresonant. The left chest was more resonant than the right, 
 and moved more. ‘The breathing was much diminished on the right. 
 At the right apex in front there was dullness below dull tympany. 
 There was no coin sound and no amphoric phenomena of any 
 sort. The left chest showed increased compensatory (resonance). 
 In the right lung the breath sounds were almost absent, high-pitched, 
 with an occasional musical rale. (See Fig. 17.) On the left there 
 was compensatory breathing. The abdomen was distended, dull 
 
132 
 
 in the flanks. 
 
 The right pupil was greater than the leit. 
 reacted to light. 
 
 Duration 
 of Disease 
 Dejections 
 Days of Month 
 
 Four-Hourly | 
 
 FACTS ON THE HEART 
 
 Food pad mead og eas ph dd 
 fe Ee 
 pe fl Be PS ES 
 oe Fd a BSE 
 fe OS ed BS aE 
 ah | 
 
 ok log Dale a 
 od AY 
 Coa 
 
 9°| “he 
 
 60 H, 
 i eS 
 
 Fie. 18. 
 
 51617 1819 Vols || 
 imme oe 
 
 The liver dullness extended from the fifth rib. to 5 cm. 
 below the costal margin; tender. 
 
 The feet showed slight edema. 
 
 with position. No tactile 
 Voice much dim- 
 Whisper = ? 
 
 fremitus. 
 
 ‘Dull to flat, not shifting 
 jen 
 
 FIG. 37; 
 
 Both were dilated. They 
 
 The other reflexes were normal. 
 
 The temperature and pulse are 
 shown in Fig. 18. The respiration 
 was 50 at entrance, afterwards usually 
 30. 
 the specific gravity 1.030-1.032. The 
 sediment showed some pus and granu- 
 lar casts at one of two examinations. 
 The hemoglobin was 60%. The 
 leucocytes were 28,o00 at entrance, 
 5400 January 11, the polynuclears 
 88%, the reds 4,048,000, with moder- 
 ate achromia. A Wassermann was 
 negative. The sputum showed 
 tubercle bacilli. A radial tracing and 
 electrocardiogram at entrance showed 
 auricular fibrillation. Fluoroscopic 
 examination showed right hydro- 
 pneumothorax with extreme displace- 
 ment of the heart to the left. 
 
 The patient was put upon magne- 
 sium sulphate 3ss in the morning, 
 ammonium chloride gr. v t.i.d. p.c., 
 and sodium veronal gr. v. January 
 6 the right chest was tapped and 50 
 ounces of thick pea-soup-like fluid 
 withdrawn. 
 
 notrecorded. The smear snowed pus cells and small mononuclears; no 
 
 organisms. 
 
 A culture showed pneumococci. 
 
 A guinea pig inoculated 
 
 The output of urine was normal, - 
 
 The specific gravity is © 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 133 
 
 with the fluid showed a negative necropsy February 11. The patient 
 was very much more comfortable after the tap. The heart, however, 
 did not come back at all. The fluid did not reaccumulate during the 
 next three days, and the general condition and heart rate and quality 
 remained about the same. There was a very definite coin sound 
 over the right chest. January 9 a throat consultant reported com- 
 plete paralysis of the left recurrent laryngeal nerve. 
 
 January 11, just as she was in preparation for another tap, she 
 grew more dyspneic and cyanotic. The heart became rapid and 
 more irregular, and a mass about the size of a grape-fruit appeared 
 in the abdomen in the region of the umbilicus, firm and definite in 
 outline, not fluctuating. She grew rapidly worse, and died January 
 
 12, asphyxiated by her sputum. 
 
 Clinical Diagnosis (from Hospital Record) —Pyopneumothorax, 
 right. 
 
 Acute cardiac dilatation. 
 
 Mitral stenosis and insufficiency. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 mitral valve; stenosis and regurgitation. 
 
 Ball thrombus in the auricular appendage. 
 
 A piece in the mesenteric artery. 
 
 Tuberculosis of the lungs. 
 
 Probably pyopneumothorax. 
 
 Probably compression atalectasis. 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral valve; 
 mitral stenosis. 
 
 Pyopneumothorax, right. (2000 c.c. of frank pus.) 
 
 Left laryngeal paralysis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Chronic passive congestion of the liver. 
 
 Hydropericardium. : 
 
 Ascites. 
 
 Anasarca. 
 
 Arteriosclerosis of the aorta and its great branches, moderate. 
 
 Arteriosclerosis of the pulmonary artery and its branches, 
 moderate. 
 
 Cholelithiasis. 
 
 Old infarcts of one kidney. 
 
 Chronic pelvic peritonitis. 
 
 Chronic appendicitis. 
 
 Chronic pleuritis. 
 
I34 FACTS ON THE HEART 
 
 Heart: The myocardium was negative. The left ventricle wall 
 was 11 mm., the right ventricle 8 mm., (greatly thickened). The 
 cavities were enlarged. The mitral valve was of the button-hole 
 type, 16 X 5mm. The chordae tendineae were fused with the valve 
 all the way down to the papillary muscles. The valves were other- 
 wise negatve. There were no fresh vegetations. There was a clot 
 in the left auricular appendage, presumably an ante-mortem clot. 
 
 Lungs: The pus was walled off in the pleural cavity on the right for 
 about the lower two-thirds. That portion of the lung was collapsed 
 against the spinal column in compression atalectasis. At one point 
 the pleura showed an area suggesting that a portion of the lung had 
 been adherent, and had pulled off, establishing communication 
 between the bronchi and the pleural cavity; hence pyopneumothorax. 
 The other third of this lung, isolated in its own compartment, was 
 not remarkable. The apex and the bronchial lymphatic glands were 
 negative. The left lung was voluminous, and showed chronic passive 
 congestion. Otherwise it was negative. No record as to the cause 
 of recurrens paralysis. There was no tuberculosis anywhere and no 
 abdominal tumor! 
 
 Necropsy 2646 
 
 An American housewife of twenty-nine entered June 27, 1910. 
 Her father died of trouble with the heart and liver after suffering 
 with acute rheumatism. She had had scarlet fever, kidney trouble, 
 chickenpox and mumps. At fourteen she was ill a year with rheu- 
 matic fever and was in bed six months. She had one miscarriage at 
 twenty-two. About once each winter she had a cold. She had 
 occasional attacks of nausea and vomiting. She urinated three or 
 
 four times at night. She had frequent frontal headache. A few | 
 
 months before admission she weighed 200 pounds, her best weight. 
 She now weighs 1509. 
 
 In the summer of 1909 she began to have dyspnea and backache 
 and to tire easily. During the winter she had a cold, but worked in 
 a laundry until a month before entering the hospital; when she began 
 to feel worse. 
 
 Examination showed a well nourished woman breathing some- 
 what rapidly. The skin was moist, hot and loose, the muscles flabby, 
 the mucous membranes slightly cyanotic. Her only tooth was a 
 carious stump. The tongue showed a dry brown-gray coat. The 
 throat was reddened, the pharynx dry. The left side of the chest 
 over the precordia was more prominent than the right. ‘There was 
 diffuse tumultuous heaving over this area. The apex impulse of the 
 
 . 
 A 
 p 
 f 
 t 
 ‘ 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES Ia 
 
 heart was seen and felt in the fourth, fifth and sixth spaces, with the 
 point of maximum intensity at the fifth space. The left border of 
 dullness was 16 cm. from midsternum in the left fifth space, anterior 
 axillary line, the right border 4.5 cm. to the right in the fourth space. 
 There was no increase in the substernal dullness. The action was 
 irregular, rapid. There was a short powerless impulse at the apex 
 with a presystolic leading up to a first sound which was practically 
 replaced by a harsh blowing systolic murmur heard over the entire 
 precordia, loudest just inside the apex and transmitted to the axilla 
 and back. The pulmonic second sound was greater than the aortic 
 second, snapping, accentuated and reduplicated. The pulses were 
 equal, irregular in rhythm, rapid, of low volume and tension. Not 
 all beats reached the wrist. The artery walls were not palpable. 
 The systolic blood pressure was 105. The lungs showed fair expan- 
 sion, good resonance throughout except in the left axilla below the 
 fourth rib, where there was dullness to flatness. Posteriorly there 
 was good resonance except at the left base below the angle of the 
 _scapula. The breath sounds were rather harsh. There were a few 
 moist rales at both bases, more marked on the left. The abdomen 
 was full and held somewhat rigid. It was tympanitic throughout, 
 with slight general tenderness, more marked in the region of the sig- 
 moid and the liver. ‘The liver dullness extended from the fifth rib 
 to two finger-breadths below the costal margin, where the edge was 
 felt, tender. The fingers and toes were slightly clubbed. The pupils 
 were normal, the knee-jerks very sluggish. 
 
 The temperature was 98° to 102.8° until July 20, when there was a 
 terminal drop from 97.9° to96°. The pulse was 69 to 120, the respira- 
 tion 24 to 46. The amount of urine was normal, the specific gravity 
 1.009 to 1.016. The urine was cloudy at four of five examinations, 
 showed aslight trace to theslightest possible trace of albumin at three, 
 hyalin and granular casts with cells attached at two, with blood 
 attached at one, a few red blood cells at another. The hemoglobin 
 was 95% to 85%, the leucocytes 36,000-12,000-39,600, the poly- 
 nuclears 90%-70%-91%. The reds showed polychromatophilia at 
 one of three examinations. No Wassermann is recorded. 
 
 At entrance the patient was very. uncomfortable, breathing 
 rapidly, and had considerable pain in the right arm and leg. Aspirin 
 gave relief but was followed by marked delirium and some vomiting. 
 After this she had a feeling of weakness in the entire right half of the 
 body. From entrance she had had a feeling of numbness on this side. 
 After digipuratum had been given for four days the apex and wrist 
 
136 FACTS ON THE HEART 
 
 beats became synchronous and the pulse rate was much slower and 
 steadier. There was a definite presystolic thrill and murmur, a loud 
 first sound and a systolic murmur at the apex. No murmurs at the 
 base were made out. The lungs showed a few rales at the bases. 
 There was considerable edema over the sacrum and a small amount of 
 shifting dullness in the abdomen. There was very little edema of the 
 legs. A small bed sore over the coccyx healed very slowly. 
 
 From July 7 the patient lost ground. Her memory was very poor. 
 She looked very pale and weak. She had very little dyspnea and no 
 palpitation. The temperature was very irregular. She had three 
 sudden attacks of sharp pain in the region of the spleen lasting half 
 an hour to two hours and keeping her awake. She seemed to be ina 
 kind of stupor most of the time, and fell asleep while people were talking 
 with her, but could easily be roused and then seemed perfectly rational. 
 A blood culture showed a slight growth of staphylococcus aureus. 
 
 By the 17th she was much worse. There was a steady aching in 
 the splenic region with attacks of sharp-pain. July 21 a blood 
 culture showed a growth of atypical streptococci in chains and 
 clumps, weakly Gram-staining. For two days the pulse could not 
 be felt in the left hand, and for several hours before death none in the 
 right. The heart became permanently enlarged. The apex impulse, 
 very diffuse and flapping, could easily be felt as far as the midaxillary 
 line, the right border two inches from midsternum, and the lower 
 border in the sixth and seventh spaces. The action was very irregu- 
 lar and rapid, and so tumultuous that the thrill could not be timed. 
 Still a fairly definite presystolic murmur and a tremendous systolic 
 murmur were heard at the apex. No murmurs were made out in the 
 aortic area. The left lung showed dullness at the base with dimin- 
 ished breath sounds. This lung was full of moist rales. The right 
 lung was clear. The patient lay on her left side. There was only 
 slight edema, and no shifting dullness, but the abdomen was con- 
 siderably distended so that it was impossible to palpate the liver or 
 spleen. Finally she had almost constant attacks of pain in the region 
 of the spleen, with considerable tenderness there. July 23 she died. 
 
 Clinical Diagnosis (from Hospital Record) —Acute ulcerative 
 mitral endocarditis. 
 
 Aortic disease? 
 
 Chronic mitral endocarditis. 
 
 Perisplenitis. 
 
 Chronic passive congestion. 
 
 Multiple infarcts. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES Lai] 
 
 Dr. Richard C. Caboi’s Diagnosis —Chronic endocarditis of the 
 mitral valve. 
 
 Mitral stenosis and regurgitation. 
 
 Acute endocarditis. 
 
 Thrombosis and embolism. 
 
 Infarcts of kidney, spleen, brain (?) 
 
 Chronic passive congestion. 
 
 Hypertrophy and dilatation of the heart. 
 
 Streptococcus septicemia. 
 
 Anatomical Diagnosis.—1. PRIMARY FATAL LESIONS. 
 
 Fibrous endocarditis of the mitral and aortic valves. 
 
 Verrucose endocarditis of the aortic valve.. 
 
 Polypous endocarditis of the mitral valve. 
 
 Streptococcus septicemia. 
 
 2. SECONDARY OR TERMINAL LESIONS 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Infarcts of spleen and kidneys. 
 
 3. HISTORICAL LANDMARKS 
 
 Urethral caruncle. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 There is nothing in the record about anasarca or edema. 
 
 Dr. CazotT: There was very little in life. 
 
 Dr. RICHARDSON: There was a good amount of subcutaneous fat. 
 The peritoneal cavity contained no fluid. Scattered over the perito- 
 neum were small purplish-red ecchymotic areas, and there were a 
 few on the pericardium. 
 
 Dr. Casot: But there were none of those areas on the skin? 
 
 Dr. RIcHARDSON: None. 
 
 The liver was two fingerbreadths below the costal border. The 
 aiaphragm was at the third interspace on the right and the sixth on 
 the left. For some reason the diaphragm was perhaps a little high 
 on the right and it was low on the left, indicating of course, so far as 
 it goes, the presence of fluid or something abnormal in the left cavity. 
 
 The right pleural cavity contained no fluid. In the lett there 
 was a small amount of thin pale fluid. There were no adhesions, 
 which is rather unusual at almost any age. 
 
 The glands were out of the picture. 
 
 The lungs showed no areas of infarction or serena The 
 tissues were a little leathery, brownish-red, yielding a brownish-red 
 fluid showing the so-called heart cells, that is the large cells filled with 
 
138 FACTS ON THE HEART 
 
 pigment,—chronic passive congestion of the lungs, moderate in 
 amount. 
 
 The pericardium was out of the picture except for the spots 
 mentioned. The heart weighed 470 grams. In a woman of twenty- 
 nine, if the heart had weighed 230 or 240 grams, it would have been 
 all right for her. So there is considerable hypertrophy. The right 
 ventricle wall measured four mm., the left twelve,—both fairly thick. 
 The left auricle wall measured two to four mm. That is rather 
 unusual. Acthick left auricular wall should mean that it was working 
 against something. The columnae carneae were flattened in the left 
 ventricle, fairly marked on the right. The cavities, more especially 
 on the leftside, wereenlarged. That would indicate something on the 
 aortic valve. The mitral valve circumference was 12 cm., the aortic 
 7cm., the tricuspid 12cm. The mitral and the tricuspid in this heart 
 were of the same dimensions; that is a little large for the mitral, and 
 the tricuspid was about what it might be if this heart was normal. 
 The mitral and the aortic valve showed some diffuse fibrous thicken- 
 ing,—a certain amount of chronic endocarditis. 
 
 Along this thickened mitral valve there was a mass of grayish to 
 yellowish soft vegetations. It was very large and irregular, present- 
 ing, tit-like projections and extended down along the chordae 
 tendineae. At one point it extended for a short distance on to the 
 body of the mitral valve. A short distance above this, on the inner 
 surface of the auricle, there was another flattened mass of these 
 vegetations. 
 
 The aortic cusps showed the fibrosis mentioned and running along 
 them some verrucose endocarditis,—that is, chronic and acute. So 
 that these two valves showed chronic and acute endocarditis, 
 the acute being more massive on the mitral valve and in minute 
 amount on the aortic but still present on both valves. The tricuspid 
 and pulmonary valves and the coronary arteries were out of the 
 picture. The aorta and great branches, the pulmonary artery, veins 
 and vena cava were negative. 
 
 The liver weighed 2413 grams, a large liver, but all it showed was 
 chronic passive congestion. 
 
 The gall-bladder showed no stones, the bile ducts were free the 
 pancreas negative, the duct free. 
 
 The spleen weighed 417 grams, considerably hypertrophied, and 
 showed definiteinfarcts. There was a question raised which makes of 
 value a statement as to whether the infarcts in this spleen were soft. 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES 139 
 
 They were soft. The largest one measured 314 cm. across. That is 
 quite large. | 
 
 The kidneys were a little large, the cortex rather wide, but other 
 than for some chronic passive congestion and a few infarcts they were 
 negative. 
 
 The uterus and adnexa were negative. 
 
 The gastro-intestinal tract showed no definite lesions of any 
 sort except a little congestion. 
 
 Culture from the heart blood at the time of necropsy showed a 
 moderate growth of micrococci growing in long chains and clumps 
 with many involution forms after three days,—the streptococcus 
 viridans. 
 
 The vegetations on the mitral were so massive that we used the 
 term polypous to describe them. 
 
 Dr. Casot: The only thing we got wrong was that I thought 
 there was a mitral stenosis due to a chronic lesion. There was a 
 mitral stenosis due to these fresh vegetations. I do not know how 
 we are ever going to tell the difference between a mitral blocked by a 
 chronic permanent lesion and a mitral blocked by acute vegetations 
 like this. 
 
 It is obvious that there is something in this case which has 
 produced hypertrophy and dilatation of the heart. We are not accus- 
 tomed to thinking that acute endocarditis produces cardiac hypertro- 
 phy and dilatation. Is it possible that this disease has been going on 
 over a year? She had very little chronic endocarditis, not enough, I 
 should think, to produce hypertrophy and dilatation. It seems to 
 me we have to say that this is a case which has been going on for a 
 year, that these vegetations have been going on for months and 
 months; they have obstructed the circulation and so produced this 
 hypertrophy. It is an idea which has not yet taken its place in our 
 ideas about the heart that a purely soft process can last so long and 
 make so much obstruction of the valve that hypertrophy and dilata- 
 tion occur as in this case. I do not know what else to say as to 
 the cause of the big heart. Did that problem present itself to you, 
 Dr. Richardson, why that heart was so big? 
 
 Dr. RicHARpDSON: Yes, it did. It makes me think of the hearts in 
 chorea. In those cases we find changes on the valves, sometimes on 
 all three valves. It is a fibrosis not so very marked, but still there is 
 some hypertrophy of the heart and more than one would think the 
 chronic endocarditis accounted for. It seemed to throw it back into 
 the physiological pathology rather than the anatomical. 
 
I40 FACTS ON THE HEART 
 
 Dr. Casot: Otherwise I do not see that we have need to change 
 anything of the reasoning we made here. We notice that the nyc- 
 turia, if it was a real thing, was present without kidney disease. 
 
 Dr. RICHARDSON: The anatomy here is interesting when we note 
 the thickness of the auricular wall which is accounted for by the . 
 stenosis produced by the mass of vegetations. | 
 
 Dr. Casot: There is a little fibrous process, Dr. Richardson says, 
 on the aorta and on the mitral,—not enough to do anything in the 
 way of stenosis or regurgitation, which has to be accounted for by 
 the soft vegetations. There is nothing in the aorta itself except 
 these vegetations. 
 
 Dr. R1icHARDSON: How does the pulse work in these chorea cases 
 —is it high? 
 
 Dr. Casot: I do not think it is any different from the pulse in 
 any other failing heart. It is not high over long periods ordinarily. 
 
 Necropsy 861 
 
 A married Canadian laundress of sixty entered March to. She 
 gave a history of scarlet fever and smallpox in childhood; no other 
 serious illnesses until the present one. She had had to do hard work 
 to support her husband and three children for twenty years and felt 
 worn out. For five weeks she had felt miserable. 
 
 Two weeks and a half before admission she had sudden onset of 
 cramps in her feet, and both legs felt numb to the knees. There was 
 pain below the knees. The right leg was better in a few hours, but 
 the left had continued numb and painful. A little over two weeks 
 ago she began to be dyspneic and noticed that her heart beat fast and 
 irregularly. She had had cough recently, especially at night. 
 
 Examination showed a fairly well nourished woman. ‘Themucous 
 membranes were pale. ‘There was a systolic murmur in the axilla. 
 The pulse was weak, irregular and intermittent. The lungs showed 
 numerous squeaks and grunts. The abdomen was negative. ‘The 
 left leg below the knee was enlarged, firm, and painful on pressure. 
 The vessels in the calf were blue and cord-like. The foot was blue- 
 black to above the ankle. The femoral pulse was felt in the groin 
 and above the popliteal space. The right foot was negative. 
 
 Before operation the temperature was 97.2° to 100°. The pulse 
 was 150 at entrance, afterwards 90 to 110. The respirations were 
 27 to 31. The urine and blood are not recorded. 
 
 The patient was given one-fortieth of a grain of strychnia every 
 four hours and tincture of digitalis ten minims three times a day with 
 
MITRAL STENOSIS. ILLUSTRATIVE CASES t4t 
 
 good result. The pulse became much more steady and better in 
 quality. The toes became dry and black, and an area of redness 
 appeared below the knee. She complained of pain in the precordia 
 and the right thigh and leg. March 16 the right foot was slightly 
 cold. An icebag over the heart gave some relief. March 17 she felt 
 better, had less pain, and the pulse was better, though still rather weak 
 and very irregular. 
 
 March 18 the left leg was amputated at the junction of the lower 
 and middle thirds of the thigh. Pathological examination showed 
 the foot and leg entirely black and gangrenous. The cutaneous 
 and deep veins were found thrombosed throughout, and there was an 
 embolus at the bifurcation of the popliteal artery, above which the 
 artery was also thrombosed. ‘The patient was in poor condition at 
 the end of the operation. The next day the pulse was irregular. 
 The night of March 1g she was delirious. She complained of severe 
 pain in the right leg. Next day the night foot and leg were mottled 
 and purple to the knee. No pulse was felt in the tibials or the 
 popliteal. 
 
 March 22 the right leg was amputated at the junction of the 
 lower and middle thirds. There was very little bleeding. The femo- 
 ral vessels were plugged by thrombi. Pathological examination 
 showed an area of commencing gangrene on the outer side of the foot. 
 The entire leg as high as the knee was slightly yellowish. Dissection 
 showed the veins everywhere thrombosed, and in the popliteal artery 
 at its bifurcation a grayish, more or less discolored thrombus. 
 Below, the arteries contained but little blood, while above they were 
 filled with clots, and several thrombi were adherent to the walls. 
 The patient was in better general condition after this operation than 
 after the first. 
 
 March 30 she had an attack of pain and discomfort in the epigas- 
 trium and tingling and numbness in the right arm. The arm and 
 hand became cold and white. The pulse was present in the subcla- 
 vian artery but not in the brachial. April 1 there was a suggestion 
 of pulse in the right wrist, and the hand was warm. On the fourth 
 there was a feeble right radial. The wounds were clean and solid. 
 She felt very well. April 16 there was a flicker of pulse in the right 
 brachial and the radial. 
 
 April 17 she had right hemiplegia. April 18 she died. 
 Clinical Diagnosis (from Hospital Record) —Embolic gangrene of 
 leg. 7 
 
I42 FACTS ON THE HEART 
 
 Dr. Maurice Fremont-Smith’s Diagnosis —Embolism and throm- 
 bosis. 
 
 Chronic and endocarditis (mitral stenosis ?). 
 
 Hypertrophy and dilatation of the heart. 
 
 Anatomical Diagnosis —Chronic endocarditis (mitral stenosis). 
 
 Hypertrophy and dilatation of the left auricle. 
 
 Streptococcus septicemia. 
 
 Thrombosis of the left auricular appendix. 
 
 Embolic thrombosis of the right axillary artery. 
 
 Hemorrhages into basal ganglia on the left side. 
 
 Multiple infarcts of the spleen and kidneys. 
 
 Double amputation at lower third of the thighs for eribeHe 
 gangrene. 
 
 Obliterating thrombosis of the left common iliac and external 
 iliac veins. 
 
 Infarcts in the left lung. 
 
 Ulcer of the duodenum. 
 
 Hemorrhage into the small intestine. 
 
 Malformation of the left common iliac vein. 
 
 Chronic perihepatitis. 
 
 Cholelithiasis. 
 
 Dr. FREMONT-SMITH: Was that a hemorrhage into the basal 
 ganglia? It was not a hemorrhagic infarct? 
 
 Dr. Ricuarpson: I should think from the description that those 
 were of the nature of infarcts, because the cerebral vessels were not 
 remarkable. 
 
 A PuysictAn: Was there any evidence of bacterial endocarditis 
 on that mitral? 
 
 Dr. FREMONT-SMITH: The temperature never went above too’. 
 
 Dr. RicHARDSON: No, there was not. 
 
 Dr. Casot: Was this mitral stenosis pathologically like any 
 other mitral stenosis? 
 
 Dr. RICHARDSON: Yes. 
 
 Dr. Casot: I am interested in this case because it is a type of 
 mitral stenosis that does not get adequate mention in the literature. 
 We have quite a group of cases of mitral stenosis in our necropsies 
 in which the first thing that anybody knows is gangrene. The very 
 first event is not congestion or anything suggesting the heart at all. 
 It is peripheral gangrene. 
 
 Dr. Bock: There is another group of which we had three examples 
 in one year, of extreme mitral stenosis in patients between twenty 
 
POINTS ON MITRAL DISEASE I43 
 
 and thirty years of age with no cardiac symptoms until the sudden 
 onset of pulmonary edema followed by death. 
 
 Dr. Casot: Would you call that passive congestion, only very 
 sudden? 
 
 Dr. Bock: I should hesitate to call an acute pulmonary edema, 
 which comes on very suddenly, passive congestion. 
 
 Dr. CaBot: How many years ago were those cases? 
 
 Dr. Bock: One or two. There were three cases. I think we 
 had two and Dr. Magrath the medical examiner had one. I saw 
 all three. Dr. Magrath said-that that was an event that he had seen 
 before occurring in uncomplicated mitral stenosis in young people. 
 
 POINTS ON MITRAL DISEASE 
 
 1. As to etiology our knowledge may be summed up by saying the 
 rheumatic infection (including arthritis, chorea, and probably some 
 cases of tonsillitis), is the only one which has any known relation to 
 chronic valvular disease involving the mitral valve. The cases of 
 acute or subacute streptococcic endocarditis probably represent a 
 different type of disease which, however, may be superimposed upon 
 a rheumatic valvular scar. 
 
 2. In these 180 cases there was no evidence either of the gonococ- 
 cus or of the influenza bacillus as an etiological factor. 
 
 3. There is a definite predominance of females over males among 
 the cases of pure mitral disease. When the other valves are also 
 involved there is no such predominance. 
 
 4. Mitral disease is compatible with long life, and if the patient 
 gets beyond the second decade his valvular lesion is usually not the 
 cause of his death. Intercurrent infections, trauma or surgical 
 operations are more likely to end life, the mitral lesion remaining 
 latent. 
 
 5. Over half the patients with mitral disease die a non-congestive 
 death, that is, half do not die of heart disease itself. In the cases of 
 pure mitral trouble only two-fifths die a congestive death. 
 
 6. Even when the mitral disease is complicated by stenosis at the 
 aortic or one of the other valves, dropsy supervenes before death in 
 only half of the cases. 
 
 7. The size of the slit left in the stenosed mitral curtains has no 
 relation to the clinical signs during life. Patients with only a small 
 slit left in the mitral aperture may have no more serious symptoms 
 or signs of congestion than those with a much larger orifice. 
 
144 FACTS ON THE HEART 
 
 8. Chronic passive congestion is no commoner in the cases of 
 mitral disease complicated by aortic disease than in the cases of 
 mitral disease alone. 
 
 g. Fever and leucocytosis when they occur, usually turn out to be 
 due to causes within the heart itself, that is, to acute endocarditis or 
 to intracardiac thrombosis. 
 
 to. Thrombosis in the auricular appendages, especially the left, 
 is to be expected in a quarter of the decompensating and fibrillating 
 mitral cases. 
 
 11. Glomerulonephritis acute or chronic is to be expected before 
 the end of life in one-fifth of the cases of mitral disease. 
 
 12. Arrhythmia due to auricular fibrillation is twice as common in 
 pure mitral disease as in the mitral cases with aortic stenosis as well. 
 
 13. When mitral disease occurs alone, uncomplicated by stenosis 
 on any other valve, the reduction in the size of the orifice reaches a 
 greater degree than when aortic disease complicates the picture. 
 
 14. Over half the cases of mitral disease are not recognized during 
 life in hospital patients. This is presumably dué to the considerable 
 number of such cases occurring in surgical wards or dying of pneu- 
 monia and other infections without having presented any cardiac 
 complaints during life. 
 
 ' 15. The importance of suspecting and especially investigating the 
 possibility of mitral disease, even when no presystolic or diastolic 
 murmur is detected, should be remembered in the following. 
 conditions: 
 
 (a) In cases of cerebral or peripheral embolism occurring in 
 relatively young persons and presumably not due to arteriosclerosis. 
 
 (b) Arrhythmia and decompensating heart disease without evi- 
 dence of syphilis or hypertensive cardiovascular trouble, and especially 
 if there is a rheumatic history. 
 
 (c) Evidence of an acute endocarditis (since a chronic mitral 
 endocarditis usually underlies this lesion). 
 
 (d) The presence of a sharp first sound and a dull or feeble second 
 sound at the apex; doubling of the second sound (or a third heart 
 sound) along the left sternal margin; absolute arrhythmia without 
 known cause in a young person. 
 
 16. Pure mitral stenosis without any other valve lesion is more 
 than twice as common as the combination of mitral stenosis with 
 valve lesions (mitral-and-aortic, for instance), and considerably more 
 common than all the other combinations put together. 
 
SYMPTOMATOLOGY I45 
 
 17. Mitral regurgitation is one of the rarest of valve lesions, and 
 cannot with any certainty be recognized in life. 
 
 MULTIPLE VALVE LESIONS 
 
 Although most of the tables in the preceding pages include the 
 valve lesions other than “‘pure”’ mitral stenosis and show the statisti- 
 cal difference between this lesion and the more complicated stenoses, 
 it seems well to recapitulate here the main features of the commoner 
 combined lesions separated by themselves. 
 
 MITRAL AND AORTIC STENOSIS 
 
 Sex.—Males predominate 27 to 13 in the necropsied cases and 59 
 to 30 in the living cases. This is in sharp contrast with the series of 
 pure mitral cases,—females 62, males 45 in the necropsies and 149 
 to 68 in the living patients. Why this is so I have no idea, but it is 
 one of the items going to make up the widespread association between 
 diseases of the aortic valve and the male sex. 
 
 Age.—The age incidence at the first attack of rheumatism or 
 chorea, at the time of first seeking medical advice, and at the time of 
 death, is about the same in the mitral-and-aortic cases and in the 
 pure mitral cases, yet (as already noted) the term of life in mitral-and- 
 aortic cases from first complaint to death is (in those necropsied) 
 strikingly shorter than in the pure mitral cases or in the other “‘com- 
 bined lesions” (see Table 17, p. 44). | 
 
 Thus the ‘‘pure”’ mitral case’s average duration is 15 years. 
 
 The mitral-and-aortic case’s average duration Is 3 years. 
 
 The ‘‘combined lesions”’ case’s average duration is Io years. 
 
 The significance of these figures however is somewhat diminished by 
 comparison with the non-necropsied cases (Table 10, p. 36). Here of 
 course x.e have no such certainty as to the diagnosis as we have in 
 the nec vsied cases. But on the face of the figures the Mitral-and- 
 Aortic .ases live longer than the pure Mitral cases. 
 
 Multiple Attacks of Rheumatism or Chorea—Here there is a dis- 
 tinct difference between the mitral-and-aortic cases, thirteen out of 
 seventeen of which had multiple attacks and the pure mitral cases, 
 only t- elve out of forty of which had had multiple attacks. 
 
 SYMPTOMATOLOGY 
 
 Dyspnea is relatively more frequent (73%)as an early complaint 
 in mitral-and-aortic cases than in pure mitral cases (50%). The 
 
 same thing is true of other ‘‘cardiac symptoms.” ‘This is another 
 10 
 
146 FACTS ON THE HEART 
 
 way of stating the fact that in relatively few of the mitral-and-aortic 
 cases is the cardiac lesion latent. The patient is less apt than is the — 
 ‘‘pure”’ mitral patient to die of some infection, operation, or trauma 
 before compensation has failed. 
 
 In the clinical picture of ‘‘living cases” (not necropsied) precordial 
 pain of some sort was an early feature in sixteen out of twenty-seven 
 mitral-and-aortic cases, and of only eight out of twenty-five “pure” 
 mitral cases. In the later course of the living cases pain was also a 
 feature more often in mitral-and-aortic cases than in pure mitral 
 cases. 
 
 Arrhythmia and palpitation (-fibrillation?) were less commonly 
 noticed in the mitral-and-aortic cases (ten out of thirty-four) than in 
 the pure mitral cases (thirty-eight out of sixty-seven). 
 
 Nutrition was poor in sixteen of forty mitral-and-aortic cases, 
 (40%) as contrasted with twenty-eight out of 107 pure mitral cases 
 (267%). 
 
 In the Physical Examination of cases which ultimately came to 
 necropsy decided enlargement of the heart was not found any more 
 often in mitral-and-aortic cases (twenty out of thirty-three) than in 
 the pure mitral cases (fifty-two out of eighty-seven). This is some- 
 what surprising. But the figures are practically the same in the 
 non-necropsied cases,—which showed definite enlargement in 127 to 
 150 pure mitral (84%) and in 81 of 89 mitral-and-aortic (91%). 
 
 Transverse enlargement was not found more common clinically 
 in the pure mitral cases than in the mitral-and-aortic. It was the 
 rule in both groups. 
 
 Heart Weights at Necropsy.—Hypertrophy was present in thirty- 
 seven of forty cases, distinctly more than in the ‘‘pure mitral” series, 
 89 of 107. The degree of hypertrophy is also greater in the mitral- _ 
 and-aortic series, nineteen of thirty-nine over 500 grams (50%) as 
 against thirty out of 107 in the pure mitral series (28%). This shows 
 how unreliable are our clinical estimates of cardiac enlargement as. 
 reported in the last section. 
 
 Dilatation of Cavities.—Preponderant dilatation of the right side 
 of the heart was present at necropsy in twenty-five pure mitral cases 
 out of 107 (or 23%), andin five of forty mitral-and-aortic cases (12%). 
 
 Preponderant dilatation of the left ventricle was present in ‘five 
 of forty mitral-and-aortic and in three of 107 ‘‘pure mitral’’ cases. 
 
 Preponderant dilatation of the left auricle was present in twenty- 
 seven of 107 pure mitral cases, and in only three of forty mitral-and-_ 
 aortic cases. Obviously the strain of the double lesion is more 
 
i 
 
 DIAGNOSIS 147 
 
 equally distributed while that of the single mitral lesion falls on the 
 right side of the heart and on the left auricle. 
 
 DIAGNOSIS 
 
 The heart was considered enlarged in life in twenty-nine cases 
 of forty. An apical presystolic or diastolic murmur was heard in 
 21 out of 40 or 52%, so that in 14 the cases we had some reason to 
 make a diagnosis of mitral stenosis, especially when a clear rheu- 
 matic history was present without evidence of syphilis and in a young 
 person. : 
 
 In five cases no murmur was heard, and in fourteen a systolic 
 murmur only. In eight cases (20%) a sharp or accented first sound 
 was noted at the apex, but only three of these were associated with 
 presystolic or diastolic murmurs. In the mitral-and-aortic “living 
 patients” sixty-three out of eighty-nine (70%) showed a sharp first 
 sound at the apex. 
 
 In seven cases the second sound was absent at the apex. : 
 
 Doubling of the second sound along the left sternal margin was 
 noticed only four times in forty cases (probably from inattention). 
 Accentuation of the pulmonic second was recorded eighteen times in 
 forty cases. 
 
 Arrhythmia (presumably fibrillation) was noted only ten times. 
 The rheumatic history was clear in eighteen cases only. 
 
 So far I have been assembling data relative to the diagnosis of 
 the mitral stenoses found post-mortem, and I conclude that on the 
 evidence ‘iis diagnosis was recognized in eighteen out of forty cases. 
 
 How about the aortic lesion? A diastolic murmur loudest along 
 the sternal margin or in the second right interspace was heard in 
 sixteen cases. This was associated with cardiac enlargement in 
 
 fourteen, and a collapsing (‘‘Corrigan’’) pulse and other arterial 
 
 phenomena in ten cases. This justifies a diagnosis of aortic regurgita- 
 tion in sixleen cases out of 40. 
 
 Direct evidence of aortic stenosis was seldom sufficient for diagnosis. 
 A basal systolic thrill was recorded in only four cases. Plateau pulse 
 was never recorded. A diminished or absent aortic second sound is 
 noted in six cases, but not one of these is associated with any of the 
 four systolic thrills just mentioned and only four times was the 
 
 weak aortic second sound associated with a diastolic basal murmur. 
 
 It is of no considerable value therefore. 
 Any diagnosis of aortic stenosis in the forty cases of this series 
 which showed it at necropsy had to be based on the assumption that 
 
148 FACTS ON THE HEART 
 
 in rheumatic lesions (such as eighteen of these cases appeared from their 
 history to be) aortic disease almost always produces stenosis as well 
 as regurgitation. With direct evidence of aortic regurgitation in a 
 rheumatic case it is safe to assert that stenosis 1s present in about 
 4< of the cases (see “‘pure”’ rheumatic regurgitant lesions p. 252). 
 
 Diagnostic Summary.—Of forty cases, the aortic and the mitral 
 stenoses found at necropsy were both recognized in life in eight cases 
 or 20%. The mitral lesion was recognized in ten cases and the aortic 
 
 alone, in eight, while neither was detected in fourteen. 
 
 MITRAL AND AORTIC STENOSIS 
 
 Both lésiohs* recognized in ie.37 2 St J ee 8 cases 
 
 Mitral alone recognized ‘in 2) n5.0% 22.2 2... 2s i ee IO cases 
 
 Aortie*alone:recogmized in ©. tig. c/ie pec ops 62,0 pe 8 cases 
 
 Neithér recognized in cycvs'o cet i. ss ve Pte wing 
 40 
 
 Passive Congestion.—Aortic disease when superadded on a mitral 
 lesion produced neither more nor less congestion and dropsy than 
 mitral disease alone. 
 
 Fever and Leucocytosis—Fever was present in twenty-two of forty 
 cases (cf. “‘ pure’’ mitral, 51 of 107), 1.e., slightly more often in the mitral 
 and-aortic series. Leucocytosis was found in nineteen of forty 
 (cf. ‘‘pure”’ mitral, 66 of 107). 
 
 The percentage of infarcts was the same in mitral-and-aortic as in 
 ‘“‘pure”’ mitral disease. 
 
 Thrombt in the Auricles—Auricular thrombi are recorded in five 
 of forty cases (one in eight) whereas in ‘‘pure”’ mitral disease there 
 were twenty-eight of 107 cases (one in four). Apparently these 
 auricular thrombi are only one-half as common in mitral-and-aortic 
 disease as in “‘ pure”’ mitral. 
 
 Infectious pulmonary complications are apparently less common in 
 
 mitral-and-aortic disease (five out of forty’ than in pure mitral | 
 
 cases (seventeen in 107). 
 
 Nephritis is commoner (thirteen of forty cases) than in Pure 
 mitral (18 of 107). 
 
 Positive Cultures at necropsy are also more common eas of 
 forty cases) than in “‘ pure” mitral (25 of 107). But these differences 
 between the two groups are probably not significant (see Tables 45 
 and 46). 
 
 As to the degree of narrowing of the mitral it appears from Table 
 47 that the “‘pure mitral” cases tend to a greater degree of stenosis 
 than the mitral-and-aortic cases. 
 
SUMMARY OF CONTRASTS I49 
 
 » 
 
 MODE OF DEATH IN MITRAL AND AORTIC STENOSIS 
 
 21 of 40 cases died from passive congestion. 
 4 of 40 cases died from passive congestion with sepsis. 
 8 of 40 cases died from sepsis alone. 
 7 of 40 cases died from non-cardiac causes. 
 o of 40 cases died from embolism. 
 
 Of the eight septic cases five were overshadowed by the effects 
 of an acute endocarditis with septicemia, three were cases of surgical 
 sepsis, two of them with general peritonitis. 
 
 Of the four cases combining passive congestion and sepsis, three 
 were cases of active septic acute endocarditis engrafted on a chronic 
 process, which had been severe enough to produce marked passive 
 congestion. The remaining case was complicated by pulmonary 
 abscesses due to stenosis of a bronchus from pressure of a gland 
 (tuberculous?) in an Italian boy of fourteen. 
 
 Among these seven deaths classed as due to non-cardiac diseases, 
 four were due to pneumonia, one to apoplexy, and two were post- 
 operative deaths. 
 
 Comparing these with the ‘‘pure mitral’ cases we get the follow- 
 ing results: 
 
 TABLE 52 
 
 M; 
 Mitral Mitral and 
 
 Manner of death Aortic 
 107 cases 
 40 cases 
 
 Congestive deaths 49 or 47% 21 or 52% 
 
 Acute septic deaths Io or 9% 8 or 20% 
 
 Non-cardiac causes. ‘ 33 Or 31% 7 or 17% 
 
 12 OF 21.9% 
 
 Mepemaverantseptic death... 30. oeisi oven weet ek 
 
 SUMMARY OF THE CONTRASTS BETWEEN THE 107 “PURE MITRAL” CASES 
 AND THE 40 “MITRAL-AND-AORTIC CASES 
 
 1. Etiology—Mitral-and-aortic disease is common in males, 
 lasts only three years (instead of fifteen) on the average fromthe 
 first symptom to death, and is much more apt to give a history of 
 multiple attacks of rheumatism (or chorea.) 
 
I50 FACTS ON THE HEART 
 
 2. Symptoms.—Mitral-and-aortic begins more often with dyspnea, 
 i.e.is less often a latent lesion in a patient dying of non-cardiac disease, 
 is more apt to have precordial pain among its symptoms, and less 
 apt to show palpitation and arrhythmia. 
 
 3. Physical Examination Nutrition is more often poor. 
 
 We should expect a record of greater cardiac enlargement than in 
 ‘‘pure”’ mitral cases. But this is not so; neither is there any differ- 
 ence in the shape of the cardiac dullness in the two groups. 
 
 4. Necropsies—Hypertrophy of the heart is commoner but is 
 less preponderant on the right side. Passive congestion is no more or 
 less common than in “pure” mitral disease. 
 
 Auricular thrombi are but half as common. WNephritis and post- 
 mortem cultures are commoner. 
 
 The mode of death—as is to be expected from the relative rarity 
 of intracardiac thrombi—is less often embolic. Indeed there were 
 no embolic deaths in our forty cases. Congestive and septic deaths 
 are commoner and those from intercurrent disease or trauma much 
 rarer. 
 
 5. Diagnosis —Some lesion was recognized in twenty-six of 
 forty cases, but both lesions in only eight. The stenotic part of the 
 aortic lesion was hardly ever recognized by physical examination, 
 but might have been inferred with 80% of accuracy from the diag- 
 nosis of aortic regurgitation which was made in sixteen out of forty 
 cases. 
 
 ILLUSTRATIVE CASES. MITRAL STENOSIS AND AORT:C STENOSIS 
 Necropsy 4401 
 
 An American factory operative of fifty entered September 7, 
 1922, complaining of dyspnea and weakness. One sister died of 
 tumor of the stomach. The patient’s health had always been good 
 except for the present illness. He had influenza in 1918 and ques- 
 tionable influenza in 1921. He and the rest of his family always ° 
 had pale yellow skin. | 
 
 At twenty-one he was ill in bed for a week or two with acute 
 rheumatic fever. Since that time he had continually done hard work 
 and had been troubled only a little by dyspnea. At twenty-eight 
 years he was passed for life insurance. His second wife, to whom he 
 had been married nine years, said his heart had been irregular as 
 long as she had known him. Two years ago he noticed that his 
 ankles were slightly swollen for two months. The winter before 
 admission the dyspnea increased both on exertion and at night. A 
 
ILLUSTRATIVE CASES. MITRAL STENOSIS AND AORTIC STENOSIS I5I 
 
 physician gave digitalis, which slowed his heart but increased the 
 dyspnea and orthopnea. Under some other medicine the condition 
 improved considerably, though the dyspnea and orthopnea were worse 
 than the previous year. A month before admission these symptoms 
 returned, more intense than ever before, and the medicine gave less 
 relief than formerly. During the past few weeks there had been 
 occasional attacks of palpitation during which he had to stop work 
 and spend a few minutes lying flat. Two weeks before admission all 
 the symptoms began to grow progressively worse. He had more 
 . dyspnea on the slightest exertion. Orthopnea frequently awakened 
 him at night. He had slight swelling of the ankles. His appetite 
 generally was poor, and he grew weak. 
 
 Examination showed a fairly well developed, poorly nourished, 
 orthopneic man, pale, cyanotic and in considerable distress. The 
 tonsils were small and buried. There were a few very small sub- 
 
 Slight 
 dullness. 
 esistance, Many moist 
 Moderate tender- rales. 
 ness, Liver edge Fremitus, 
 not definitely >reath and 
 felt because of voice sounds 
 rigidity. normal, 
 
 Flatness. Absent 
 tactile fremitus. 
 Distant bronchial 
 breathing. 
 Occasional rales 
 Edema. 
 
 Fic. 10. 
 
 maxillary glands. The apex impulse of the heart was seen and felt 
 in the sixth space 12 cm. to the left in the anterior axillary line; also 
 seen in the fourth and fifth spaces, diffuse and heaving, The borders 
 of percussion dullness were 13 cm. to the left, 5.5. cm. outside the 
 
 nipple line, 4 cm. to the right; the supracardiac dullness 5 cm.. At 
 the apex was a loud blowing systolic murmur transmitted to the 
 axilla and back, obscuring the first sound. The second sound was 
 not made out. A low-pitched rumbling diastolic murmur was heard 
 over a small area at the apex. Over the whole base a well marked 
 systolic thrill was felt. There was a loud rough systolic murmur at 
 the base filling all of systole. The second sound was not heard. 
 There was an early diastolic murmur, loudest to the left of the ster- 
 num, of different character from that at the apex. There was abso- 
 lute irregularity of rhythm and force. The action was not very rapid 
 (95). The pulses were absolutely irregular, of poor quality, plateau 
 type. The highest systolic blood pressure was 115, the usual 105, 
 the diastolic 85.' The lung signs were as shown in Fig. 19. The 
 abdomen was slightly distended, tympanitic except in the flanks. 
 
152 FACTS ON THE HEART 
 
 (See diagram.) There was moderate edema over the sacrum and 
 marked edema of the feet and ankles extending halfway to the knees. 
 The pupils reacted sluggishly to light. The reflexes were normal. 
 The temperature and pulse were as shown in Fig. 20. The 
 respirations were g to 29. The amount of urine is not recorded 
 except 31 ounces September 8. The specific gravity was 1.026 to 
 1.028. The urine was cloudy at one of two examinations and showed 
 a slight trace of albumin and leucocytes at both, fine granular and 
 hyalin casts at the first. The hemoglobin was 
 m= 1. 11 70%. There were 8000 to 11,000 leucocytes, 
 —— te 70% polynuclears, 4,800,000 reds, slight achromia. 
 ~»{ { | | || The platelets were normal. A Wassermann was 
 oft 4 negative. A chest tap September 8 in the right 
 TLE] posterior axillary line and below the tip of the 
 
 ott | | | | scapula gave 20 ounces of beet-colored clear fluid 
 mE an which coagulated quickly; specific gravity 1.012, 
 
 LLIALL] 2 3 leucocytes, 2410 red blood cells, no organisms; 
 faoPlort tlt | culture negative. 
 200 oot ay | | : : 
 100] loos f-N-E afk The patient showed no improvement. He had 
 
 Ltt constant nocturnal orthopnea, failure and irration- 
 io ed ES ality. The edema increased. September 9g the 
 sot +t 11 | lungs were full of wet rales, with fluid at both 
 es Ee bases. September 11 he died. : 
 ro OT a ES EB Clinical Diagnosis (from Hospital Record) — 
 Rh ic h i ith mitral is and 
 Delon PTA eum aa eart disease with mitral stenosis an 
 be TAY I | «regurgitation. 
 c Aortic stenosis with regurgitation. 
 
 Pasta | Auricular fibrillation 
 
 pS itp ee 6a] ie uricular 10N. 
 Congestive failure. 
 
 =is 
 So S&S 
 PULSE 
 o 
 
 Fic. 20 
 Chronic passive congestion of lungs and liver. 
 Hydrothorax. 
 Bronchopneumonia. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 aortic and mitral valves. 
 
 Aortic stenosis and regurgitation. 
 
 Mitral stenosis and regurgitation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Hydrothorax. 
 
 Ascites. 
 
 Pneumonia? 
 
ILLUSTRATIVE CASES. MITRAL STENOSIS AND AORTIC STENOSIS 153 
 
 Anatomical Diagnosis —Chronic endocarditis of the aortic and 
 mitral valves (stenosis). 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax. 
 
 Edema of the legs and feet. 
 
 Meckel’s diverticulum. 
 
 Obsolete tuberculosis of the mesenteric glands. 
 
 Dr. RICHARDSON: Clinically do you find a large heart with 
 aortic stenosis if it is a real stenosis? 
 
 Dr. CasorT: Yes, certainly. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 The legs and feet were slightly swollen pitted on pressure. The sub- 
 cutaneous tissues were moist but not wet. There were a few c.c. of 
 thin pale fluid in the peritoneal cavity. The esophagus, stomach, 
 and intestine showed well marked chronic passive congestion,—red- 
 dened, velvety, juicy mucosa oozing thin bloody fluid. 
 
 Two of the mesenteric glands were transformed into stony fibro- 
 calcareous material, obsolete tuberculosis. 
 
 The right pleural cavity was half full of clear fluid; on the left 
 there was 200 c.c.—hydrothorax, more marked on the right, and 
 some compression atelectasis. The lungs showed frank chronic 
 passive congestion, but I could not find any pneumonia. That does 
 not mean to say absolutely there is no pneumonia in those lungs. It 
 means that I could not find any definite pneumonia. If we took the 
 lung from the apex to the base and cut up every part of it there might 
 be found in it some bronchopneumonia. I was unable to find any- 
 thing from the culture in the heart blood. So that so far as our 
 evidence goes there was nothing in the way of terminal infection. 
 The trachea and bronchi showed congestion of the mucosa. 
 
 The pericardium was negative. The heart weighed 685 grams, 
 markedly enlarged, with a thick myocardium of good consistence, pale 
 brown-red. The left auricular wall showed some thickening, measur- 
 ing 15 mm., the right three to four mm. That is a thick heart, 
 the kind of heart we expect with aortic stenosis. The left cavities 
 showed considerable dilatation, the right slight dilatation. The cavi- 
 ties were all distended with currant-jelly-like blood clot,—apparently 
 death in diastole. There was a small adherent thrombotic mass in 
 the left auricular appendix. The mitral valve measured seven cm., 
 the orifice of the aortic valve was represented by a slit-like opening 
 114 cm. by one cm.—a fairly well marked stenosis in the mitral and 
 
154 FACTS ON THE HEART 
 
 a classical picture of stenosis of the aortic. Of course that connotes 
 a fibrocalcareous fusion of the cusps of the aortic valve and marked 
 fibrocalcareous thickening and deformity of the mitral. There was 
 no evidence on either of these valves of acute endocarditis. The 
 tricuspid valve showed increase of circumference but was otherwise 
 negative. The pulmonary valve was negative. 
 
 The coronaries were free, capacious and showed only a slight 
 amount of fibrous sclerosis. There was also a slight amount of fibrous 
 sclerosis in the first portion of the aorta and elsewhere. 
 
 The liver showed the typical nutmeg markings of chronic passive 
 congestion. The gall-bladder, bile ducts, pancreas were out of the 
 picture. The spleen did not weigh so much, 115 grams, but was 
 chunky, thick, elastic and dark brown-red,—chronic passive conges- 
 tion. The adrenals were negative. The kidneys showed chronic 
 passive congestion, otherwise frankly out of the picture. The 
 microscopical examination of the kidneys corroborates what I have 
 said about them. In this case there was a Meckel’s diverticulum, but 
 it was perfectly free and negative. 
 
 Dr. Cazsot: I think the fever must be laid to the thrombosis. 
 
 Necropsy 3827 
 
 An American clerk of forty-eight entered April 1. His maternal 
 grandparents died of tuberculosis, one brother of epilepsy. In child- 
 hood he had scarlet and typhoid fevers, and strained his back by 
 carrying too heavy weight, ‘with resulting prominence of the shoulder 
 blades and lack of chest development.’’ He had urinated once at 
 night and had had dull fronta] headaches once in two or three weeks 
 “fall his life,” especially brought on by overwork. At thirteen he 
 had what he believed to be epidemic cerebrospinal meningitis, though 
 no lumbar puncture was done. He made a complete recovery. 
 For thirty years he had suffered from gas eructations beginning two 
 hours after meals and lasting one or two hours, somewhat relieved ~ 
 by hot water. At sixteen, twenty-five, and thirty he had attacks of 
 ‘“‘muscular rheumatism,’—painful, tender but not swollen joints, 
 especially the elbows and knees, and muscles of the calves and arms, 
 lasting about two months. Four years ago he was ill in bed with 
 ‘“‘grippe’’ for five weeks, and ever since this had had attacks of dysp- 
 nea on exertion with pain in both sides of the chest in front and pal- 
 pitation. He had to sleep on two pillows. He urinated six times a 
 day and once or twice at night. Three years before admission he had 
 epithelioma of the left cheek, curetted at a hospital. Twelve years 
 
ss 
 
 ILLUSTRATIVE CASES. MITRAL STENOSIS AND AORTIC STENOSIS 155 
 
 before admission he weighed 155 pounds, his best weight. His usual 
 weight was 148. In the past year it had fallen ta rgo. | 
 
 His illness was the third of a series of similar attacks, the first of 
 which followed his “‘grippe”’ four years.ago. The second kept him 
 from work for two months the year before admission. March 29 he 
 had a third attack of dizziness lasting half a day, followed by weakness 
 and dyspnea on even very slight exertion. He had since this required 
 three pillows at night. 
 
 Examination showed a poorly Est anyiteal and nourished man in 
 distress with dizziness and faintness when sitting up. The mucous 
 membranes were slightly cyanotic. The anterior-posterior diameter 
 of the chest was greater than the lateral diameter. There was 
 slight bulging over the precordia. The apex impulse of the heart 
 
 was in the fifth space 9 cm. from midsternum and 3 cm. inside the 
 
 nipple line, corresponding with the left border of dullness. The 
 right border was 6.5 cm. to the right, the supracardiac dullness 9 cm. 
 The pulmonic second sound was accentuated. The sounds were of 
 poor quality. At the apex they were obliterated by loud murmurs, 
 
 systolic and diastolic in time. The systolic was heard over the 
 
 precordia. The pulses were thready and of poor volume and tension. 
 The artery walls were palpable. The blood pressure was 85/50. 
 The lungs were normal. The abdomen was retracted. There was 
 tenderness over the liver. The liver dullness extended from the 
 
 _ fourth rib to 8.5 cm. below the costal margin in the midclavicular 
 
 line, 9 cm. below in the parasternal, and 5 cm. below the xiphoid. 
 The liver pulsated. The edge was felt. The genitals and extremities 
 showed nothing of importance. The pupils were irregular, but equal 
 and reacted. The knee-jerks were not obtained. There was a 
 suggestion of a bilateral Babinski; no Kernig. 
 
 The temperature was 100° by mouth to 105.4° by rectum, the 
 pulse 91 to 135, the respiration 18 to 32. The amount of urine is not 
 recorded. The specific gravity was 1.025 to 1.010. There was the 
 slightest possible trace to a trace of albumin at both of two examina- 
 tions, a question of diacetic acid at the first, many leucocytes at the 
 second. The hemoglobin was 80%. There were 21,600 to 26,000 
 leucocytes. Blood cultures showed staphylococcus albus. The 
 blood urea nitrogen was 24 mgm. per 100 c.c. of blood. A Wasser- 
 mann was negative. The stools were negative. A lumbar puncture 
 April 2 gave 15 c.c. of clear fluid under 180 mm. pressure, showing 244 
 cells per cu. mm., 42% polynuclears, 58% mononuclears. Alcohol 
 was slightly positive, Nonne questionable, Wassermann negative. 
 
150 | FACTS ON THE HEART 
 
 There was a small fibrin clot in one-half hour in a stained specimen 
 of which no organisms could be demonstrated. A culture showed 
 staphylococcus albus. A lumbar puncture April 3 gave 30C.c. 
 of cloudy fluid under 140.mm. pressure, showing 840 cells, 59% 
 polynuclears, 41% lymphocytes... Another puncture the same day 
 gave 30 c.c. of cloudy fluid under 200 mm. pressure, cell count 
 1100, 64% polynuclears, 36% lymphocytes. <A clot formed in one 
 hour. Cultures on agar and blood serum showed staphylococcus 
 albus. : 
 
 The patient was put upon Karell diet,* with fluids limited to 
 tooo c.c. April 2 his mind was fogged and there was definite Brudzin- 
 ski. April 3 he was still irrational. 45 c.c. of anti-meningococcus 
 serum was injected, with definite rigidity and struggle on the part of 
 the patient. There was active reflex on the left, and positive Babin- 
 ski, but no clonus; on the right no reflex and no Babinski. None of 
 the fluids obtained at lumbar puncture showed tubercle bacilli. 
 April 4 the patient suddenly died. 
 
 Clinical Diagnosis (from Hospital Record)—Acute endocarditis. 
 
 Mitral insufficiency and stenosis. 
 
 Pulmonary embolism. 
 
 Acute meningitis. 
 
 Poliomyelitis? 
 
 General septicemia. 
 
 Dr. William H. Smith's Diagnosis —Extensive chronic endocardi- 
 tis of the mitral valve. 
 
 Possibly staphylococcus albus septicemia. 
 
 Possibly fresh vegetative endocarditis. 
 
 Possibly staphylococcus albus meningitis. 
 
 Anatomical Diagnosis ——Chronic and acute endocarditis of the 
 mitral and aortic valves. Stenosis. 
 
 Chronic and acute pericarditis. 
 
 Septicemia, staphyloccus, pale variety. 
 
 Hypertrophy and dilatation of the heart. 
 
 Infarcts of the spleen and kidneys. 
 
 Abscesses of the kidneys. 
 
 Septic arteritis and thrombosis of the hepatic artery with infarcts 
 of the liver. 
 
 Phlegmonous enteritis. 
 
 Soft hyperplastic spleen. 
 
 * 200 c.c. of milk at 8a.m., 12 m., 4 p.m., 8 p.m.; total 800 c.c. Or 9 iv at 6-8-10 
 Aa0s, b20n..72-4-0-4p, 10; 
 
ILLUSTRATIVE CASES. MITRAL STENOSIS AND AORTIC STENOSIS 157 
 
 Partial agenesis of liver with cyst. 
 
 Cholelithiasis. 
 
 Slight chronic pleuritis. 
 
 Chronic interstitial orchitis. 
 
 (Brain not examined.) 
 
 Dr. RicHARDSON: A staphylococcus of the pale variety was 
 recovered from the blood and the spleen. Scattered over the skin 
 in many places were minute to small purpuric spots, accounted 
 for, of course, by the staphylococcus septicemia. 
 
 The heart weighed 560 grams (normally 200-300), and showed 
 considerable hypertrophy and dilatation. ‘The left ventricle wall 
 
 Fic. 21.—Staphylococcus albus septicemia, mitral and aortic stenosis with acute 
 endocarditis. Section of heart valve showing staphylococcus albus. (Photomicro- 
 graph by Lewis S. Brown. xX1500. Dr. William H. Smith.) 
 
 was beefy,—good muscle. The cavities were dilated markedly on 
 the left and considerably on the right. Both layers of the pericar- 
 dium, visceral and parietal, were closely bound together by fibrous 
 membranous adhesions, but at one point there was an area about 
 three fingers’ breadth on the postero-lateral aspect of the left ventricle 
 where the adhesions were soft, reddish, and mushy. In other words, 
 there was an area of acute pericarditis within the chronic. 
 
 The aortic valve orifice would not admit a lead pencil. The cusps 
 were fused into a fibrocalcareous, irregular-surfaced mass, the 
 so-called fish-mouth valve. The surfaces of this irregular mass, both 
 superior and inferior, were coated with a felt-like layer of granular 
 thrombotic material. The mitral valve showed much fibrous thicken- 
 ing and deformity, with a large fibrocalcareous area, the central 
 
158 FACTS ON THE HEART 
 
 portion of which was depressed and the surface roughened, with at 
 one point a coating of thrombotic material. The tricuspid and 
 pulmonary valves were negative. The aorta and its great branches 
 were negative. There was no arteriosclerosis. 
 
 The lungs showed some edema; otherwise they were negative. 
 
 The spleen was enlarged, soft, pulpy, and showed several infarcts. 
 
 There was cholelithiasis; about fifty small gall-stones were 
 recovered. The bile ducts and the gall-bladder were negative. 
 
 The kidneys weighed 330 grams (normally 200-400). On remov- 
 ing the capsules the surfaces showed scattered over them minute 
 purplish spots like those on the skin. In other places there were 
 areas that looked like infarcts, the central portions of which were a 
 little softer than usual. They were margined in instances by red 
 borders. 
 
 We have in this case, therefore, an old endocarditis established 
 some time ago, with stenosis of the aortic and mitral valves. To this, 
 and within recent times, he has added a staphylococcus infection 
 which finds expression in the acute endocarditis, and, although I did 
 not examine the head, zn all probability a meningitis due presumably 
 
 to septic infarcts. The infarctions in the case were really septic; 
 
 that is, portions of the.septic vegetations on the valves containing 
 staphylococci were carried by the arteries to other organs. The 
 spleen and kidneys were the organs in which the infarcts arose 
 because they have the so-called end arteries. 
 
 Microscopical examination of the kidneys and of the tissues 
 generally showed a very characteristic picture, corroborative of 
 what we have been saying. In the arteries in the kidneys and in the 
 spleen we found collections of staphylococci. We found the staphy- 
 lococci also in the liver, and if we had had permission to examine the 
 brain I think we should have found them there. | 
 
 In the intestine there were purplish areas the central portions of 
 
 some of which on the mucosal side contained small yellowish-purple 
 
 areas; that is, septic infarcts in the intestine. In cases of sepsis we 
 may have intestinal disturbance associated with diarrhea, and in 
 some of them we find definite lesions, as we did in this case. The 
 anatomical picture as a whole was as though you had taken a hypo- 
 dermic syringe containing staphylococci and injected them into the 
 blood in the left ventricle; then, carried by the blood stream, the 
 
 organisms were distributed throughout the body. It was an experi- 
 
 ment conducted by Nature. Unusual as the anatomical conditions 
 were, they formed a good basis for the clinical picture. 
 
OTHER COMBINED LESIONS 159 
 
 There was some question about the conditions in the liver. At 
 one point there was an area of thickening of the capsule, and atrophy 
 of the liver tissue underneath. Below that area of atrophy the 
 liver showed areas not unlike septic infarcts, although infarcts very 
 rarely occur in the liver. A branch of the hepatic artery leading to 
 the region of these areas showed occlusion by thrombotic material. 
 The microscopical examination of the liver tissue showed septic 
 thrombosis of this branch, and also showed that the areas were areas. 
 of infarction. 
 
 Septicemias due to infection with the pale variety of the staphy- 
 lococcus are quite rare. 
 
 Dr. SmitH: The previous typhoid history is of interest as an 
 ‘etiological factor for his gall-stones. It would be of interest to know 
 whether typhoid bacilli were still present in the gall-bladder, sug- 
 gesting the possibility of his being a typhoid carrier. 
 
 OTHER COMBINED LESIONS 
 
 Mitral-and-Aortic-and Tricuspid Stenosis... ..............0c.0e0cee0+0+.22 CASES 
 Mitral-and-Tricuspid Stenosis. . Pee a oe ee I OAs eee 7 CASES 
 Pulmonary-and-Tricuspid E enoste Je Peel <r Meath clive Ste 2 CASES 
 Mitral-Aortic-Tricuspid-and- Bainonsey PGtetetiee Pe i cae at Rae SE CAGES 
 
 re ee er ee cases 
 
 Emphasizing some points already alluded to in the chapter on 
 mitral disease we see: 3 
 
 1. Etiology.—That in most cases (thirty out of thirty-three) there 
 has been recorded only a single attack of rheumatism. In the 
 “pure mitral’’ cases we have multiple attacks recorded in nearly one- 
 third, and of the mitral-and-aortic cases two-thirds have had multiple 
 rheumatic attacks. 
 
 2. Symptomatology.—The mode of death is congestive in two- 
 thirds of the cases as against one-half the cases in the simpler lesions 
 (see Table 52), but it is striking that the cases with mitral-and-tri- 
 cuspid lesions do not show passive congestion before or after death. 
 Only one out of seven cases died a congestive death or showed chronic 
 passive congestion at necropsy. 
 
 3. Necropsies.—The evidences of passive congestion are, as one 
 would expect, more often severe in these. multiple lesions than in 
 the simple cases. Dyspnea and cyanosis in life, cardiac hyper- 
 trophy, ascites, enlarged liver, and infarctions are all more often pres- 
 ent in the ‘‘combined lesions,” except as above specified. 
 
 4. The Diagnosis of the More Complicated Valve Lesions.— 
 Besides the 107 ‘‘pure mitral” cases and the 4o mitral-and-aortic, 
 
160 FACTS ON THE HEART 
 
 there were in our series twenty-two cases of Mutral-aortic-and- 
 iricus pid stenosis. Out of this group we recognized the mitral lesion 
 alone or in combination in eighteen. We recognized the aortic lesion 
 alone or in combination in nine. We raised the question of a tricus- 
 pid lesion in one. We missed all three lesions in four. 
 
 In the seven cases showing post-mortem stenosis of the mitral and 
 of the tricuspid valves, we recognized the mitral lesion in five, the tri- 
 cuspid lesion in none at all. In two cases we missed both the mitral 
 and the tricuspid. 
 
 We had two cases involving stenosis of the pulmonary and tricuspid 
 valves, in one of which we recognized the pulmonary stenosis alone. 
 In the other we missed both lesions. 
 
 In two cases necropsy showed stenosis of all four valves. In one 
 of these we recognized only the mitral lesion, in the other only the 
 mitral and aortic lesion. We missed the pulmonary and tricuspid 
 lesions in both cases. 
 
 Looking back over the whole thirty-three cases of this complicated 
 group one sees that, though the tricuspid valve was involved in every one 
 of them we only suspected this disease in one case out of the thirty- 
 three and did not even consider it in the others. The pulmonary valve 
 lesion we recognized once. So that it appears that we can often recog- 
 nize a mitral lesion especially if it has obvious congestive symptoms to 
 direct our attention to the heart. We can recognize a complicating - 
 aortic lesion (when present) in about half the cases. With uncom- 
 plicated or pure aortic stenosis we do rather better. Tricuspid and 
 pulmonary lesions we practically do not recognize at all. 
 
 ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 
 
 Necropsy 3549 
 
 A Canadian-American housewife of twenty-five entered January 
 11, 1916, for relief of dyspnea. She had one convulsion as a child. 
 She had “‘always”’ been dyspneic, and had never been strong. She - 
 had poor appetite, gas, and constipation accompanied by headache 
 over the eyes. She had scarlet fever at nine, chorea for three years 
 beginning at twelve, pneumonia at eighteen, bronchopneumonia at 
 nineteen, bronchitis several times, and many sore throats. Her 
 catamenia had always been irregular. : 
 
 For four years she had had leucorrhea and precordial pain and 
 urinated once or twice at night. For three years she had coughed 
 and had white frothy sputum. She had been married seventeen 
 months; had never been pregnant. For sixteen months she had had 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 161 
 
 pain and discharge from the right ear. Fora year she had been ortho- 
 pneic. For four months she had had edema, for three months a good 
 deal of nausea, for three weeks dysuria. A week before admission 
 she coughed up much blood. She lived near a gas plant, and thought 
 she breathed much gas. She slept poorly ten or eleven hours a night. 
 Her intelligence, memory, and speech were primitive. Her best 
 weight was 120 pounds four years before admission, her present 
 weight 112. 
 
 For four years she had had much dyspnea, for which she was 
 treated in a hospital twice for a month with relief, and again for a 
 third time. Two years before admission she developed a severe 
 cough and was sent to a tuberculosis hospital for observation. No 
 evidence of tuberculosis was found. Since her marriage she had 
 been much worse. Two weeks before admission she had “grippe.” 
 Since that attack she had been very uncomfortable, with aggravated 
 cough, dyspnea, and edema of the ankles. 
 
 Examination showed a fairly well-developed and nourished 
 woman 5 feet 614 inches in height, (weight January 22, 93 pounds). 
 The mucous membranes were slightly cyanotic, the teeth poor, the 
 tonsils large. The apex impulse of the heart was in the sixth space 
 12 cm. to the left of midsternum, two inches outside the nipple line. 
 The right border of dullness was 4.5 cm. to the right, the supracardiac 
 dullness 5.5. cm. There was a presystolic thrill. The pulmonic 
 second sound was accentuated and double, the aortic second faint. 
 There was a sharp first sound preceded by a rasping presystolic 
 murmur and followed by a high-pitched systolic. No second sound 
 was heard at the apex. The pulses were of fair volume. The lungs 
 showed many moist rales in the axillae and below the angles of the 
 scapulae, on the right nearly as high as midscapula. There was 
 tenderness over the liver. The liver dullness extended from the fifth 
 rib to eight cm. below the costal margin, where a tender edge was 
 felt. Vaginal examination was not done. The legs showed soft 
 pitting edema from the ankles to the sacrum. The pupils were 
 normal, as were the knee-jerks on reénforcement. 
 
 The temperature was 95° to 110° until January 28, then 97.3° 
 to 102° until February 7, then 96° to 99.5°, with one drop to 94.8° 
 February 11. The pulse was 71 to 146, the respiration 16 to 48. 
 The blood pressure was 140/100 to 115/80. The amount of urine 
 was normal except February 5 and 9, when it was ro ounces. The 
 specific gravity was 1.001 to 1.020. The urine showed a slight trace 
 
 of albumin at five or six examinations, a few red blood corpuscles at 
 11 
 
162 FACTS ON THE HEART 
 
 one, a large amount of pus and blood at one. The renal function 
 January 11 was 45%, January 18 30%, January 31 40%. A urine 
 culture showed a few doubtful bacilli. The hemoglobin was 85%. 
 There were 7800 to 48,000 leucocytes, 83% polynuclears, the reds 
 were normal. A Wassermann was negative. The stools gave a 
 negative guaiac at two examinations. The sputa showed many pus 
 cells and influenza bacilli; no tubercle bacilli at four examinations. 
 Two specimens settled in three layers. A dental consultant in reply 
 
 Fic. 22.—Heart symmetrically enlarged, not displaced. Seen from behind. Bron- 
 chiectasis with focal pneumonia and gangrene, especially right lung. Several areas 
 suggest cavities. (Roentgenological Department, Massachusetts General Hospital.) 
 
 to the question, ‘‘Is there alveolar abscess?” reported, ‘‘ Extraction 
 
 advised.”’ A throat consultant reported, ‘““Larynx negative as to 
 cause of cough.” 
 
 January 29 all the back teeth and roots were extracted under 
 ether. The patient was much worse from this time. She had 
 moderate fever. February 2 the pulse was elevated and the murmur 
 
 rough. For the next week she was very uncomfortable, coughing all 
 
 night and raising much sputum, occasionally blood-tinged. Evi- 
 dently she had had much morphia, as it took three-quarters of a 
 
 wy 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 163 
 
 grain to affect her. Her lungs were full of rales, especially the left, 
 where the rales at the apex were very sticky and there was slightly 
 bronchial respiration and some dullness. February 8 she was 
 cyanotic, and seemed worse. X-ray (Fig. 22) showed an extensive 
 pathological process in both lungs, especially the right, more marked 
 in the upper lobes, extending downward and obscuring the cardio- 
 hepatic angle on that side. On the left it extended down to the 
 fourth rib anteriorly. The maximum density was at the roots, 
 extending outward andupward. Enlarged and calcified glands were 
 seen at the roots. There were several areas suggesting cavities, the 
 largest the size of a quarter-dollar, at the lower border of the fourth 
 right rib, a smaller one under the third right, less distinct ones in the 
 left upper lobe. A dense line extended across the right chest hori- 
 zontally from the lower fourth costosternal angle to the upper border 
 of the seventh rib in the axillary line, near or at the interlobar cleft. 
 The heart was somewhat enlarged symmetrically, not displaced. The 
 diaphragm was low, somewhat irregular, with Jimited excursion, the 
 angles clear. | 
 
 The patient’s condition became very distressing. She coughed 
 continually, raising reddish-brown purulent sputum, had epigastric 
 pain and occasional vomiting, grew more and more cyanotic and 
 dyspneic, and February 16 died. 
 
 Clinical Diagnosis —Chronic nephritis. 
 
 Influenza. 
 
 Cardiac decompensation. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis of the 
 mitral valve with stenosis. 
 
 Possibly some chronic adhesive pericarditis. 
 
 Chronic pneumonitis with pulmonary abscesses or bronchiectasis. 
 
 Possibly old interlobar empyema. 
 
 Passive congestion of all the organs. 
 
 Anatomical Diagnosis——Chronic endocarditis of the mitral, 
 aortic, and tricuspid valves. 
 Hypertrophy and dilatation of the heart. : 
 
 Septicemia, streptococcus. 
 
 -Bronchiectasis with focal pneumonia and gangrene. 
 
 Infarcts of the superior lobe of the left lung. 
 
 Ulcer of the stomach. 
 
 Anasarca. 
 
 Slight ascites. 
 
 Vaginitis papillomatosa. 
 
164 FACTS ON THE HEART 
 
 Old infarct in one kidney. 
 
 Obsolete tuberculosis of bronchial lymphatic glands. 
 
 Chronic pleuritis. 
 
 The heart was considerably enlarged, weighing 404 grams. The 
 right ventricle wall measured 5 mm., the left ventricle wall 10 mm. 
 The auricular walls were thickened. The right side of the heart 
 contained a large amount of currant-jelly-like blood clot. The right 
 auricle was greatly dilated, the right ventricle moderately dilated. 
 The mitral orifice admitted the tip of the little finger. The curtain 
 was the seat of marked fibrous and fibrocalcareous change with great 
 deformity of the valve and decrease in its circumference. The 
 chordae tendineae were shortened, thickened, and fused to the curtain. 
 The aortic valve circumference was 5.5 cm. ‘The cusps showed a 
 moderate amount of diffuse fibrous thickening which was slightly 
 calcareous in places and rendered the walls rather rigid. The thick- 
 ened walls in places measured from one to two mm. in cross section. 
 The tricuspid valve measured 5 cm. ‘The curtain was the seat of 
 much diffuse fibrous thickening with deformity of the valve and 
 decrease in its circumference. The pulmonary valve measured 7 cm. — 
 and was negative. 
 
 Necropsy 4084 
 
 An American girl of twelve entered May 22. She gave an unsatis- 
 factory history which it was expected would be supplemented by 
 relatives. It was not, however. She was apparently a perfectly 
 normal child until a year before admission. She remembered 
 measles, chickenpox and pertussis in infancy (sic). She had always 
 been subject to sore throats, but apparently had not had tonsillitis. 
 A year before admission she had an attack of “rheumatism” and was 
 ill in bed for several weeks with swollen, red, and painful joints, 
 particularly the ankles and wrists. Since this time she had had 
 dyspnea on slight exertion, had been unable to attend school or 
 play with other children, and had had slight cough with a small © 
 amount of thin yellowish sputum. 
 
 Two weeks before admission she began to have reve and marked | 
 dyspnea, and since that time had been in bed under treatment by a 
 physician. She had had considerable pain over the epicardium and 
 frequent frontal headaches lasting a few hours each. She had 
 marked cough with considerable watery sputum. 
 
 Examination showed a fairly well developed and nourished girl 
 with pale skin and mucous membrane. The throat was slightly 
 injected. The submaxillary glands were swollen and tender. The — 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 165 
 
 chest expansion was less on the left. These was small Harrison’s 
 groove. The left border of the sternum was more prominent than 
 the right and somewhat raised: The lung signs were as shown in 
 Fig. 23. The apex impulse of the heart was diffuse in the sixth space 
 14 cm. to the left. There was a heaving precordial impulse with a 
 wave moving from the apex region toward the sternum. ‘The meas- 
 urements of percussion dullness show the borders as 14 cm. to the 
 left, 4.5 cm. to the right, the substernal dullness 4.5 cm. The action 
 was rapid. The sounds were of rather poor quality, the pulmonic 
 second sound accentuated. ‘The first sound at the apex was replaced 
 by a loud blowing systolic murmur which took up the whole of sys- 
 tole, followed by a shorter diastolic murmur. There was a rough 
 diastolic murmur over the aortic area and along the left sternal bor- 
 der. The pulses were equal; they tended to be Corrigan in type. 
 A systolic thrill was felt over the precordia. The blood pressure was 
 106/35. There was definite hyperesthesia. The abdomen showed 
 
 Kyperesthesla 
 
 of precordia. Impaired reso- 
 
 nance. Bronchial 
 
 Rales An occasional 
 
 Palpable rale. 
 
 Mier General tenderness 
 
 Operation 
 scar 
 
 Fic. 23. 
 
 general tenderness in both flanks. The liver dullness extended 
 from the fourth rib; the edge was just palpable and tender. There 
 was slight costovertebral tenderness. The genitals were not exam- 
 ined. The fingers showed definite clubbing, and the toes suggested 
 it. The pupils were normal, the knee-jerks equal but diminished. 
 There was no clonus or Babinski. 
 
 The temperature was 97°, rising with daily swings of one or two 
 degrees to 101.2°. The pulse was 120 to 140, with one drop to 105 
 May 25. ‘The respirations were 23 to 47. The output of urine was 
 16 to g ounces, the specific gravity 1.020 to 1.028. The urine was 
 cloudy at all of three examinations and showed the slightest possible 
 trace of albumin and the slightest possible trace of sugar at two, diace- 
 tic acid at two, leucocytes at all. The hemoglobin as 80 %, the leu- 
 cocytes 10,800 to 15,400, the polynuclears 69%, the platelets 
 increased. A Wassermann was negative and a blood culture negative. 
 The stools gave a positive guaiac at both of two examinations. A 
 throat culture showed streptococci, no diphtheria bacilli. 
 
166 FACTS ON THE HEART 
 
 May 26 the signs in the lungs were still more definite. A friction 
 rub was heard in the left back. May 28 the patient died. 
 
 Clinical Diagnosis (from Hospital Record) —Acute endocarditis. 
 
 Myocarditis. | 
 
 Aortic and mitral disease. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic and acute endocarditis 
 of the aortic valve and possibly the mitral. 
 
 Hypertrophy and dilatation of the heart. 
 
 Pneumonia, left lung. 
 
 Miseal 
 valve 
 
 Fic. 24.—Necropsy 4084. Heart in stenosis of the mitral, aortic and tricuspid 
 
 valves, showing the mitral valve, 7.5 cm. (Photograph by Lewis S. Brown. Dr. 
 Oscar Richardson.) 
 
 Anatomical Diagnosis——Chronic endocarditis of the mitral, 
 aortic, and tricuspid valves, stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Hemorrhagic areas, epicardium and peritoneum. 
 
 Chronic passive congestion, general. 
 
 Infarct of the right lung. 
 
 Focal pneumonia of superior lobe of right lung. 
 
 Tuberculous ulcer of small intestine. 
 
 Chronic tuberculosis, mesenteric glands. 
 
 Status lymphaticus. 
 
 Scar of old appendectomy. 
 
 Dr. Casort: There was no acute endocarditis? 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 1607 
 
 Dr. RicHARDSON: No. In the first place the hypertrophy and 
 dilatation are apparent. The valves show the kind of chronic endo- 
 carditis associated with chorea. I do not know that she had it, but 
 this is the type. In the mitral valve there is decrease of circumfer- 
 ence, not very much, 74% cm. But the curtain generally shows 
 fibrous thickening continued to the margin, where it presents as a 
 rounded fibrous ridge with markedly thickened and _ shortened 
 chordae tendineae. (See Fig. 24.) Dr. Cabot’s diagnosis as to 
 the aortic valve is borne out, for the margin of the cusps are thickened 
 and rounded in the way the free margin of the mitral is affected, and 
 
 f Kovtie valye 
 
 sss 
 
 Fic. 25.—Necropsy 4084. The same, showing the aortic valve. (Photograph by 
 Lewis S. Brown. Dr. Oscar Richardson.) 
 
 that without making much reduction of the circumference of the 
 
 aortic valve does nevertheless decrease the width of the cusp and allow 
 
 some regurgitation. (See Fig. 25.) The process in the tricuspid is 
 
 slighter than on the other valves. (See Fig. 26.) The pulmonary 
 
 valve is negative, and gives the standard for a good cusp. 
 
 Another interesting point is that extending down from one of 
 the aortic cusps is an oval area of fibrosis which of course « years ago 
 Was a patch of acute endocarditis. A cross section shows that it 
 extends slightly into the underlying myocardium. 
 
 The record should call attention to the fact that petechiae are 
 scattered through the skin and other places. They were present 
 in this case, and they were well marked in the peritoneum too. 
 
168 | FACTS ON THE HEART 
 
 The chronic passive congestion is the brown-red, salmon-colored 
 tissue, somewhat leathery, yielding a brownish-red fluid containing the 
 so-called heart cells. There was nothing in the auricular appendices. 
 There was an infarct of the right lung. These occur where there is 
 considerable chronic passive congestion. 
 
 The focus of pneumonia was in the upper part of the right lung, 
 and was rather an easy thing to miss, but I happened to be struck by 
 the resistance in feeling of it and therefore examined. With the 
 microscope it was found to be a focus of pneumonia in the superior 
 lobe of the right lung. 
 
 Tereusbrd 
 vatve 
 
 4 
 
 | 
 
 Fic. 26.—Necropsy 4084. The same, showing the tricuspid valve. (Photograph by 
 Lewis S. Brown. Dr. Oscar Richardson.) 
 
 The thymus gland weighed eleven to twelve grams, and the lymph 
 apparatus generally showed more or less hyperplasia. These condi- 
 tions we find at times associated with tuberculosis. 
 
 In this case there was only a single ulcer along the whole length of 
 the intestine, but microscopically it showed typical tuberculous 
 tissue. In the mesenteric glands there was chronic tuberculosis. 
 
 Above the diaphragm there was no tuberculosis of any sort. 
 Below we had an ulcer and the tuberculosis of the mesenteric glands, 
 and of course it is a case with strong evidence in favor of the entrance 
 of the tubercle bacillus by the gastro-intestinal tract. 
 
 A PuysictAn: This girl had a fever. What do you think it was 
 due to? | 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 169 
 
 Dr. RIcHARDSON: Fever for how long? 
 
 Dr. Casot: Two weeks before she came in and six days here. 
 
 Dr. RicHARDSON: She had tuberculous ulcer, tuberculosis of the 
 mesenteric glands, and some time within that period, of course, that 
 area of pneumonia. 
 
 A PuysictAn: What caused the leucocytosis? 
 
 Dr. Casot: I suppose it was leucocytosis due to pneumonia. 
 ‘I do not know whether the pneumonia could have been there all this 
 time. In the heart there was no source of fever. The pneumonia 
 was not in the place we suspected. It was at the right top. In the 
 left base it was merely congestion. 
 
 A PuysiciAN: Is there any means of knowing whether the ulcer 
 ~ was bovine tuberculosis? 
 
 Dr. RicHArDson: We did not secure the bacillus, but it probably 
 was the bovine type. 
 
 Necropsy 4415 
 
 An unoccupied American girl of twenty entered August 1, 1922, 
 complaining of a skin eruption and pain in the cardiac region. Her 
 mother died of Bright’s disease. The patient had the minor diseases 
 of childhood and a light case of influenza in 1918. For three weeks 
 she had had some blood stained sputum. Two weeks before admis- 
 sion for a few days she had a yellowish vaginal discharge. She had a 
 tendency to “‘nervousness.”” In 1921 she weighed 125 pounds, her 
 best weight; her present weight was 104 or less. 
 
 Six years before admission she had a severe sore throat diagnosed 
 as tonsillitis. She was in bed for a week. She returned to school 
 only to be forced to go back to bed by a sudden attack of pain in 
 the arms and legs. She had lameness of the extremities and knife- 
 like shooting pain over the precordia, aggravated by deep breathing. 
 Two months after the initial attack tonsillectomy was done. She 
 was in bed off and on for the next two years for periods of from one to 
 seven weeks. She was very short of breath and orthopneic all this 
 time, and was troubled a great deal by gas. She believed she had 
 some fever during the whole period. After this she felt quite well 
 until January, 1922, danced and walked a normal amount, and had 
 ‘no discomfort of any kind except for a somewhat more than usual 
 amount of gas. In January, 1922, she noticed a small red spot on 
 the left cheek, soon followed by one on the right and two areas on each 
 side of the jaw. These gradually increased until after a month her 
 whole face was exceedingly red. This gradually spread in the course of 
 four months to the neck, chest, arms and hands, excepting the palms. 
 
170 FACTS ON THE HEART 
 
 The lesions on the neck were decidedly painful and cracked. During 
 this time she noticed a small red spot the size of a pea on her great toe. 
 
 In May, 1922, she was operated upon at a neighboring hospital 
 for acute appendicitis. The day after the operation she developed 
 pneumonia and was in the hospital for twelve days. During this time 
 the arms cleared except fora few pigmented areas which had persisted. 
 
 After a fair convalescence she felt pretty well until six weeks 
 _ before admission. Then she began to have “a good day and a poor 
 one,’ and on the poor ones noticed that she had “catching” pains 
 in the side and occasionally in the back. ‘This continued for three 
 weeks. Then she found she could not sleep one night, and the next 
 day was very somnolent, had a heavy oppressive feeling in the chest, 
 and could get her breath only with difficulty, though she did not have 
 to sit up. She had a temperature of 103°. After placing an electric 
 pad on her chest she noticed the return of the skin condition which 
 was present at admission. She had an occasional attack of dizziness 
 and a great deal of gas, nausea and vomiting. She had eaten very 
 little, and had been very dyspneic. She said she had no cough, 
 though the examiner noticed occasional cough. For six weeks she 
 had been in bed, the first three weeks about every other day, the 
 last three weeks constantly. For twenty-one days she had had a 
 temperature of 103° and 104°. The precordial pain had been very 
 sharp and severe. It was somewhat relieved by an icebag and local- 
 ized in an area about the size of three silver dollars. 
 
 Examination showed a well nourished girl with a sharp margin- 
 ated gyrate eruption on the skin of the lower face and neck and upper 
 chest. More recent parts showed red flaking edges and paler centers. 
 The older portions showed thick crusting and the oldest portions a 
 deep dirty brownish pigmentation. The process in the mucosa and 
 roof of the mouth was red and raw. On the uvula there was a gyrate 
 patch with a whitish border and red center. The apex impulse of 
 the heart and the midclavicle are not recorded. The measurements ~ 
 of percussion dullness were, left border 11.5 cm., right border 2.5 cm., 
 supracardiac dullness 5 cm. At the apex was a presystolic and sys- 
 tolic murmur, along the left sternal border a loud rough diastolic. 
 The aortic second sound was nearly absent. The pulmonic second 
 sound was sharp. There was collapsing pulse and pistol shot in the 
 groins. The blood pressure was 140/o. The lungs showed a few 
 fine rales at both bases posteriorly. The liver edge as 2 cm. down, 
 slightly tender. The spleen was easily palpable 4 cm. below the cos- 
 tal margin. There was a scar in the right lower quadrant. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS I7I 
 
 The temperature was 103.4° to 97.5, with a terminal rise to 107.1°. 
 The pulse was 155 to 60, the respirations 19 to 71. The output of 
 urine was 8 to 4o ounces, the specific gravity 1.006 to 1.020. The 
 urine was cloudy at two of seven examinations, showed the slightest 
 possible trace of albumin at all, leucocytes at six, red blood cells at 
 four, granular casts at six, hyaline at two. The renal function was 
 50%. The hemoglobin was 55% to 75%, the leucocytes 24,000 to 
 4,000, the polynuclears 61% to 75%, the reds 3,050,000 to 4,280,000, 
 slight achromia at one examination, none at another. Three blood 
 cultures were negative; a fourth showed questionable Gram-positive 
 bacilli in one flask. A Wassermann was negative. The stools were 
 negative to guaiac. The sputum was brownish, mucopurulent. 
 
 August 6 a swelling appeared on the right arm in the region of the 
 deltoid and behind it, apparently not tender. August 9 she was 
 nauseated and vomited most of what she took by mouth. The heart 
 rate was slower and definitely irregular, without any special rhythm. 
 There seemed to be slow fibrillation. Electrocardiogram August 9 
 showed auricular fibrillation, rate 70, inverted T2 wave, left axis 
 deviation. Digitalis was stopped. After this she had no nausea 
 and felt much better. By August 12 the temperature was almost 
 normal, the pulse slower. The spleen was barely palpable. The 
 liver was not felt. The rales persisted, but to a smaller extent. 
 August 14 she had return of the precordial pain. It grew more and 
 more severe during the next few days. She required morphia for 
 any rest at all, and at times was forced to sit up and gasp. August 19 
 the pain began to diminish, and by the 24th was much less. The 
 temperature was also running lower. A swollen tender gland devel- 
 oped beneath the left jaw, disappearing in four days. She felt much 
 better. 
 
 September 1 there was dullness to a little above the angle of the 
 right scapula with diminished breath sounds and a few moist rales. 
 The next day moderate edema of the feet was noticed. September 3 
 this became marked, and she complained of feeling tired. Beginning 
 September 5 she complained of increasing pain in the epigastrium 
 and beneath the lower sternum and of increasing shortness of breath. 
 The edema of the feet was slightly less. The temperature was 
 again rising. Her general complaint was that she had ‘‘gas on the 
 heart” and felt the “‘sleep-start”’ of the cardiac patient. September 
 19 the edema of the legs and back began to increase markedly. She 
 felt generally miserable, with pain and much dyspnea. 
 
- 172 FACTS ON THE HEART 
 
 September 29 a chest tap in the seventh right space, posterior 
 axillary line, gave 600 c.c. of cloudy straw-colored fluid when the 
 patient began to cough. The specific gravity of the fluid was 1.016; 
 leucocytes 3400, rare red cells, polynuclears 87%, lymphocytes 3%, 
 epithelials 10%; no organisms; no clot; culture negative. 
 
 The night of October 9 her temperature suddenly went up to 104°, 
 the pulse to 170, and the respirations to 72. Her hands and feet 
 became cold, and she seemed to be moribund. The next morning, 
 however, she was better. The chest showed coarse rales below the 
 angle of the left scapula, dullness and bronchial breathing below the 
 right. The respiration rose to 71, falling the next day to 36-44. 
 
 October rz the right chest was again tapped in the posterior 
 axillary line, the eighth interspace, and 250 c.c. of cloudy straw- 
 colored fluid with-drawn; specific gravity 1.010, 3200 cells, 88% 
 lymphocytes, 22% polynuclears, a few red blood cells, no organisms. 
 October 12 the temperature rose to 107.1°.. The pulse was of good - 
 quality. That day she died. 
 
 Clinical Diagnosis (from Hosbital Record).—Malignant endo- 
 carditis. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic and acute endocar- © 
 ditis of the aortic and mitral valves with stenosis. 
 
 Pneumonia with acute purulent pleurisy. 
 
 Nephritis? 
 
 Chronic adhesive pericarditis? 
 
 Hypertrophy and dilatation of the heart. 
 
 Probably infarcts of spleen, liver, kidneys. 
 
 Chronic passive congestion, general. 
 
 Anatomical Diagnosis:—Chronic endocarditis of the mitral, aortic 
 and tricuspid valves. 
 
 Acute endocarditis of mitral valve.. 
 
 Chronic adhesive pericarditis. 
 
 Subacute glomerulonephritis. 
 
 Hypertrophy and diatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Edema of feet and ankles. 
 
 Slight hydrothorax. 
 
 Focal pneumonia, left lung. 
 
 Fatty metamorphosis of the liver. 
 
 Localized chronic peritonitis. 
 
 Obsolete tuberculosis of the mesenteric glands. 
 
 Scar of old operation wound. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 173 
 
 Slight chronic pleuritis. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 There was an old operation scar in the right lower quadrant and the 
 appendix was absent. The peritoneal cavity was moist. The 
 gastro-intestinal tract was out of the picture except for some redden- 
 ing of the mucosa, the beginning of chronic passive congestion. The 
 mesenteric glands showed a little obsolete tuberculosis. There was 
 none anywhere else. 
 
 The right pleural cavity contained 200 c.c. of thin pale clear fluid; 
 there was about 5o c.c. in the other cavity. There were scattered old 
 fibrous adhesions. The trachea, the bronchi and the bronchial 
 glands were negative; the bronchial glands were slightly enlarged 
 but with no evidence of tuberculosis. 
 
 Dr. CasoTt: Was there evidence of any recent pleurisy? 
 
 Dr. RICHARDSON: Not at all, except for what comes later. The 
 right lung showed chronic passive congestion. The left was similar 
 to the right except that in the upper part of the lower lobe near the 
 root of the lung there was a frank area of focal pneumonia, and over 
 that an area of acute pleuritis. 
 
 The pericardial cavity was obliterated by adhesions binding the 
 two layers together—chronic pericarditis. The heart weighed 500 
 grams. This is a very considerable enlargement for a woman of 
 twenty. The myocardium was thick on the right, fairly thick on the 
 left—four mm. on the right, thirteen on the left,—a general thick- 
 ness, rather a beefy myocardium. There was a little dilatation on the 
 left, moderate on the right. The mitral valve measured 519 cm., 
 the aortic 6 cm., the tricuspid 9 cm., the pulmonary 714 cm., indicat- 
 ing well marked stenosis of the mitral. From the measurement we 
 cannot say anything about the aortic, but there was some change in 
 the aortic valve nevertheless. There was stenosis of the tricuspid, 
 because that valve is normally somewhere about twelve cm. The 
 pulmonary valve is very rarely diseased and was not in this case. 
 The mitral curtain showed diffuse deforming fibrosis extending along 
 the free margin of the valve and showing in places fibrocalcareous 
 degeneration—a pretty fair stenosis of the mitral, and chronic enough 
 so that there was fibrocalcareous material in the lesion. The circum- 
 ference of the aortic cusps was 6 cm. It might be all right; but what 
 happened was that fibrosis had deformed the margins of the cusps 
 with consequent diminution of their width, producing some regurgita- 
 tion. The tricuspid showed some fibrosis along the margin of the 
 valve, some shortening and thickening of the chordae tendineae. 
 
174 FACTS ON THE HEART 
 
 The decrease in circumference was sufficient so that we have to say 
 stenosis of the tricuspid. Further complicating the picture, on the 
 roughened surfaces of the fibrocalcareous degeneration of the aortic 
 valve was a soft wad of acute endocarditis. A clear-cut picture of 
 chronic endocarditis and acute, with chronic pericarditis. Of course 
 the result of that was the hypertrophy and dilatation of the heart 
 and the chronic passive congestion. 
 
 It often happens here when examining the organs, as happens 
 often in the clinic, that chronic passive congestion disguises any 
 lesion that may be in the kidneys. These kidneys weighed 415 
 grams, were bluish-red, plump, rather wide cortices, and the section 
 surfaces were bluish-red. That answers well enough macroscopi- 
 cally for chronic passive congestion, but the kidneys nevertheless 
 were the seat of subacute glomerulonephritis. The pelves, ureters, 
 bladder, uterus and adnexa were out of the picture. 
 
 The liver showed fatty metamorphosis. 
 
 All together this is a clear-cut picture of endocarditis acute years 
 ago and now chronic and acute, both. 
 
 Dr. Casot: The spleen was not enlarged? 
 
 Dr. R1icHARDSON: It was slightly enlarged. Another thing—with 
 all the story not a single infarct was found. 
 
 Necropsy 4674 
 
 An Irish-American schoolgirl of nineteen came to the Emergency 
 Ward April 27. An unsatisfactory history was obtained from her 
 mother. It was negative except for tonsillectomy and adenoidec- 
 tomy at four years. When the girl was six years old her father died 
 by trauma. After fainting once the child began to feel weak and 
 
 listless. A year later she had an attack of red, painful and swollen | 
 
 joints keeping her in bed three weeks. After this she had attacks of 
 
 joint pain at least once a year, and also had “‘growing pains.” At — 
 thirteen she had a particularly severe attack of rheumatic pain, - 
 
 and following it had dyspnea. For the past six winters she had been 
 in bed a great deal, chiefly because of the joints. Two years before 
 admission she was treated by a doctor who said that she should not 
 be out of bed. It was impossible to learn how many periods of 
 dyspnea she had had. For the past ten days she had been vomiting, 
 and for the past week had been very ill indeed, vomiting, unable to 
 sleep or eat, and requiring constant fanning. 
 
 Examination showed a young girl with dyspnea and orthopnea yet 
 surprisingly comfortable. ‘The mucous membranes were cyanotic, 
 
 us 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 175 
 
 the lips red, as if painted. ‘The skin was pale and moist with diffuse 
 acne over the chest and back. The subcutaneous tissue was thin. 
 _The muscles were soft. The respiration was accelerated. There was 
 high diaphragm on both sides. The breath sounds were markedly 
 high-pitched at inspiration, otherwise the lungs were normal. The 
 heart was markedly enlarged to the right and left. The apex impulse 
 was in the sixth space ro cm. from midsternum and 3 cm. outside 
 the midclavicular line. The right border of dullness was 4 cm. from 
 midsternum. ‘The supracardiac dullness was 5 cm. There was 
 precordial heave. A thrill was felt which was difficult to time. 
 Action absolutely irregular. Soundsof good quality. Pulse deficit. 
 One sound, probably the first, markedly accentuated. Murmurs 
 dificult to time. ‘There were no signs of pericarditis or effusion 
 and no compression signs posteriorly. The blood pressure was 110/60. 
 The liver was enlarged almost to the umbilicus and slightly tender. 
 There was slight sacral and pretibial pitting. The temperature was 96 
 to 101.8°, the pulse 84 to 141 to 4o, the respiration 30 to 12. The 
 urine and blood are not recorded. 
 
 The patient weighed too pounds. One hour after the second 
 dose of digifolin it was found that the heart rate had gradually come 
 down from 140 to 96 at the apex and was irregular. Two hours after 
 the third dose, i.e. after 131¢ grains had been given intravenously, 
 the apex rate had fallen to 66. After the fall to 96 she felt much 
 better and had good diuresis. After the drop to 66 the improvement 
 was more marked. By the 29th she felt fairly well. She had been 
 vomiting all the morning. At noon the apex rate seemed fairly 
 regular. It was still about 65. ‘There was a slight odor of acetone 
 inthe breath. Rectal glucose was started. During the afternoon the 
 pulse was markedly irregular for short periods. By six o’clock the 
 whole condition was changed for the worse, though she felt about 
 the same. She was still vomiting. During the evening the heart 
 was extremely irregular in rate and rhythm over short periods during 
 which it was impossible to enumerate the separate contractions; as 
 nearly as could be made out the rate went up to go or 100. At other 
 times it was 65 to 70. At g p.m. she had not had any digitalis for 
 twelve hours. The attacks became more frequent and she was more 
 restless during them. When the rate was slow she was markedly 
 apathetic and moribund. She grew rapidly worse, and died rather 
 suddenly during an attack of marked fibrillation. 
 
 Clinical Diagnosis (from Hospital Record) —Rheumatic heart 
 disease. 
 
176 FACTS ON THE HEART 
 
 Mitral stenosis and regurgitation. 
 
 Auricular fibrillation. 
 
 Congestive failure. , 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 aortic and mitral valves with stenosis of each. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis.—Chronic endocarditis of the mitral, aortic 
 and tricuspid valves, stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Slight hydrothorax. 
 
 Slight hydropericardium. 
 
 Slight ascites. 
 
 Slight anasarca. 
 
 Chronic pleuritis. 
 
 Dr. RIcHARDSON: The lips were purple, the skin generally pale. 
 
 In the peritoneal cavity there was about soo c.c. of thin pale fluid, 
 —slight ascites. The mucosa of the stomach and intestines was 
 velvety, reddened, juicy, and saturated with thin bloody fluid,— 
 chronic passive congestion. 
 
 The anterior margin of the liver was 8 cm. below the costal border — 
 —i.e., much below.. The liver weighed toro grams,—not large, 
 although it was so far below the costal border. Yet the tissue showed 
 passive congestion. 
 
 Dr. Casort: That is an interesting point. Inever saw that before. 
 
 Dr. RicHAarDSON: The diaphragm was at the sixth rib on the 
 right, the fifth rib on the left. 
 
 The right pleural cavity contained 200 c.c. of thin pale fluid, the 
 
 left 50 c.c.,—beginning hydrothorax. There is a great variation in 
 
 the amounts of fluid found in the pleural cavities. Sometimes there 
 is a great deal in the right side and none in the left, and sometimes | 
 very little in each; to find very little in one and considerable in the 
 other is not unusual at all. There were old pleural adhesions pos- 
 teriorly in the region of the upper half of the right lung. On the left 
 there were old adhesions posteriorly. The lung tissue showed well 
 marked chronic passive congestion. 
 
 The pericardium contained too c.c. of thin clear pale fluid; slight 
 hydropericardium. . 
 
 The heart weighed 550 grams. That is marked enlargement. 
 The right ventricle wall was thickened, 5 mm. That suggests a 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 177 
 
 lesion of the mitral valve. The left ventricle wall was t1 mm. 
 There may be something the matter with the aortic, but it will not be 
 very marked. The columnae carneae were well marked. Cavities: 
 Left, much dilatation; right, considerable dilatation. That dilata- 
 tion suggests changes in probably two valves at least. 
 
 Dr. CaspotT: Was there anything about the left auricle, 
 particularly? 
 
 _Dr. RicHarpson: Dilatation. 
 
 The auricular appendices were negative. The circumference of 
 the mitral valve was about 714 cm.,—considerable stenosis. The 
 usual circumference would be 1o cm. ‘The mitral curtain showed a 
 fibrous irregular band of thickening extending along the free margin, 
 with some thickening and fusion of the chordae tendineae and con- 
 siderable diffuse fibrosis and deformity of the valve. A fibrous patch 
 extended from the valve curtain up along the endocardium of the 
 left auricle. That is not an unusual picture in these so-called 
 theumatic hearts. ‘The acute process is a spreading one, and some- 
 times extends down along the endocardium below the valve and 
 frequently up into the auricle. In the region of the aortic valve it 
 may spread to the endocardium below the cusps, and sometimes it 
 extends up along the aortic wall, a kind of aortitis, but not luetic. 
 It may confuse one a little as to whether it is syphilitic aortitis or 
 not. The tricuspid valve measured 10 cm., stenosis, and showed 
 considerable fibrosis with contraction and deformity of the curtain 
 and thickening, and shortening of the chordae tendineae. The aortic 
 was 544 cm. It showed some diffuse fibrous thickening, and the free 
 margins of the cusps were a little rigid and fibrotic; slight stenosis. 
 The pulmonary valve was negative. Of all the valves the pulmonary 
 is the least likely to be diseased; for some unknown reason it best 
 maintains its integrity. The coronaries were free and negative. 
 
 The liver showed chronic passive congestion. 
 
 The spleen weighed 120 grams,—not increased in weight, but 
 with elastic congested tissue. 
 
 Dr. Casot: The kidneys were all right? 
 
 Dr. RIcHARDSON: Chronic passive congestion. 
 
 Dr. Casot: No cause for vomiting found except digitalis. 
 
 Necropsy 1249 
 
 An Irish housemaid of forty-eight entered August 21. She 
 gave a history of measles, mumps and scarlet fever in childhood. 
 Otherwise she had always been strong and well except for dyspepsia 
 
 12 - 
 
178 FACTS ON THE HEART 
 
 of several years’ standing. For the past two years her catamenia 
 had been very irregular and scanty. The day before admission, three 
 hours after eating cabbage, she was seized with severe abdominal 
 cramps, nausea, vomiting and diarrhea. The symptoms continued 
 all through the day of admission, and she had vomited and retched 
 continually. The vomitus was dark colored and watery. She could 
 not sleep. The cramps were relieved by pressure. 
 
 Examination showed a slightly obese woman with markedly 
 irregular heart action and pulse. The heart was not enlarged and 
 showed no other abnormalities. The base of the right lung in front 
 and behind showed slight dullness, many coarse moist rales, with 
 diminished tactile and vocal fremitusand breathing. At theleft apex 
 behind there was slight dullness with marked bronchial breathing. 
 The abdomen was much distended, the navel flushed. The muscles 
 were held rigid. ‘There was slight fullness in the epigastrium and 
 slight general tenderness. To the right of the umbilicus was a soft 
 tumor about an inch in diameter under the skin. About three inches 
 below this was a small hard subcutaneous nodule, and in the epigas- 
 trium a similar one. The temperature was normal, the pulse 128 
 to 131, the respirations 23 to 36. The urine showed a very slight 
 trace of albumin; otherwise it was not remarkable. The hemoglobin 
 was 70%, the leucocytes 27,400. The vomitus was dark brown. 
 Microscopical examination showed it to be made up of fibrin and 
 normal red blood corpuscles. 
 
 The night of admission the patient did not seem in poor condition. 
 The pain was easily relieved by a hot water bag. After midnight she 
 vomited a few times, castor oil and some food and bile. In the morn- 
 ing she vomited black material which proved to be mostly blood. 
 Her abdomen was much distended and her face ashen. She con- 
 tinued to vomit quarts of black material. Operation was done that 
 morning. Considerable blood tinged fluid escaped when the peri- 
 toneum was opened. A portion of the small intestine about twenty- | 
 four inches in length seemed to be gangrenous and distended, 
 apparently at the beginning of the iieum. The demarcation line was — 
 distinct. The mesentery was thrombosed and friable. The patient 
 died on the operating table. 
 
 Dr. RicHarpson: There is a note here upon the operation. 
 Apparently Dr. Scudder must have told me himself, because I have 
 recorded, ‘“‘The surgeon, Dr. Scudder, states that at the time of 
 operation there was a twist in the jejunum in the region of the 
 involved portion.” 
 
 s 
 
/ ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS I79 
 
 Dr. YounG: A volvulus. 
 
 Dr. RrcHarpson: That is what that would describe. 
 
 Clinical Diagnosis.—Acute intestinal obstruction. 
 
 Mesenteric thrombosis. 
 
 Anatomical Diagnosis.—Fibrous endocarditis of the mitral, aortic 
 and tricuspid valves, stenosis. 
 
 Obturating thrombus of the superior mesenteric vein. 
 
 Hemorrhagic infarction of a portion of the jejunum. 
 
 Hypertrophy and dilatation of the heart. 
 
 Fibrous adhesions between the ileum and the uterus. 
 
 Chronic perihepatitis and perisplenitis. 
 
 Chronic hyperplasia of the spleen. 
 
 Chronic pleuritis. 
 
 Operation wound. 
 
 Dr. RicHARpDson: A thin brownish-red fluid exuded from the 
 operation wound. The peritoneal cavity contained a moderate 
 amount of thin brownish-red fluid. We have to account for that 
 of course. It came from the region of a strip of infarcted intestine. 
 There were adhesions between the liver and the diaphragm and 
 between the spleen and the diaphragm. These adhesions extended 
 in places to the stomach. The appendix was negative. 
 
 The first portion of the jejunum for a distance of about 70 cm. 
 
 was dark purplish red, the mesentery thickened, purplish. The 
 upper and lower margins of the infarcted strip were rather sharply 
 marked off, the lower line of demarcation being less sharp than the 
 upper. The wall of the jejunum beyond the portion mentioned was 
 slightly reddened, but this soon faded out. 
 
 The large intestine was negative. At a point thirty cm. above 
 the ileocecal valve there was a band of adhesions extending from the 
 wall of the ileum to the posterior wall of the uterus. All told there 
 was considerable chronic peritonitis. 
 
 There was some chronic pleuritis. 
 
 The heart weighed 440 grams,—moderate hypertrophy. The 
 mitral, aortic, and tricuspid valves showed a moderate amount of 
 chronic fibrous endocarditis. The mitral circumference was 7 cm., 
 the aortic 6, the tricuspid 10.5. The coronaries were free and nega- 
 tive. The aorta was negative. 
 
 The spleen was quite large, 1030 grams, but all it showed was 
 some increase in the interstitial connective tissue. There was 
 chronic perihepatitis and perisplenitis. 
 
¥ 
 
 = 
 
 180 FACTS ON THE HEART 
 
 In the region of the jejunum infarction the walls yielded a purplish 
 red fluid, the mucosa was swollen, dark purplish, and the intestine 
 contained considerable thin purplish bloody fluid. The splenic and 
 the inferior mesenteric veins were negative. In the superior mesen- 
 teric vein there was an obturating thrombus. ; 
 
 Dr. Younc: Have you any idea where this thrombus came from? 
 
 Dr. RICHARDSON: That is the reason why Dr. Scudder’s note is 
 recorded. There was no definite source in the body, but if there was 
 a twist there, that is a perfectly good source. 
 
 Fic. 27.—Infarction of the jejunum. (Photograph by Lewis S. Brown and Dr. Oscar 
 Richardson. ) 
 
 Dr. Capor: Could the cardiac lesion by slowing the circulation 
 be regarded as a cause of thrombosis in a vein as far off as this? 
 
 Dr. RicHArpDson: There does not seem to be quite enough stasis. 
 
 Dr. Casot: There was no passive congestion anywhere else? 
 The heart was doing its job? 
 
 Dr. RICHARDSON: Fairly well apparently. 
 
 Dr. Younc: Isn’t it true that there is generally some cardiac 
 lesion in most of these cases of mesenteric thrombus? | 
 
 Dr. RicHaRDsoNn: I cannot say definitely. I do not remember. 
 This thrombus was in the superior mesenteric vein. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS I8I 
 
 It happened that Mr. Brown took a very successful picture of this 
 case which is worth looking at and is much better than anything one 
 can say (Figs. 27 and 28). 
 
 A PuysiciAn: Is there anything to indicate the cause of the chronic 
 peritonitis ? 
 
 Dr. RicHarpson: Nothing definite. 
 
 A PuysiciANn: The tubes and uterus were normal? 
 
 Fic. 28.—Infarction of the jejunum. (Photograph by Lewis S. Brown and Dr. Oscar 
 Richardson. ) 
 
 Dr. RIcHARDSON: Yes. 
 
 Dr. Casot: How do you account for the blood in the stomach? 
 
 Dr. Younc: It was acute congestion, wasn’t it? 
 
 Dr. RicHarpson: At the time of necropsy the stomach con- 
 tained much undigested food material but was otherwise negative. 
 There was bloody fluid in the first portion of the small intestine. 
 
 Necropsy 3566 
 
 An Irish housemaid of thirty-two entered February 1 for the 
 relief of pain and distress in the left chest. Her father died of heart 
 disease. She had always been healthy. She normally urinated 
 twice at night. The summer before admission she weighed 150 
 
T82 FACTS ON THE HEART 
 
 pounds, her best weight. She now weighed 113. She drank five 
 quarts of water and a quart of milk a day. 
 
 For two months she had had night sweats. A month before 
 
 admission she had moderate epigastric pain, relieved after a week 
 
 5 of treatment for dyspepsia. After a few 
 
 days she had sharp shooting pains in the 
 
 arms, legs, and feet. A few days later her 
 
 legs began to swell and her appetite to 
 
 15 10.5 grow poor. January 29 she began to have 
 
 Fic. 29.—Dimensions by | Severe continuous pain in the cardiac region, 
 
 Sec aetrgs not affected by eating or change of position. 
 
 A previously slight dyspnea became worse. She had palpitation on 
 
 strong exertion. 
 
 Fic. 30.—Seven-foot plate of hypertrophied and dilated heart with mitral, aortic, 
 and tricuspid stenosis. 
 
 Examination showed a well nourished woman. The apex impulse 
 of the heart was in the fifth space. The dimensions by percussion 
 are shown in Fig. 29, the measurements by X-ray in Fig. 30. There | 
 was a slight thrill over the apex, whether systolic or diastolic is not. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 183 
 
 recorded; possibly also over the second right intercostal space. The 
 action was regular, rapid. The sounds were of good quality. The 
 pulmonic second sound was accentuated. A blowing systolic mur- 
 
 Distant 
 
 tubular A few 
 
 breathing. coarse 
 
 No rales, rales, 
 FIG23T: 
 
 mur and a soft diastolic were heard over the aorta area, transmitted 
 to the neck; also at the apex, the systolic transmitted to the axilla. 
 The pulses were of fair volume, low tension, Corrigan in char- 
 
 Fic. 32.—Same case showing apparently effusion at left base. Enlargement of 
 the heart, especially in the region of the pulmonary artery and the left auricle. 
 Pathological process at the left base, involving the pleura. ; 
 
 acter. The lung signs are shown in Fig. 31. The abdomen was 
 negative. There was slight edema of the ankles. The pupils and 
 reflexes were normal. 
 
184 FACTS ON THE HEART 
 
 The temperature was 97.5° to 103.5°, the pulse 80 to 120, the 
 respiration 20 to 38. The amount of urine was normal, the specific 
 gravity I.o1o to 1.024. There was a very little albumin at all of 
 eight examinations, rare granular casts at five, cellular at one. A 
 urine culture showed staphylococci; no streptococci. The renal 
 function was 55%. The hemoglobin was 75 to 60%. There were 
 13,200 to 34,700 leucocytes, 81% polynuclears, 3,954,000 to 3,112,000 
 reds, slight achromia, irregularity in sizeand shape. Blood cultures 
 February 2 and 24 showed no growth, February 15 showed doubtful 
 bacilli, February 7 and March 15 streptococci. “Two Wassermanns 
 were negative. A stool was negative. X-rays of the roots of the 
 teeth showed a pus pocket and absorption. The chest showed opac- 
 ity at the left base as high as the fourth ribin front. The diaphragm 
 could not be made out on this side. (See Fig. 32.) The heart was 
 a little displaced to the right. 
 
 February 6 the patient suddenly lost power over her left arm 
 could not speak clearly, had a left facial paresis and loss of the pharyn- 
 geal reflex. The uvula was pulled to the left. The tongue could 
 not be protruded. The speech grew somewhat clearer; otherwise the 
 condition did not improve. February. 11 there was musical mur- 
 mur in the aortic area. She grew increasingly pale. March 14 
 she began to complain bitterly of ‘‘feeling sick all over,’ with pain 
 especially in the abdomen. ‘That night she quietly died. 
 
 Clinical Diagnosis (from Hospital Record).—Mitral stenosis and 
 regurgitation. 
 
 Ulcerative endocarditis. 
 
 Septicemia, streptococcus. 
 
 Cerebral embolus. 
 
 Mesenteric infarcts? 
 
 Dr. Richard C. Cabot’s Diagnosis—Streptococcus endocarditis, 
 acute; also chronic, endocarditis with deformity of the aortic valve, 
 stenosis and regurgitation. 
 
 Perhaps some lesion at the mitral valve. 
 
 Septicemia, streptococcus. 
 
 Serofibrinous pleuritis. 
 
 Embolic hemiplegia. 
 
 Anatomical Diagnosis——Chronic and acute endocarditis of the 
 mitral and aortic valves. 
 
 Chronic endocarditis of the tricuspid valve. 
 
 Hypertrophy and dilatation of the heart. (Weight 375 gm. 
 Right ventricle 3-4 mm. Left ro mm. in thickness.) 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 185 
 
 Chronic passive congestion, general. 
 
 Purulent infarct of the spleen. (Weight 600 gm.) 
 
 Infarcts of the kidneys. 
 
 Acute glomerulo-nephritis. 
 
 Slight fatty metamorphosis of the liver. 
 
 Chronic pleuritis, bilateral. 
 
 Focus of obsolete tuberculosis, upper lobe, right lung. 
 
 Obsolete tuberculosis of a mesenteric lymphatic gland. 
 
 The head was not examined. 
 
 The circumference of the mitral valve was 8.5 cm. (normally 10), 
 of the aortic valve 7 cm. (normally 7), of the tricuspid valve 9 cm. 
 (normally 11), of the pulmonary valve 8.5 cm. (normally 7). 
 
 The aortic and mitral orifices were so much obstructed by masses 
 of acute vegetative endocarditis that it was hard to make a definite 
 statement as to permanent deformities. 
 
 The absence of fluid in the left chest post mortem is explainable by 
 the difference in date between the X-ray and the necropsy. Possi- 
 bly the shadow was due in part to the big spleen. 
 
 A streptococcus (probably the s. viridans) was cultivated from 
 the spleen. Yet curiously enough cultures from the heart’s blood 
 were sterile. 
 
 It is notable though not at all unprecedented that the renal func- 
 tion remained good despite the existence of an acute glomerulonephri- 
 tis wholly unsuspected during life: 
 
 Necropsy 3596 
 
 A widowed American waitress of thirty-four entered April 22 
 for relief of palpitation. One sister died at thirty of hemorrhage in 
 the brain. The patient’s husband died of tuberculosis, one child of 
 tuberculous meningitis six months later. 
 
 She had children’s diseases and St. Vitus’ dance in childhood. 
 She had one miscarriage. At twenty-five she was told she had heart 
 trouble and was advised to rest in the country. She felt perfectly 
 well until the present illness, except for occasional slight dyspnea on 
 exertion for a year. She drank a bottle of porter every night before 
 going to bed. She urinated three or four times by day, two or three 
 times at night. Her catamenia was regular except for four months, a 
 year before admission, when it occurred every two weeks. Her best 
 weight was 121 pounds, her weight a year ago 118. She worked asa 
 Waitress, not hard. 
 
186 FACTS ON THE HEART 
 
 A month before admission she became nervous and was unable 
 to sleep. She worried about family affairs, which came to a crisis 
 a week before admission. Six days ago she felt weak, but worked 
 until eleven at night. While walking home she suddenly felt a sense 
 of constriction around the throat, ‘electric pains” in the arms, and rapid 
 and violent thumping of the heart. Half an hour later she began to 
 vomit, and continued to do so all night and the next day. The pal- 
 pitation had been less and the pains had disappeared. She had 
 developed a dry cough. 
 
 Examination showed a well nourished woman with slightly prom- 
 inent eyes. The tonsils were ragged. There was possible slight 
 
 Fic. 33.—Seven-foot plate of hypertrophied and dilated heart in stenosis of the 
 mitral, aortic, and tricuspid, with chronic adhesive pericarditis and auricular flutter. 
 Enlargement of the right side of the heart. 
 
 fullness of the thyroid. The apex impulse of the heart was in the fifth 
 space 10 cm. to the left of midsternum. The right border of dullness 
 was 5 cm. to the right. X-ray showed the measurements as in Fig. 
 33. There was a possible thrill at the apex. The action was regular, 
 very rapid. Electrocardiogram however showed auricular flutter.. 
 The first sound at the apex was very loud. The pulmonic second 
 sound was accentuated. There was a harsh systolic murmur at the 
 apex transmitted upward and to the left and a possible diastolic to 
 the right of the apex. The liver dullness extended from the fifth 
 space to two cm. below the costal margin. The edge was felt 5 cm. 
 below the costal margin. The lungs, extremities, pupils and reflexes 
 were normal. There was no tremor. 
 
 The temperature, pulse, blood pressure and apex beat are shown 
 in Fig. 34. The respirations were 22 to 44. The amount of urine 
 
 } 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 187 
 
 was 10 to 35 ounces, the specific gravity 1.018 to 1.008. There was 
 the slightest possible trace of albumin at one of three examinations. 
 Occasional red blood corpuscles were seen once. The renal function 
 was 20%. The hemoglobin was 75%. There were 13,400 to g600 
 leucocytes, 73% polynuclears. The reds showed moderate varia- 
 
 “mz1llTTITIT TTI 
 ETUC P53 a a ba 
 lSxemosalssb dst do beady lo 
 ies (aepsecheetel se halasle l(t cl 
 
 ll 200 99° N [aN abel 
 Hoo} | oof RAE hE ht ThA oh ANE - 
 Heol loft ttt Wi MT TY 
 
 “sie bd eg ea 0 
 yl eet Wie EC 
 peal op CE TTT 
 hel la 
 
 fc fo EE 
 
 mae 
 90 6 
 
 feo | eof LE ITT a 
 0 
 og SO 
 SAS SR ee 
 Pee letaclar bale [ela lie lec} 
 
 x-—-— xX = apex beat, 
 
 Fic. 34. 
 
 tion in size and shape, many polychromatophilic cells, rare stippling. 
 A Wassermann was negative. The stools were negative to guaiac 
 at three examinations. The sputum showed no tubercle bacilli 
 
 _ at two tests. X-ray (Fig. 35) showed the right chest less radiant 
 _ than the left, especially at the apex; considerable thickening of the 
 
 lung roots, especially on the right and running toward the apex; 
 
 _ glands at both roots, some of them calcified; the heart enlarged to 
 
 the right and left. 
 
188 FACTS ON THE HEART 
 
 April 26 the patient was nauseated, vomited, and her pulse dropped 
 105 points (180 to 75) and became irregular. Electrocardiogram 
 showed auricular fibrillation. Digifolin was omitted. April 29 the 
 visiting physician heard a loud, very harsh systolic murmur at the 
 aortic area, and wrote, ‘‘I believe a diastolic is present different from 
 the one at the apex. This I believe originates at the aortic valve.” 
 May 1 digifolin was given again. By May 3 she was responding well 
 to it. The pulse was still irregular. At midnight she was given an 
 
 Fic. 35.—Hypertrophied and dilated heart in stenosis of the mitral, aortic and tricus- 
 
 pid, with chronic adhesive pericarditis and auricular flutter. Heart enlarged to right 
 and left. Findings not definite on tuberculosis; rather more like passive congestion. 
 
 enema, and felt very well. She sat up to have a sheet changed, and 
 was very comfortable and laughing when she suddenly fell over in a 
 convulsion, more marked on the left side, and died. 
 
 Clinical Diagnosis (from Hospital Record)—Cardiac flutter. 
 
 Auricular fibrillation? 
 
 Mitral stenosis? 
 
 Cerebral embolism and infarct of the lung? 
 
 Dr. Richard C. Cabot’s Diagnosis —Goiter heart (to be shown 
 post-mortem by hypertrophy and dilatation). 
 
 i 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 189 
 
 Possibly a lesion at the aortic, stenosis and regurgitation, though 
 on the whole I vote against it. 
 
 Healed tuberculosis of the right lung. 
 
 Anatomical Diagnosis.—Chronic endocarditis of the mitral, aortic 
 and tricuspid valves, (stenosis). 
 
 Chronic adhesive pericarditis. 
 
 Thrombus in the left auricular appendix. 
 
 Thrombus in the right auricular appendix? 
 
 Hypertrophy and dilatation of the heart. 
 
 Pulmonary embolism. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, right. — 
 
 Slight hydropericardium. 
 
 Slight ascites. 
 
 Slight arteriosclerosis of the aorta. 
 
 Slight chronic pleuritis, left. 
 
 Small portion of persistent thymus gland. 
 
 Slight chronic salpingitis. 
 
 _ Dr. Ricuarpson: The heart weighed 466 grams,—considerably 
 enlarged. (Normal weight 200 to 300 grams.) The myocardium 
 of the right ventricle was thick, of the left about normal. The cavi- 
 ties were considerably dilated. The circumference of the mitral 
 valve was 6 cm. (normal 10). The aortic ring was 5 cm. (normal 7). 
 
 Death was from pulmonary embolism. 
 
 The thyroid was not obviously enlarged. This, however, is 
 perfectly compatible with thyrotoxicosis. Moreover, persistent 
 thymus (which we found) goes very often with thyrotoxicosis. 
 
 Dr. Cazor: I believe this patient had two things, chronic endo- 
 carditis and thyrotoxicosis. A pulse of 180 without arrhythmia is 
 very rarely seen except in thyrotoxicosis. 
 
 A Puysicran: She had had heart trouble nine years. Had she 
 had thyrotoxicosis nine years? 
 
 Dr. Casot: No. She had had the valve lesion nine years. 
 
 Necropsy 2556 
 
 An English housewife of twenty-eight was referred February 28 
 | from the Out-Patient Department, where urine examination showed 
 many red blood corpuscles. Her father died of “‘shock”’ at fifty- 
 eight. At twenty-one she had “rheumatism.” At twenty-seven 
 she was ill in bed a week with “‘inflammation of the stomach.” 
 
Igo FACTS ON THE HEART 
 
 For three years she had had dyspnea and palpitation. For two 
 years she had had almost continuous sharp pain a little to the left of 
 the navel, increased by exertion, especially by walking, which caused 
 nausea and vomiting. A hot drink usually started or aggravated the 
 pain. It was the same day or night. For two weeks it had been so 
 severe that she had vomited two or three times a day. She had pain 
 between her shoulders most of the time. Her appetite and sleep 
 were poor. She had a heavy feeling when she lay down. Her best 
 weight was 95 pounds, her weight two years before admission go 
 pounds, her weight February 27, 87 pounds. 
 
 Examination showed a fairly well developed and nourished 
 woman with slightly pale skin and mucosae. The apex impulse of 
 the heart was felt in the third space 1514 cm. from midsternum, 4 cm. 
 outside the nipple line. The right border was 3! cm. from midster- 
 num. A soft blowing systolic murmur was heard all over the pre- 
 cordia. The pulmonic second sound was greatly accentuated, very 
 loud and snapping. The pulses were normal. The blood pressure is 
 not recorded. The lungs were negative. The abdomen was held 
 a little rigid. The point of greatest tenderness was an inch to the 
 left of the umbilicus and a little below it, shading off from this point 
 in all directions. The right pupil was greater than the left. Their 
 reactions and the other reflexes were normal. 
 
 The temperature was 97.4° to 101.8°, the pulse 81 to 139, the 
 respirations 24 to 33. The urine was normal in amount, dark green 
 and alkaline at one of seven examinations (bile present), cloudy at 
 two. The specific gravity was 1.017 to 1.026. There was the slight- 
 est possible trace to a slight trace of albumin at all examinations, 
 rare hyalin casts at three, red blood corpuscles at one, rare leucocytes 
 at two. Culture from a catheter specimen showed one colony of 
 staphylococcus albus. The hemoglobin was 85% the leucocyte 
 count 13,000 to 36,000. A blood culture was negative. Skin tuber- 
 culin test negative. The stool showed a slight amount of admixed 
 blood. Cystoscopy showed a normal bladder, no obvious bleeding 
 from either kidney, the functional activity of both kidneys equal 
 and normal (indigo-carmine). ‘“‘If she has noticeable hematuria I 
 should like to see her during an attack.”’ 
 
 March 3 the visiting physician heard a presystolic murmur 
 before some beats and found at least half the right kidney palpable 
 but not obviously enlarged or tender. By X-ray it appeared 
 enlarged, but the plate was not conclusive.» March 6 the double 
 murmur was clear. March 8 the patient rapidly grew blue, the pulse 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS I9QI 
 
 became rapid and poor, the respiration labored. Early the next 
 morning she suddenly died. 
 
 Bacteriological Report-—Three guinea pigs inoculated with cathe- 
 ter specimens of urine, two from the right kidney, one from the left, 
 were all negative at necropsy. 
 
 Clinical Diagnosis (from Hospital Record) —Malignant endo- 
 carditis. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 mitral valve, with stenosis and regurgitation. 
 
 Acute endocarditis of the mitral valve. 
 
 Infarcts in the kidneys and spleen? 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral valve. 
 Stenosis. 
 
 Chronic and. verrucose endocarditis of the tricuspid valve. 
 Stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hemorrhagic infarcts of the lower lobe of the right lung. 
 
 Slight chronic pleuritis, left. 
 
 Focus of obsolete tuberculosis, upper lobe of left lung. 
 
 Dr. RicHarDson: This was a case of disease of the heart valves. 
 The kidneys were negative. Nothing was found to give any anatom- 
 ical basis for the pain mentioned below the diaphragm. But the 
 incision was restricted to the thoracic wall, and the organs were 
 examined in situ. 
 
 Dr. Capot: Here I think the PERSO, is ata loss. He did 
 not find the thing that was there. 
 
 A PuysictiAn: How do you account for the cardiac impulse in 
 the third space? 
 
 Dr. RICHARDSON: The hypertrophy of the heart in this case was 
 
 on the right side. It was behind an obstructed mitral, and the other 
 — lesion was on the tricuspid; that is, all the lesions were on the right 
 side. The work was consequently thrown on the myocardium of 
 the right side of the heart. In mitral stenosis we do not get hyper- 
 trophy and dilatation of the left side of the heart. An added load 
 in this case was the lesion on the tricuspid valve. The valve meas- 
 ured about 7 cm., about one-half its normal circumference. In 
 addition to the chronic endocarditis it showed also some verrucose 
 endocarditis which possibly was acute. The mitral would not admit 
 the tip of the little finger. That threw the whole load on the right 
 side of the heart and gave a wide heart. I did not notice at the 
 
Ig2 FACTS ON THE HEART 
 
 time that the apex was as high as the third interspace. It shows 
 that in making necropsies many points that seem insignificant are of 
 value. Of course I did not know at the time that they called it in 
 the third interspace, and there was nothing to attract my attention ~ 
 to it. {do not think it was as high as that. 
 
 A PuysictAn: Was a blood culture taken? 
 
 Dr. RicHarpson: Yes. It was negative. Septicemia is not 
 always positive by culture. 
 
 A Puysictan: Would that be the same reflex pain that we get in 
 a child from pneumonia giving symptoms in the abdomen? 
 
 Dr. Casot: I do not think so. It persisted two years. We 
 have to leave as a mystery that pain which we worked so hard over. 
 That does not surprise me. We have many cases in which the post- 
 mortem does not supply us with the information we seek. 
 
 A PuysictAn: Was that the patient’s word for the pain, or was it 
 the observation of the man who had charge of the case? 
 
 Dr. Cazsor: I should judge it was the patient’s word. 
 
 A PuysictAn: There is quite a difference sometimes. 
 
 Dr. Casort: You are right. But they did notice tenderness in 
 the place the patient complained of. It certainly sounded as if 
 there had been something there. 
 
 A PuysicrAn: She had a pleurisy. 
 
 Dr. Capsor: Yes, but it is just a chronic adhesion which we find 
 in about half of all our cases, without pain. 
 
 Necropsy 3982 
 
 An American housewife of forty-eight entered August 18, 1919. 
 A grandmother died of gastric carcinoma. The patient considered 
 that she had always been strong and well. From the age of ten to 
 fifteen she had chorea. She had the minor diseases of childhood, 
 scarlet fever, and diphtheria. For twenty-five years she had had 
 hemorrhoids, which in 1902 began an intermittent bleeding, stopping 
 in 1909. At thirty-four she had bronchopneumonia. For ten 
 years she had had occasional sharp grinding precordial pain, better 
 of late, referred to the abdomen or axilla, once in 1907 to the shoulder, 
 when it nearly took her breath away. Her bowels had always been 
 more or less constipated. She passed the menopause at forty-five. 
 That year she weighed 155 pounds, her best weight. Her usual 
 weight was 135, her present weight 125. She thought she had lost 
 25 or 30 pounds during the past year. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 193 
 
 For eight months she had had intermittent smarting, burning and 
 itching of the rectum several times a day, not growing worse, but 
 severe enough to interfere with sleep. There had never been severe 
 pain. Since January she had taken cathartics which had made her 
 bowel movements loose. She thought she had lost flesh, color, and 
 strength. At entrance she was very weak. 
 
 Examination showed a fairly well nourished woman with slightly 
 cyanotic skin and mucous membranes. The sclerae were slightly 
 injected. There was right structural scoliosis with slight left lumbar 
 compensating scoliosis and much deformity of the thorax,—promi- 
 nence of the left chest, the right back, and the left thorax in the 
 midaxillary line. Expansion of the right chest was greater than of 
 the left. There was slight dullness and bronchovesicular breathing 
 at the apex of the left lung. The apex impulse of the heart is not 
 recorded. The borders of percussion dullness were 8.5 cm. to the 
 right, 4.5 cm. to the left, the supracardiac dullness 5.5. The action 
 was irregular. The pulmonic second sound was markedly accen- 
 tuated. There was a presystolic roll and an apical thrill. The 
 systolic blood pressure was 120, the diastolic 70. The abdomen was 
 somewhat protuberant. The liver edge was 4 cm. below the costal 
 margin. The pelvic examination showed good perineal support. On 
 bearing down the patient began to urinate. She said there was no 
 incontinence. The cervix was bilaterally torn. It was bound down 
 to the posterior cul-de-sac. The fundus was apparently also bound 
 down posteriorly. Rectal examination showed a hard, irregular 
 mass, not tender, completely encircling the rectum, more prominent 
 on the left, extending to the internal sphincter. The fingers 
 showed questionable slight clubbing. The right pupil was greater 
 than the left; otherwise both were normal. The reflexes were 
 hyperactive. 
 
 Before operation the chart was not remarkable, the amount of 
 urine not recorded, the specific gravity 1.014 to 1.022; the blood is 
 not recorded. A Wassermann was negative. The stools showed 
 blood and pus and a positive guaiac. 
 
 The patient complained of pain in the anus. August 27 operation 
 was done. After the peritoneum was opened palpation revealed 
 an irregular mass in the neighborhood of the left anterior brim of 
 the pelvis. The liver was studded with carcinomatous nodules. 
 The sigmoid was brought into the wound and the mesentery sepa- 
 rated from it widely enough to permit the passage of a glass rod over 
 
 which the sigmoid was sutured to the peritoneum and the fascia. 
 13 
 
194 FACTS ON THE HEART 
 
 The loop was not opened. The pathological report on small pieces 
 from the rectum was “‘carcinoma.” 
 
 The patient made a good recovery from anesthesia. August 29 
 the wound was opened and found in good condition. ‘The chart 
 was flat. August 31 she complained of pain in the right side, anda 
 short time later had a rather severe chill. The pulse was 136, the 
 respirations 36, the temperature 99°. Later she complained of pains 
 all over. There was some tenderness in the right flank. The tem- 
 perature continued to range from 99° to ror.9°, the pulse from 84 
 to 113. September 3 she was feeling much better, and the wound 
 was in good condition. September 9 she had been vomiting. Medi- 
 cal consultants advised stopping digitalis. The vomiting ceased, 
 the heart action was much better, and by September 12 the chart 
 was flat, yet for no discoverable cause the patient lost ground. 
 September 15 her heart action was very poor. That day she died. 
 
 Clinical Diagnosis (from Hospital Record)—Carcinoma of the 
 rectum and metastases. 
 
 Mitral stenosis. 
 
 Phlebitis. 
 
 Colostomy. 
 
 Dr. Hugh Cabot’s Diagnosis —Cancer of the rectum. 
 
 Acute peritonitis? or 
 
 Acute endocarditis? 
 
 Anatomical Diagnosis—Carcinoma of the rectum with metas- 
 tases in the retroperitoneal and bronchial lymph nodes and the liver. 
 
 Thrombosis of the inferior cava and iliac veins. | 
 
 Embolic thrombosis of branches of the pulmonary artery. 
 
 Infarcts of the lungs. 
 
 Chronic endocarditis of the mitral and tricuspid valves; stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Edema of the ankles and feet. 
 
 Hydropericardium. 
 
 Slight chronic passive congestion, general. 
 
 Operation wound, colostomy. 
 
 Scoliosis. 
 
 The heart weighed 335 grams. The mitral valve measured 4.5 
 cm., the aortic 7, the tricuspid 7, the pulmonary 8. 
 
 Necropsy 1533 
 
 An electrician of twenty-seven came to the Accident Room Nov- 
 ember 25. His mother died of a paralytic stroke. Except for an 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 195 
 
 attack of typhoid fever seven years before admission and for rheu- 
 matic fever confining him to bed for eight months he had been well. 
 He drank two or three glasses of beer daily and an occasional glass 
 of whiskey. He smoked thirty cigars, six boxes of cigarettes and 
 forty cents worth of plug tobacco weekly. His present illness began 
 four days before admission with sharp pain in the side, chill, and 
 
 cough, all of which had persisted, 
 with considerable fever. His anal PER Wh Wa a fh aoe Meee FT] 
 
 | Days of Month [R912 G27R6R7 p01 # [2 |9 |¥ [5 [ 6/7 | 
 appetite and sleep were poor. ee 
 Examination showed a well I]o| |o4-LLILILTI LI 
 
 : : na : eel 
 nourished man with pallor of the POE RIS belch Tek Noles 
 
 skinandmucousmembranes. The _ |} 240 y 
 
 apex impulse of the heart and the RASS aah wie 
 
 left border of dullness were in the | 2!2 vo VN ET 
 
 fifth space just outside the nipple 74 ES sa PA, ae os 
 aoe Pie Wola bielie tak bdo 
 
 line, 414 inches from midsternum. |}! | |” 
 
 TEMPERATURE 
 
 160 
 There was no enlargement to the Mele sates gat elec lal 
 Brees Nemsounds. ands action Oiia.| liste eer PT 
 lL The fi 4 Due ye ie hele tape pepe (cr 
 were normal. e first sound at || 5 me Pala ae 
 Es Ho J} 110 {1 LV of 
 
 the apex was markedly accen ee) 
 tuated, heard over the whole ff | | a fe FE 
 : Aah ah ba ea cod ad 222 A 
 
 precordia. A presystolic and a a 
 
 163-40; 
 
 systolic murmur were heard at the 
 mitral area, loudest at the apex, transmitted to the axilla. A soft 
 diastolic murmur was heard at the aortic area. The pulmonic second 
 sound was greater than the aortic. The pulses and arteries were 
 normal. The right upper chest in front and back showed dullness, 
 increased vocal and tactile fremitus and whispered voice; the front 
 showed also bronchial breathing. Attheright base behind weremany 
 fine moist rales. The abdomen showed slight general tenderness. 
 There was a nodule in the right epididymis. The knee-jerks were not 
 obtained. The other reflexes were normal. The temperature and 
 pulse were as shown in Fig. 36. The respirations were 28 to 45. The 
 urinary output was 65 to 85 ounces until the day before death, then it 
 felltonormal. The specific gravity was 1.020 to 1.032. There wasa 
 trace to a slight trace of albumin at two of three examinations and 
 a few to rare red blood corpuscles at two. The hemoglobin was 
 100%, the leucocytes 11,000 to 20,000. 
 
 November 29 the temperature had dropped to normal. Coarse 
 moist rales were heard over the right back and at the upper right 
 front. December 2 a diastolic murmur was heard best in the third 
 
196 FACTS ON THE HEART 
 
 left interspace, but also in the second right interspace. Fine moist 
 rales were heard all over the base of the right lung behind and at the 
 side. The patient complained of pain in the right shoulder joint 
 and of sharp pain in the splenic region. December 7 the diastolic 
 murmur had become very loud and could be heard all over the pre- 
 cordia. The heart sounds were very loud and snapping. ‘The pulse 
 at the wrist was of rather poor volume and tension. The patient had 
 failed rapidly during the past two days. That night the breathing 
 was somewhat harsh at the left apex and in the axilla. Vocal and 
 tactile fremitus were somewhat increased. The evening of Decem- 
 ber 8 he suddenly took a turn for the worse, sank rapidly, and in three 
 hours died. 
 
 Clinical Diagnosts—Croupous pneumonia. 
 
 Arthritis. 
 
 Mitral and aortic disease. 
 
 Acute endocarditis? 
 
 Dr. Maurice Fremont-Smith’s Diagnosis—Chronic and acute 
 endocarditis. 
 
 Multiple infarcts to the lungs, kidneys and spleen. 
 
 Possibly bronchial pneumonia. 
 
 Anatomical Diagnosis—Pneumococcus septicemia. 
 
 Lobar pneumonia. 
 
 Organizing pneumonia. 
 
 Chronic and acute endocarditis of the mitral, aortic, tricuspid 
 and pulmonary valves. 
 
 Hypertrophy and dilatation of the heart. 
 
 Infarcts of the spleen and kidneys. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 
 The lungs were voluminous. The pleura here and there was 
 coated with fibrinous exudate. Of course there was some passive 
 congestion in the lungs, and in addition in the upper half of each lung 
 areas of pneumonia which in portions resembled a pneumonia in the 
 stage of resolution and in places an organizing pneumonia,—that is, 
 an older combined with a more recent pneumonia. 
 
 The heart weighed 493 grams,—considerably hypertrophied—and 
 all of the valves, the mitral, aortic, tricuspid and pulmonary, showed 
 chronic endocarditis in the form of fibrous deforming thickening with 
 if anything decrease in their circumferences,* and on this basis what 
 is called here polypous endocarditis, that is, smaller and larger soft 
 
 * The mitral valve measured 8 cm., the aortic 7 cm., the tricuspid 8144 cm., the 
 pulmonary 7 cm. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS I197 
 
 frank masses of vegetations. That is an acute endocarditis on top 
 of an old. The organism is the pneumococcus all through. 
 
 A pneumococcus septicemia, and in the vegetations on the heart 
 valves many pneumococci. 
 
 The kidneys were not remarkable except for infarcts. There 
 was a hypertrophied spleen, in places soft, and with infarcts here and 
 there. 
 
 I could not make out any infarcts of the lungs, but of course with 
 a source for emboli as there was on the tricuspid valve there might 
 have been some small ones, but none were found. 
 
 Dr. FREMONT-SMITH: I think we have to assume that the pneu- 
 monia was primary, don’t we? 
 
 Dr. RIcHARDSON: Yes. 
 
 Dr. Casot: That is, you believe that the heart trouble came from 
 the pneumonia? 
 
 Dr. RICHARDSON: Yes, the acute trouble. 
 
 Dr. FREMONT-SMITH: Do we ever get a primary pneumococcus 
 septicemia without a pneumonia? 
 
 Dr. RICHARDSON: Yes. 
 
 Dr. G. C. CANER: Wouldn’t you expect a more sudden onset if 
 it were? There is a long history of smoking up to his admission. 
 
 Dr. Cazsot: Yes. That is a good point. People with acute 
 endocarditis do not smoke that way. Isn’t it true, on the other hand, 
 that these vegetations are bigger than those you ordinarily see in a 
 heart accompanying pneumonia? Aren’t the vegetations accom- 
 panying pneumonia generaily little ones? 
 
 Dr. RIcHARDSON: I don’t think one can make a definite statement 
 in regard to that. 
 
 Dr. FREMONT-SmITH: Is pulmonary infarct a common symptom 
 in subacute bacterial endocarditis? There is no reason why it 
 should not occur, but does it happen? 
 
 Dr. Casot: I do not remember it. Ido not believe it is common. 
 
 Necropsy 2213 
 
 An American housewife of thirty-five entered September 21. 
 She gave a history of measles in childhood, two miscarriages, malaria 
 at thirty, rheumatism at thirty-two,—soreness of the knees and ankles 
 without redness and swelling. She was in the habit of taking 
 whiskey about once a week. She passed the menopause eight 
 months before admission. In April, five months before admission, 
 
198 FACTS ON THE HEART 
 
 she was ill in bed six weeks with an attack like the present one. 
 After being up and about for two months she was laid up again for 
 six weeks. After this she was fairly comfortable until two weeks 
 before admission, when her feet began to swell, more at night, and she 
 began to have cough with very little sputum until the past few days. 
 The sputum was thick and yellow, once blood-tinged. She had much 
 dyspnea and palpitation and could not sleep at night because of 
 nervousness. 
 
 Examination showed a well nourished woman lying flat without 
 discomfort with very cyanotic and mottled skin, cyanotic lips, and 
 frequent dry cough. The apex impulse of the heart was seen and 
 felt in the fifth space in the anterior axillary line, 14 cm. to the left 
 of the midsternum, 614 cm. outside the nipple line, corresponding to 
 the left border of dullness. The right border of dullness was 514 cm. 
 to the right. The heart was fibrillating, the action rapid and very 
 irregular in force and rhythm. A systolic murmur was heard all 
 over the precordia and in the axilla, where it was musical. A 
 presystolic murmur was heard at the apex, loudest just inside the 
 nipple line, where a presystolic thrill was palpable. The pulmonic 
 second sound was slightly accentuated. The pulses were irregular, 
 only about a third of the beats reaching the wrist. The volume was 
 variable. The artery walls were normal. The systolic blood pres- 
 sure was 130. The lungs showed slight dullness below the lower 
 angles of the scapulae. The abdomen was rather prominent, with 
 diastasis of the recti and lineae albicantes. The liver dullness 
 extended from the sixth rib to 10 cm. below the costal margin, where 
 the edge was felt on a line with the umbilicus. The liver pulsated. 
 There was moderate edema of the legs and slight edema of the thighs. 
 The pupils and reflexes were normal. The temperature was 96.1° 
 at admission, afterwards normal, the pulse 60 to 81, the respirations 
 20 to 34. The urinary output was 5 to 15 ounces, the specific gravity 
 1.022. At the single examination there was a very slight trace of 
 albumin and the sediment showed rare red cells. The blood was 
 normal. 
 
 September 23 ascites was demonstrated which was not found 
 at entrance. The left border of cardiac dullness was two cm. 
 nearer the median line than at admission. The next day one 
 thousandth of a gram of strophanthin was given intravenously. 
 The heart action was much stronger and steadier for a few hours. 
 The next morning the heart showed alternating strong and weak 
 beats. Only the forcible beat could be felt at the wrist. One- 
 
ILLUSTRATIVE CASES. VARIOUS CONBINED VALVE LESIONS 199 
 
 ‘thousandth of a gram of strophanthin was given intravenously again 
 with transient good effect similar to that of the day before. Septem- 
 ber 26 one thousandth of a gram was given again. Ten minutes 
 after the injection the patient was in good condition. A few minutes 
 later she was very cyanotic, breathing heavily. Twenty-eight 
 minutes after the injection she died. 
 
 Clinical Diagnosis —Mitral stenosis and regurgitation. 
 
 _ Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Digitalis heart block (strophanthin). | 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis of the 
 mitral (and other valves?). 
 
 Mitral stenosis. 
 
 Chronic adhesive pericarditis. (?) | 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Infarcts. 
 
 Anatomical Diagnosis—Chronic endocarditis of the mitral, 
 aortic, tricuspid and pulmonary valves, stenosis. 
 
 Slight’ chronic adhesive pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Hydropericardium. 
 
 Hydrothorax. 
 
 Ascites. 
 
 Anasarca. 
 
 Chronic pleuritis. 
 
 Chronic perihepatitis and perisplenitis. 
 
 Slight arteriosclerosis. 
 
 Dr. RicHARDSON: We were not permitted to examine the head. 
 
 The abdomen was distended. ‘There was a great amount of fluid 
 in the peritoneal cavity. The extremities were swollen and pitted 
 easily—ascites and anasarca. The liver was-four fingers below the 
 costal border, not very far down. The diaphragm on the right was 
 at the fifth rib, on the left at the fifth interspace. Nevertheless the 
 pleural cavities contained a large amount of clear straw-colored fluid 
 
 —hydrothorax. There were the usual evidences of chronic pleuritis, 
 fibrous adhesions generally. 
 
 The trachea and bronchi showed a slightly reddened mucosa and 
 contained a moderate amount of brownish mucus material,—pas- 
 sive congestion. The lungs showed no areas of consolidation, no 
 
200 FACTS ON THE HEART 
 
 evidences of pneumonia, but general well-marked chronic passive 
 congestion. 
 
 The heart weighed 415 grams,—considerably enlarged for her. 
 The myocardium was twelve mm. on the left, 3 mm. on the 
 right. The heart muscle generally was thick. The cavities were 
 enlarged, the auricles more especiallyso. The mitral, aortic, tricuspid 
 and pulmonary valves all showed a definite chronic fibrous endocarditis. 
 In the case of the mitral there was a small mass of fibrocalcareous 
 material. The fibrosis appeared as irregular fibrous thickening of 
 the valves and shortening and thickening of the chordae tendineae 
 with consequent marked deformity of the valves and decrease of 
 their circumferences. The mitral circumference was six cm., the 
 aortic four cm., the tricuspid six cm., the pulmonary five and a quar- 
 ter cm. ‘Those are all decreased, most markedly so the mitral and 
 tricuspid. On this chronic endocarditis basis there were on all the 
 valves minute gray-red granulations which were firm. In one or two 
 places there was some questionable fibrinous material, but all told 
 not enough so that we could definitely state that there was an acute 
 endocarditis. Of course these minute granulations occurring on the 
 valves are very discouraging. If they are definitely firm and tough 
 they of course are at least subacute or chronic. But if they are soft 
 and fibrinous it is reasonable to assume that they are acute. It not 
 infrequently happens however that it is difficult to say, and so it has 
 been called “‘verrucose endocarditis.” The only thing we have to 
 go by is the question of consistence, the character of the material, 
 whether firm or soft, and its relation to the underlying fibrosis. At 
 the time this was not regarded as acute endocarditis. 
 
 The liver weighed 1047 grams. That was rather small. The 
 organ showed very well-marked chronic passive congestion, and 
 there were adhesions about it to the diaphragm. The spleen also 
 showed adhesions to the diaphragm. ‘That is, chronic perihepatitis 
 and perisplenitis, without much definite idea as to why. It may be 
 in association with the chronic passive congestion which was present 
 in each of these organs, as there was some increase histologically of 
 the interstitial tissue. 
 
 The gall-bladder and pancreas were negative. Thespleen weighed 
 155 grams. The tissue was dark red, firm, elastic, the follicles and 
 trabeculae visible,—a good example of chronic passive congestion. 
 
 The kidneys weighed 250 grams. The capsules stripped leaving 
 fairly smooth surfaces, negative cortex. The tissue generally showed 
 passive congestion. 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 201 
 
 The gastro-intestinal tract showed marked chronic passive 
 congestion. 
 
 Between the layers of the pericardium there were membranous 
 fibrous adhesions,—slight chronic adhesive pericarditis. 
 
 There was a slight amount of arteriosclerosis, mentioned because 
 this woman was said to be thirty-five years of age. 
 
 A typical picture of that condition which is of course rather rarely 
 found, all four valves of the heart affected. 
 
 Dr. Cazort: That is about as near as we are going to get for the 
 present. We can hit the mitral, we cannot the others. I am inter- 
 ested in the perisplenitis because she had had a very early arterio- 
 sclerosis and two miscarriages. I tend to think that perisplenitis 
 and perihepatitis may mean syphilis. 
 
 Necropsy 3252 
 
 An American teamster of fifty-one entered September 2 for relief 
 of dyspnea on exertion and edema. His wife had had two miscar- 
 riages. At thirty four he first had rheumatism. Three years later 
 he was ill four months with rheumatic fever. Since that time his 
 joints had troubled him in bad weather. He had gonorrhea at 
 forty-two. He occasionally urinated at night. Until three years 
 before admission he was a steady but not very heavy drinker. For 
 three years be had taken very little alcohol. A year ago he had 
 slight dyspnea on exertion and slight edema of the ankles, growing 
 worse until four months ago he gave up work. He had been in bed 
 on and off, and for three months had at intervals slept in a chair. 
 For two months he had had an occasional dull headache, some swell- 
 ing and stiffness of the wrists, and ‘dancing spells’? when his eyes 
 became blurred. Six weeks ago he had some cough and vomiting. 
 He had slight paroxysms of cough on exertion. Lately his legs had 
 been especially swollen and a little painful, and he had occasional 
 attacks of dyspnea without exertion. 
 
 Examination showed a well nourished man breathing rapidly. 
 His cerebration was slow and suggested toxemia. The skin and 
 mucosae were slightly cyanotic, with many dilated venules on the face. 
 The sclerae were slightly injected. There was arcus senilis. A few 
 hard cervical glands were felt. The apex impulse of the heart was 
 in the sixth space 16 cm. from midsternum and 6 cm. outside the 
 nipple line, coinciding with the left border of dullness. The right 
 border was 6cm. to the right of midsternum. ‘The action was regular, 
 
202 FACTS ON THE HEART 
 
 the sounds were of fair quality; the first and second sounds were 
 heard best at the left sternal margin. The aortic and the mitral 
 second were very faint. The pulmonic second sound was accentu- 
 ated but faint. There was a loud explosive systolic murmur at the 
 apex replacing the first sound, heard all over the precordia and trans- 
 mitted to the axilla, as was a loud blowing diastolic which was heard 
 best at the second and third spaces at the left sternal border and was 
 transmitted also to the neck. At the base, loudest at the second 
 right costal cartilage, was an early rough scraping systolic, without 
 thrill, transmitted to the neck. ° The pulse was an atypical Corrigan. 
 
 Diminished 
 breathing, 
 Slight dullness, 
 Coarse moist 
 rales, 
 
 Dullnsss, 
 diminished 
 respiration 
 and coarse 
 moist rales. 
 Voice 
 slightly 
 
 Liver dullness diminished, 
 
 Liver edge 
 
 Shifting dullness 
 
 ee? 
 
 Fre; *3°7; 
 
 The artery walls were bare:y palpable. The lung signs are shown in 
 Fig. 37. There was spasm and tenderness in the right upper quad- 
 rant and shifting dullness in both flanks. The liver dullness extended 
 from the fifth rib to two centimeters below the costal margin, where a 
 tender edge was felt. The lower abdominal wall, the chest wall, 
 and the sacrum were slightly edematous. There was diastasis of 
 the recti. . The penis and right scrotum showed marked edema. 
 There was a large right scrotal hernia, easily reducible. There was 
 marked edema and brawny induration of the legs and thighs. The 
 pupils were normal. The knee-jerks were sluggish, the plantars 
 normal. 
 
 For the first three days the temperature was 97.8°—100° and the 
 pulse 89-100; then the temperature usually 96°—-98.4° and the pulse 
 usually 80-92 until October 2. The later chart (Fig. 38) is shown. 
 The respirations were 15-40. The systolic blood pressure was 110, 
 the diastolic 65. The output of urine was 17-89 ounces, the specific 
 gravity 1.016-1.021. Albumin in small amounts was shown at three 
 
ILLUSTRATIVE CASES. VARIOUS COMBINED VALVE LESIONS 203 
 
 of six tests, red blood cells at three, leucocytes at two, granular casts 
 at one. The renal function was 45%. ‘The hemoglobin was 85%. 
 The leucocyte count 7109-16,000, polynuclears 88%. There was 
 achromia, some variation in size, rare 
 poikilocytosis. A Wassermann was 
 negative. 
 
 The patient was given two tablets of  [fessetenm b 
 digipuratum a day, reduced September 5 ZZ BRO 
 toone. September 3 the visiting physician 
 thought him toxic from alcohol. He heard sy 
 practically no heart sounds. September 9 
 diuretin gr. xv was given three times. 
 September 11 there was a systolic thrill in jlasol2 102° 
 the manubrial and aortic areas, and the_ |]220/ehor 
 first sound at the apex and the pulmonic — 
 second sound were audible. There was 
 increased diuresis coincident with the 
 addition of diuretin to digipuratum. Sep- flizo} | 96 
 tember 14 the former was omitted. Sep-_ {1604 95° 
 tember 16 the patient was much more _ |}!50} |'5 
 comfortable, the toxicity gone and the ti See eile 
 edema almost gone. A week later he was |f.05| |ioo po 
 
 having occasional short but very uncom- fhj0 
 
 fortable attacks of dyspnea, often fft00 tt 
 
 nocturnal. The heart sounds were of | 99} | 9 SAA 
 better quality, the pulse remarkably good ers Pay By 
 
 considering the general condition, the 
 edema entirely gone. 
 
 From this point he grew much worse. He became increasingly 
 delirious at night and stuporous during the day, with orthopnea and 
 weakening heart sounds. ' October 6 the respiration began to grow 
 rapid. The lungs showed a few rales at the bases, becoming many 
 October 7 and obscuring the breath sounds so that no changes in 
 breathing could be heard. ‘There was no definite dullness. October 
 8 the lungs were full of rales. No patch of pneumonia could be made 
 out. The patient was comatose, and died quietly that day. 
 
 Clinical Diagnosis (from Hospital Record) ——Mitral and aortic 
 endocarditis. 
 
 Broken compensation. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 aortic and mitral valves, with stenosis of both. 
 
 ae 
 bel 
 al 
 SI 
 
 Ss 
 a 
 ~ 
 
 200} | 99° 
 190} | 98° 
 
 ie BESS SBBes 
 
 PULSE 
 = 
 ba 
 = 
 
 Fic, 38. 
 
204. FACTS ON THE HEART 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Terminal infection, probably pneumococcus. 
 
 Anatomical Diagnosis —1. Origin of fatal illness. Chronic endo- 
 carditis of the aortic, mitral, tricuspid, and pulmonary valves, 
 (stenosis). 
 
 2. Secondary or terminal lesions. Hypertrophy and dilatation of 
 the heart. Chronic passive congestion. Very slight hydropericar- 
 dium, hydrothorax, ascites and anasarca. 
 
 3. Historical landmarks. Cholelithiasis. Slightly defective clos- 
 ure of the foramen ovale. Slight chronic interstitial hepatitis. 
 
 The heart weighed 795 grams. The mitral valve measured 5.5 
 cm. The aortic valve opening was triangular in shape, each arm of 
 the triangle measuring about 13 mm. inlength. The tricuspid valve 
 measured 11 cm., the pulmonary valve 6.5 cm. 
 
 APPENDIX 
 
 Fibrocalcareous Mass (Arteriosclerotic?) in the Mitral Valve—Three Cases 
 
 1. Necropsy 534 
 
 A man of fifty-five died of chronic nephritis associated with a 
 chronic adhesive pericarditis. He had had much pain in the left 
 side of his chest for a month and some dyspnea two days before his 
 death, but in general ran the course of a case of chronic nephritis. 
 There were no cardiac manifestations in life not easily accounted 
 for by the moderate cardiac hypertrophy associated with his chronic 
 glomerulonephritis. 
 
 Necropsy.—The mitral valve in this case showed in its substance 
 and projecting from its surface an irregular calcified mass the size of 
 a split pea. This was thought to be due to arteriosclerosis, as were 
 the similar masses in necropsies 3332 and 3999. 
 
 2. Necropsy 3332 
 
 Fibro-calcareous cylindrical mass in the region of the insertion 
 of the mitral valve. Marked arteriosclerosis in aorta and its great 
 branches, in the cerebral arteries, in the pulmonary artery and its 
 branches. Arteriosclerotic nephritis. Clinically the patient was a 
 woman of 60 with chronic nephritis, uremia and cerebral hemorrhage, 
 all of which was confirmed post-mortem. The examination of the 
 heart in life showed nothing characteristic of the heart lesions found 
 post-mortem. It was moderately enlarged, showed systolic murmurs 
 at the apex and base, and nothing else. 
 
AORTIC STENOSIS AND REGURGITATION 205 
 
 3. Necropsy 3999 
 
 An essentially similar condition, namely a fibro-calcareous column 
 about the size of the little finger at the base or insertion of one mitral 
 curtain. The valve curtain over it, though wrinkled to correspond 
 to the roughening of the fibro-calcareous material underneath, yet 
 was otherwise smooth. The mass was situated near the insertion 
 of the valve and did not appear to interfere with its function at all. 
 This patient, like the last, suffered primarily from arteriosclerosis with 
 hypertension (b.p. 235/120). She was a woman of 67 and was ill 
 only two days, dying of cerebellar hemorrhage. Aside from a cir- 
 rhotic liver and general arteriosclerosis there were no lesions of impor- 
 tance. In life there was a loud blowing systolic murmur at the apex 
 but nothing any more distinctive. The picture was one of hemiplegia, 
 coma, and death. 
 
 Comment.—These data are presented because of the question 
 which’ they suggest. Are the lesions arteriosclerotic? Do similar 
 but more extensive lesions ever interfere with the heart’s conduction 
 system or with the function of the valves? In these three cases appar- 
 ently the calcareous masses did no harm. 
 
 AORTIC STENOSIS AND REGURGITATION 
 
 The rheumatic lesions of the aortic valve associated with those of 
 the mitral and others valves have already been described in Chapter II. 
 I tried there to make clear that the difference between “‘pure mitral” 
 disease and mitral disease complicated by aortic was for practical 
 purposes very slight and that the differential diagnosis between the 
 two conditions was often difficult. I showed that in relation to age, 
 sex, rheumatic, and choreic history the two groups (‘‘pure mitral” 
 and mitral plus aortic) were essentially the same, and that both 
 groups differed only in unessentials from the rarer cases in which the 
 disease had spread to the tricuspid or pulmonary valves. 
 
 But when we come to the cases of aortic disease not associated 
 with any other valve lesion—‘‘ pure aortic disease’’ as I shall fre- 
 quently call it—without any syphilitic aortitis, we face a problem 
 in etiology. 
 
 ETIOLOGY 
 
 The incidence of age and sex is in marked contrast with that of the 
 rheumatic lesions of the mitral and other valves. In the pure aortic 
 cases the males out-number the females by more than eight to one in 
 
206 FACTS ON THE HEART 
 
 this series. Out of 28 cases, 25 were male and only three female, 
 while it will be remembered that with the mitral group the females 
 were always definitely, sometimes markedly in excess. As to age the 
 contrast is also striking. In our 28 cases only six, or less than a 
 quarter were under the fortieth year when they came under observa- 
 -tion. As regards the time of onset, the data are not very clear, but 
 appear to be as follows: 
 
 TABLE 53 
 YEAR CaSES 
 
 Duration of disease from first complaints to death.............. 1 I 
 Duration of disease from first complaints to death.............. 2-3 3 
 Duration of disease from first complaints to death.............. 4 4 
 Duration of disease from first complaints to death.............. 5 3 
 Duration of disease from first complaints to death.............. 6 I 
 Duration of disease from first complaints to death.............. 8 I 
 Duration of disease from first complaints to death.............. I0 I 
 Duration of disease from first complaints to death............. Over to 2 
 Duration of disease from first complaints to death.............. Several I 
 Duration of disease from first complaints to death............. Doubtful 12 
 
 28 
 
 Average duration .% occu ka ck ay 
 
 TABLE 54.—AGE 
 
 BOs Saas eine coke ee kaha |e tae ce nee ee I 
 TOFIOG Ds pote rr aio ese cae ae 3 
 2OREY) Nive Phe Nod vba pave ste ee le ° 
 BOER O oak tae Udit karan ya eye anes Ch 2 
 BOTAD 2 od nels eee ae ees cose okt ey ne oleh eae 7 
 OSES fact We Loe Aer areata vt Siakg Cen 7 
 OOK00 std cle a Bc tees dow hk en 7 
 FORIO Ora Ws mito eves GLP Oy Unhinged I 
 
 28 
 
 In Table 54 it appears that half the cases were beyond the fiftieth 
 year when they first came under our notice, while eight out of twenty- 
 eight were beyond the sixtieth year, and only four were under thirty. 
 Such an incidence as regards age and sex, contrasting strongly as it 
 does with that of the recognized rheumatic cases, cannot help making 
 us suspect at once that these cases belong to a separate group, and 
 are very possibly of a different etiology. Yet the history of rheu- 
 matic fever, chorea, or tonsillitisis about as frequent in these cases as in 
 those which it is generally agreed to call rheumatic. Thus there was, 
 in this group of 28 cases, a clear history of rheumatic fever in fourteen, 
 two of which had also a history of tonsillitis and one of tonsillitis 
 and chorea as well. Beyond this there were also three cases with a 
 
ETIOLOGY 207 
 
 questionable history of rheumatism, two with a definite history 
 of chorea, and two with frequent attacks of tonsillitis; leaving only 
 seven cases or 14 without any known etiological clue. Comparing 
 these figures with those in the mitral group we see that the two are 
 practically the same. 
 
 If these cases are not rheumatic what are we to callthem? They 
 certainly show no evidence of being syphilitic. The usual presump- 
 tion has been that some or all of them are of arteriosclerotic origin. 
 In favor of this is the age and sex incidence already referred to, and 
 the association with definite arteriosclerosis in other parts of the 
 circulatory system, an association which is somewhat more frequent 
 than in the mitral series. Out of 28 cases sixteen showed an asso- 
 ciated arteriosclerosis, and only twelve were free from this. But 
 these twelve cases militate strongly against the general hypothesis of 
 an arteriosclerotic etiology for the whole group, unless one is to 
 assume that arteriosclerosis can be confined to the aortic valve, 
 which seems altogether improbable. In the cases associated with 
 arteriosclerosis of the aortic arch it is very natural to assume that 
 the process has extended on to the valves, as we remember that 
 syphilitic aortitis does. This is further supported by the fact that in 
 old people’s heart valves a certain amount of fibrous thickening and 
 stiffening is the rule. Why, therefore, should one not suppose that 
 in certain cases this is exaggerated into the rigid, calcareous ring of 
 aortic stenosis? 
 
 Against this it is to be said, in the first place, that we cannot 
 disregard the definite rheumatic types of aortic stenosis associated 
 with mitral stenosis in young people, which present on the valve a 
 pathology identical with that of the group now under discussion. 
 The same rigid, calcified ring, the same adherence and fusion of 
 adjacent cusps, are seen in this group and in the juvenile cases with- 
 out any possible suspicion of arteriosclerosis. Is it probable that two 
 diseases as diverse as the acute endocarditis of rheumatism and the 
 sclerosis of old age, produce identical results in the aortic valve? 
 Moreover, five of these cases of pure aortic disease are associated 
 with an acute aortic endocarditis such as we are very familiar with, 
 breaking out as what we believe to be a recurrence or recrudescence . 
 of the chronic endocarditis of rheumatism. Certainly arteriosclerosis 
 cannot cause this acute process. It is natural to suppose that the 
 acute process is a recrudescence or relapse, in this group as in the 
 mitral group,—in other words, to suppose it ‘an acute infection recur- 
 ring on the basis of a healed process of like type. 
 
208 FACTS ON THE HEART 
 
 If one adopts the rheumatic hypothesis in these cases one has to 
 leave largely unexplained the incidence in relation to age and sex. 
 But on the whole the age and sex seem to me less difficult of explana- 
 tion than the results of the opposite hypothesis of an arteriosclerotic 
 origin for some or all of these cases. It may well be (z) that the heart 
 and circulatory system accommodates itself more easily to be a pure 
 aortic lesion than to any of the other valve lesions or combinations 
 of such, that, (2) as a result of this the patients live on and have 
 time to acquire in other parts of their bodies the usual arterio- 
 sclerosis of elderly people. The sex difference remains still a mystery 
 unexplained. But we shall see in studying acute endocarditis and 
 also in the cases of chronic non-deforming endocarditis that the 
 aortic valve is more often hit in men andinold men. We may think 
 of its lesions as especially men’s not women’s. 
 
 On the whole it seems to me best to consider these cases as due to 
 a peculiar subtype of endocarditis belonging under the rheumatic 
 
 group. 
 PATHOLOGICAL ANATOMY 
 
 1. Enlargement of the Heart—In Table 55 are listed the heart 
 weights correlated with the valve circumferences and with the 
 clinical diagnoses as regards cardiac size. To the last of these points 
 I shall return later. But at a glance it is clear that one can find large, 
 middle-sized, or small hearts in association with aortic stenosis and 
 regurgitation, and that there is not much correlation between the 
 heart weight and the size of the slit left between the edges of the 
 stenosed valves. Thus the four hearts weighing 700 grams or more 
 were associated with an aortic valve circumference averaging 4.5 
 cm. Hearts weighing from 500 to 700 grams went along with aortic. 
 circumferences slightly larger, the average being 5.3 cm. But the 
 hearts weighing less than 500 grams were associated with valve 
 circumferences averaging slightly smaller than those of the group 
 just referred to. So that viewing the whole 28 cases I should say 
 that there seems to be very little connection between the size of the 
 heart and the size of the aortic orifice. 
 
 It is also particularly to be emphasized that decidedly small 
 hearts occurred in this series, for example, 278 grams, 305 grams, and 
 370 grams. On the other hand, one heart weighed 1000 grams, which 
 is among the largest of our whole series. There was nothing either 
 in the pathological anatomy or in the history of the cases to explain 
 these differences. 
 
PATHOLOGICAL ANATOMY 209 
 
 2. Type of Endocarditis.—In 23 cases the lesions were altogether 
 chronic and hard. In five these chronic lesions were associated with 
 an acute endocarditis. 
 
 3. Size of the Aortic A periure—Table 56 shows that in twenty-two 
 cases the aperture was obviously reduced by actual measurement, 
 many times very greatly reduced. On the other hand, one can 
 never conclude from normal or even increased valve circumferences 
 that stenosis is mot present, because a rigidity of the valves, holding 
 their margins into close approximation and immobility is quite 
 possible even though their circumference when they are dissected 
 apart is not diminished and even if it is increased. 
 
 TABLE 55.—CORRELATION OF CLINICAL MEASUREMENTS OF CARDIAC ENLARGEMENT 
 WITH POST-MORTEM DATA OF HEART WEIGHTS AND WITH AORTIC VALVE 
 MEASUREMENTS 
 
 Clinically et Aortic valve circum- | Mitral valve Tricuspid 
 Weight : : 
 enlarged ference cire; valve circ. 
 
 6.5) cia. : TAM SACI 
 8) eon. ; normal 
 5.5 cm. 4 ; ay 
 Ans cms ; : 13 
 “small’’ 
 ““small”’ ‘ ; II 
 Be Seok : : 12 
 Onscins : : P22 
 Sesitt 
 5.5 cm. ; } £35 
 
 “tip of little finger’’ : : 13. 
 yy Susies 4 é Es 
 serine Cm: I4. cm. 
 weyanks Uae ¢ normal normal 
 
 900 MWAH RW DH 
 
 HH 
 bOoH 
 
 I3 
 14 
 I5 
 16 
 17 
 18 
 
 Slightly + 
 Slightly + 
 
 Not enlarged 
 Not enlarged 
 Not enlarged 
 
 ‘slit admitting closed 
 blades of enterotone”’ 
 Qn 7 cn. 
 Average = 
 580 
 
210 FACTS ON THE HEART 
 
 TABLE 56.—AorRTIC VALVE APERTURES IN AORTIC STENOSIS 
 
 i 
 : 
 tr. 
 2% 
 3: 
 4. 
 ve 
 ce 
 6. 
 6. 
 6. 
 
 4. Infarcts—The lungs contained infarctions in three cases, the 
 liver in one, the kidney and spleen in one. This proportion of five 
 out of 28 cases is somewhat smaller than that observed in the mitral 
 group, as recorded in Table 42, page 69. 
 
 I have already mentioned the rather frequent association of 
 artertosclerosis, 1.e., in sixteen out of 28 cases. : 
 
 SYMPTOMS 
 
 In Table 57 is shown the order in which symptoms were noted. 
 There is nothing notable so far as I see about this showing or about 
 the general incidence of symptoms (Table 58). They are the symp- 
 toms of uncompensated heart disease in general, and differ from those 
 shown in the other groups considered in this book, only in that pre- 
 cordial pain and angina are somewhat more frequent than in the 
 other rheumatic types. This 1s what we should expect from the 
 greater average age of the patients in this group and from the pre- 
 ponderance of males. Obviously aortic stenosis when compensation 
 fails, shows itself by dyspnea, cough, and cyanosis, like any other type 
 of heart disease. It is somewhat notable, however, that palpitation 
 (auricular fibrillation?) was noted so infrequently in this group. 
 
 The incidence of hydrothorax (1 in 8) is also somewhat less than 
 in the mitral cases (1 in 2).. On the other hand cyanosis is fully 
 
SYMPTOMS ait 
 
 as prominent as in any other group. I think it is very doubtful if 
 anyone could guess, by symptoms alone, whether or not a given 
 case was likely to turn out aortic stenosis. Only the age and sex 
 would give one an inkling. 
 
 TABLE 57.—SYMPTOMS 
 
 Symptoms Ist sign 2d sign 3d sign 
 
 Dyspnea 
 Palpitation 
 Anginal pain* 
 Weakness 
 Dizziness 
 
 NY O NS H O HR HN 
 N’e-O  O. ©. 7° 0. © HH 
 OL ee OM Om yt Ou Ono 
 
 (of feet 1, legs 1, feet to chin 1, ? 1) 
 Ascites 
 
 *In 2 other cases angina appeared late in the course of the disease. 
 
 TABLE 58.—GENERAL INCIDENCE OF SYMPTOMS 
 
 Total showing edema 
 Of lower extremities 
 (Of these, in addition, anasarca 1, edema 
 of lids 1, of abd. wall 1) 
 No record of place 
 Total showing cough 
 (cough with sputum, 16 
 
 cough with blood, 8) 
 Cyanosis (slight 6, 1 lips only, 1 hands only) 
 Precordial pain (fairly clear angina 3) 
 Ascites (absent in 9, ? in 15) 
 Gastric symptoms 
 Hydrothorax (single 4, double 1) 
 Jaundice 
 
212 FACTS ON THE HEART 
 
 PHYSICAL SIGNS 
 
 TABLE 59.—NUTRITION 
 
 Well developed’and nourished ..... .)... 5 2 as ace 14 
 Well developed; obese) \. ac0.hih dan 1 ols eeu ae are ee I 
 Obese: ots Ya hed fey EF aaa os ooh e's A ewe atey nay Biv ee ei 2 
 Poorly developed-and nourished.) 3 45. cc ve oe 3 
 Fairly developed and nourished ~.:-.//...5... s, aes. cee oe ee 3 
 Well developed, poorly. nourished.) .2. | 302. oc. se I 
 Fairlydeveloped pemaciated. css te eee a to. wk wy ge I 
 Ipmacia ted ah a. mew esas PITS eRe Reo iy I 
 Not .tecotded 20 a5. Parca ok We cae Se oe 2 
 
 28 
 
 Table 59 lists the data as regards nutrition and development of 
 these patients, and calls for no special comment. 
 
 Fever.—Seventeen were afebrile and eleven febrile. Of these 
 eleven cases, two died of pneumonia and may naturally be thus 
 explained, one was associated with urinary sepsis, and one with acute 
 endocarditis. One of the remaining seven was associated with a 
 small auricular thrombus; in the other six fever is altogether 
 unexplained. 
 
 TABLE 60.—LEUCOCYTES 
 
 Under: 60004 te'So ee ot intone 2 sop yp ce eee I 
 6000—-QO00 ANCIUSIVEs.c% 0: wey wie! sued wins enact ee te teaie ack oe he eee 5 
 T0,000=15°600 SNClUSIVE Pas. esa sks co ess os ep a re 9 
 ADOVE'T 5, C0025. 5 THU Ga. i ALS toe ee see ee 8 
 No white count. 2). cwekoG 4 Se Bie ane ele ee cet oe 5 
 
 28 
 
 Leucocyte Count.—Table 60 shows the figures in 28 cases. Cor- 
 relating these with the febrile cases it appears that the highest counts 
 (34,000, 30,000, 24,000) accompanied high fever due to streptococcus 
 infection in all 3 cases. The more moderate counts were associated 
 with pneumonia. For one count of 16,000 (temp. 98°—100°) no 
 cause was found. 
 
 CLINICAL DIAGNOSIS OF CARDIAC ENLARGEMENT 
 
 Referring again to Table 55, it appears that most of the notably 
 enlarged hearts were recognized in life as greatly enlarged. On the 
 other hand the same diagnosis was made on one heart which weighed 
 
CLINICAL DIAGNOSIS OF CARDIAC ‘ENLARGEMENT 213 
 
 only 305 grams, and no note of enlargement is recorded in three 
 cases weighing respectively goo, 872,.and 682 grams. The note 
 “slightly enlarged”? occurs in the clinical record of cases which 
 showed after death a cardiac weight of 528 grams and 487 grams 
 respectively, and a definite note of “‘not enlarged”’ correlates rather 
 poorly in three cases with cardiac weights of 543, 490 and 370. In 
 general we got a fairly correct idea of the facts in twenty cases out of 
 28 cases, or about three-quarters. These facts are further shown 
 in Table 61. | 
 
 TABLE 61.—CARDIAC WEIGHTS IN 18 CASES OF AorTIC STENOSIS 
 
 18 cases showed “‘marked enlargement”’ clinically. 
 Of these, 1 weighed 305 grams (6 cm. aortic aperture) 
 4 weighed 400-500 grams 
 7 weighed 500-600 grams 
 2 weighed 600-700 grams 
 3 weighed 700-800 grams 
 o weighed 800-900 grams 
 1 weighed 1000 grams 
 
 18 
 
 2 showed slight enlargement clinically, weighing 487 
 and 528 grams respectively, with aortic apertures 
 2X 5 cm. and 1.5 X 2.3 cm. respectively. 
 
 8 not recorded as enlarged clinically weighed 
 the following: 
 
 278 grams 573 grams 
 370 grams 682 grams 
 490 grams 872 grams 
 543 grams goo grams 
 
 Cardiac Murmurs.—I think it fair to assume that in all these cases 
 there was some regurgitation of the blood stream as well as an 
 obstruction to its passage from the heart. Yet in twelve out of 28 
 cases no diastolic murmur or other evidence of aortic regurgitation 
 was obtained in life. The concomitart stenosis ordinarily prevents 
 the appearance of marked peripheral vascular phenomena such as 
 Corrigan and capillary pulse, and the pulse-pressures are not at all 
 significant for the reason just given. The sixteen cases in which a 
 diastolic murmur was looked for are listed in Table 62. It appears 
 that the diastolic was widely distributed as regards its place of appear- 
 ance and maximum intensity, as Is apt to be the case in all types of 
 aortic regurgitation. 
 
214 FACTS ON THE HEART 
 
 TABLE 62.—Dt1Astotic Murmurs IN AorTIC STENOSIS 
 
 hat otal 
 
 Present | Absent ey ft 
 
 DiastohGatiapexierer sa atc eae ee 
 2 at apex alone. 
 2 at apex and left sternal margin. 
 5 at apex and over whole precordia. 
 I at apex aortic area, and left sternal 
 margin. 
 
 1 at apex, aortic area, and pulmonary area. 
 1 at apex, aortic area and pulmonary area 
 and left axilla. 
 t at apex and left axilla. 
 Diastolic at pulmonic area alone.............. 
 Dilastoliciateortic al ea wlONCsee eee Ge ee 
 Diastolic:in lett-axilla’andtback. .see esc. oe 
 
 TABLE 63.—Systotic Murmurs 1n Aortic STENOSIS 
 
 Present | Absent Riss Total 
 recorded 
 
 DYStOUCIAL ADEs © saat glee Sah waren tae ae 
 4 at apex alone, except 1 in axilla. 
 7 at apex and over whole precordia. 
 
 4 at apex and pulmonic and aortic areas. 
 5 at apex alone and aortic area. 
 1 at apex and pulmonic area. 
 ro show extension to other places: 
 4 to axilla. 
 2 to neck, 1 to clavicle. 
 1 to axilla and back. 
 
 Systolic murmurs were present in 22 cases and absent or not 
 recorded in six. Their distribution and place of maximum intensity 
 is shown in Table 63. In most of these cases the murmur was loudest 
 at or near the orthodox aortic area, though four were very apt to 
 lead to error in diagnosis because of their presence solely at or to the 
 left of the cardiac apex instead of at the base of the heart. The 
 extension of these murmurs to the neck, axilla, or back seems to me 
 of no diagnostic or other significance, and merely means that in a 
 considerable number of cases there were notably Joud murmurs. 
 
CLINICAL DIAGNOSIS OF CARDIAC ENLARGEMENT 215 
 
 All loud murmurs are widely transmitted, whatever their place of 
 production. 
 
 Presystolic murmurs at or near the apex were noted as present 
 in six cases and absent in three. Knowing what I do of the routine 
 of examination pursued in these cases, I think it fair to assume that 
 such murmurs were absent in most of the unrecorded residuum of 
 cases. So that we may say with tolerable accuracy that the ‘‘ Austin 
 Flint murmur” was here present in six out of 28 cases. 
 
 Thrills.—Table 64 sums our results on this point. But I am 
 loath to believe that it represents the actual state of things in these 
 cases. Unless one is definitely looking for aortic stenosis I know that 
 we often fail to investigate the question of a thrill. So that I believe 
 it may well have been present in many of the seventeen unrecorded 
 cases. 
 
 TABLE 64.—THRILLS 
 
 PV BLOUCIALYDASE Ate Star sg, th eatntn ey ROR Wc de <. oy/ Ne des SOUR A? Rese 7 
 RIDES VRCO UG. te OB DOxe ners ys tons mac a Ns et cae GY Riku, eh aa Deeds I 
 Peron VeLGlucr dee PLMONIG areas? sarees Cts eal eee es la Seige I 
 Moca CAECS ipo) RSC RU anne RG er Ne a OOM EY yd Sane ere 2 
 BIE RPOCICLIOCC emt pen Sk at NN eine git ae 2 annie She ace 17 
 28 
 
 TABLE 65.—AORTIC 2ND SOUND 
 
 POPC TOG EOIN ANSCN La tne a oer en aat AIR ee Gre LP a eh 9 
 POLL Cw ei SOU CLNINISNe ote Sai uk che Mla Kaede ees ekg noon ds 2 
 PA GOLLICM tr SOUDCE NOLINAL grater cep all ete ela IA. nl way athe ire Bees I 
 Lelie A SOUNC aa Chel tdi ad hacties i a ear ee ci dsc NEE ky Bat a eta oles I 
 UR ERTOGOTLICC ARI NT otra Wiyiiel Praee re woe nly ace cleo eat ete en, Lae Laer & ts 
 
 28 
 
 Aortic Second Sound.—From Table 65 it would appear that the 
 aortic second sound was diminished or absent in only eleven of these 
 28 cases. In fact I believe more careful observation would have 
 shown it to be faint or absent in a considerable number of those in 
 which no record was made. It is worth noticing, however, that in 
 one case the aortic second sound is recorded as definitely accentuated, 
 a fact very difficult to reconcile with the known post-mortem findings, 
 that is, with rigid aortic cusps. In two cases not included in this 
 series I have faced this mystery before. So far as I see it definitely 
 attacks the theory ordinarily held by physiologists, that the aortic 
 second sound is due to the closure of the aortic valves and to this 
 cause alone. 
 
210 FACTS ON THE HEART 
 
 TABLE 66.—PULSE IN AORTIC STENOSIS 
 
 “Plateau” of “low volume and‘tension’’*).......).... 5+. + ae 6 
 isin pistol shot........ ey | 
 “Corrigan” j with capillary pulse..... Abo. lia Se eee 6 
 with bounding pulse.....1 
 Normal st 2-6 ae te eh eos Re er gee 10 
 NO TOCOLG wees cre tie hy Peele tee Serre kk et ete Re ere ae 6 
 
 Pulse.—The most notable fact about these pulse records as 
 factors in diagnosis is the absence of any sign of ‘‘Corrigan pulse”’ 
 in twenty-two out of 28 cases. This substantiates the usual belief 
 that when aortic stenosis is associated with aortic regurgitation, 
 as is the case in almost all non-syphilitic disease of this valve, the 
 ordinary arterial phenomena of aortic regurgitation are neutralized 
 or absent. On the other hand there are not many cases to sustain 
 the classical belief in the flat-topped or plateau pulse as a frequent 
 concomitant of aortic stenosis. We noticed it in only six out of 28 
 cases. 
 
 Blood Pressure.—The scanty observations available in our cases 
 are shown in Table 67, which is, however, of interest because it 
 proves that despite very considerable narrowing of the aortic valves, 
 as for example in Necropsy 3320, a high systolic and diastolic pressure 
 (presumably due to a complicating nephritis) may be present. In 
 the other cases with still higher systolic pressures (Necropsies 2919, 
 2629) the valve stenosis is not obvious from the measurement of its 
 circumference but was nevertheless stated to be considerable in the 
 post-mortem record. In Necropsy 3928 one notes a pulse pressure 
 of 86, which should correspond with a very tolerable degree of Corri- 
 gan pulse. 
 
 TABLE 67.—BLOOD PRESSURE IN AORTIC STENOSIS 
 
 Blood ; Arterio- Valve 
 pressure z sclerosis circumference 
 
 TOS (Ba Leah “4. Br Ace oh Ral ole a cee ee 
 
 210/? 
 
 -210/? 
 150/? 
 
 160/110 " ++ general 
 
CLINICAL DIAGNOSIS OF CARDIAC ENLARGEMENT 217 
 
 TABLE 68.—ARTERIAL WALLS IN AORTIC STENOSIS 
 
 MER ALAC tee, UN aa aes lene yale! tale aide Ga sly ate ite I 
 Smee as Ae. DIO. ANd CAICHTEOUS. oc ctoc Sp ph ca a ke be cab ee I 
 RES SLAXLU UCTS hire Lite Me etate rn aig hey Tee vnte'e soereid Gr ata tenis wa I 
 RPM G ECO EEUU S Gile AT..2-2 oh Gs) bas a eco Ge cab ln wls lca ns BAe ut 
 Pe CLLACEOPTUOUS ANG) CHICK, oh N5 06a). eais's Gamboa sike say Oh by «cle ak I 
 MO Leni ee ae MME es WB aig Sai atSs ada w wie oe hee 6 
 ME LL Se SOL RTT Mtn ee RA Se ail, Siigie als okie dos wulisdielu Gee ee eats I 
 SRI LIENALISE LOLS ee an bees, Shee Oe ne ete tcc 7 ete Nae velies 4-4 wh a ae I 
 ME DESEEERESTRINU LER et koe Ee I tint Age what Cres, Sie, fades Arete we sliehe 2 
 MME OL LOTT CONGILION tai fie ue timtlets sa BU. saya el tele cele ace Oe 13 
 
 28 
 
 Arterial Walls.—The condition of the artery walls as listed in 
 Table 68 shows about the amount of arterial thickening that one 
 would expect from the age of the patients and the amount of arterio- 
 sclerosis to be expected at that age. But it is decidedly in contrast 
 with the condition of the artery walls in mitral disease, pure or 
 complicated. 
 
 Evidences of Chronic Passive Congestion.—A good deal of the 
 stasis present in these cases appears in the items recorded in Table 58. 
 In Tables 69 and 70 we get some further corroboration of facts 
 obviously to be expected. 
 
 TABLE 69.—CONDITION OF THE LIVER IN AORTIC STENOSIS 
 
 Seeme cet ely DELO wi fiLsuig ey iuacls se he ree a lcci nie Wisteselh he spas Bee Rhee Ge We 17 
 REPEAT CRLC LE. ae AAP) See OES Gi wa elec e hcl. a. aha. ble dre wos ein a Scare 9 
 PERE eTTO LT RCOTOCU A font Fa otter es del uses wale sehe wale 2 
 
 TABLE 70.—CONDITION OF THE SPLEEN IN AORTIC STENOSIS 
 
 MERIAL CCU MMI ey Net teete te C iS eute Ce aka ot clae ak oe 2 
 NMED ie (1 Cees Br en er vig Me fev a, ots Shove ns te occ Paktom, 6 pes aes 8 
 REEIETIC AL CCOCCCC oe B ic itl PART oie sad ETE DR SK poets ehy fs biel ge 18 
 
 The Blood.—The condition of the leucocytes has already been 
 explained. ‘There was no notable abnormality about the red cells 
 in any of these cases. 
 
 Bacteriology.—Streptococci were found post-mortem in the blood 
 of five out of 28 cases, staphylococci in one, pneumococci in one, a 
 total of seven, or one-quarter of the cases. Four of these positive 
 blood cultures, all of them showing streptococci, were associated with 
 
 ‘the finding of acute endocarditis. I have already referred to these 
 
 facts as tending to show that arteriosclerosis can hardly explain all of 
 the facts in these cases. 
 
 Urine.—There is nothing worthy of note. Albumin was present ~ 
 in seventeen cases and absent in eleven. Fifteen showed casts. But 
 
218 FACTS ON THE HEART 
 
 there was nothing herein to distinguish the cases of nephritis pre- 
 sently to be referred to from those of simple passive congestion. 
 
 Complications.—Obsolete tuberculosis was present in four cases. 
 There was no case of active tuberculosis in this series. Chronic 
 pericarditis was found in one case, acute pericarditis in one, and 
 hyrdopericardium in four. Chronic pericarditis was also diag- 
 nosed during life in two other cases, in neither of which was the 
 diagnosis verified. The same is true of one of the clinical diag- 
 noses of pulmonary infarct. Nothing was found to correspond to 
 it post-mortem. 
 
 Nephritis was present in ten cases out of 28, a surprisingly large 
 proportion. It was of the arteriosclerotic type in four cases, of the 
 glomerular type in four, and suppurative in two. Of the glomerular 
 cases one was acute, two subacute, and one chronic. Some of the 
 high blood pressures are doubtless associated with these facts. 
 
 Jaundice was present in three cases without any adequate explana- 
 tion post-mortem. In one it was associated with high fever (104°) 
 and a leucocytosis of 30,000; in the others with passive congestion. 
 
 Angina pectoris. Three cases out of 28 suffered from pain 
 definitely of the anginoid type. In five others precordial pain was 
 distressing but did not possess the characteristics distinctive of angina. 
 Correlating these cases with the state of the coronary arteries and of 
 the aortic arch, we find that there is no definite anatomical basis for 
 the pain; in one case the patient was syphilitic (chronic interstitial 
 orchitis) but with no aortitis or coronary disease. 
 
 TABLE 71.—ESTIMATED DURATION 
 
 FVCAT sg oe eb en ae os a ee I 
 B= YOATS soa ey eked acg gees 9 hae ee Sete nee et ee ) 
 A VOATS org Mee oes BS cs Ve le deb bet rca gs Be 3 
 SeVOOrs. ey 34 SEN oo eM ceaciet cloh cages eee re 3 
 O Years 3. Fe.. ein Be egies Ohcois Dees ok ie I 
 Ss VeOaTts.< ook ie ee ye SERA SPs 5S a ee A, Gee ee I 
 LO VEArsi goss Soa ow Pee «olde woolen wht pauses toile Soci ee ee ee ee I 
 Over ro years dc his 5 5 ese UO hen ee ee 2 
 Several years! cn vel sere Se eve ves mad eine: o Wena eer emi age I 
 Doubtfulee ee onc. ier 29 ee, Gare oy ate oo eae ee 12 
 28 
 
 Estimated Duration of the Disease.—Table 71 lists the known 
 
 facts in our 28 cases. It is of interest, as evidence of the long dura- 
 
 tion of symptoms in some cases, though it is hard, even in the doubt- 
 ful cases, to picture the disease as having lasted ever since the age 
 when rheumatic infections usually occur. 
 
 ital 
 
SUMMARY AND CONCLUSIONS 219 
 
 Mode of Death.—Pneumonia was present in four cases post-mor- 
 tem, and pulmonary abscess in two. Death was notably sudden 
 and unexpected im six cases though no special explanation was found 
 for this posi=mortem. In one case the patient died in the hospital 
 corridor. As a rule, however, the death was preceded by the usual 
 symptoms of passive congestion and stasis. 
 
 Involvement of the Bundle of His.— Necropsy 3424 showed well 
 marked lesions in the interventricular septum including the bundle 
 of His. During life this patient suffered typical attacks of angina 
 pectoris but had nothing to suggest heart block. 
 
 SUMMARY AND CONCLUSIONS 
 
 1. As-in all types of aortic disease, the male sex strongly predomi- 
 nates, 25 out of 28 cases. 
 
 2. More than half the patients were beyond the fiftieth year when 
 they first came for treatment at the hospital. 
 
 3. [he cases appear to be of rheumatic origin, judging by the 
 history and the post-mortem findings. 
 
 4. The degree of cardiac enlargement is greater on the average 
 than that found with any single valve lesion except syphilitic aortitis 
 with aortic regurgitation. 
 
 5. The symptoms are like those of other types of uncompensated 
 valve lesions save that faintness, precordial pain and angina pectoris 
 are more frequent. 
 
 6. In twelve of twenty-eight cases no diastolic murmur was heard 
 in life though the valve lesions were such that some regurgitation 
 seemed inevitable. | 
 
 7. In six of twenty-eight cases a presystolic murmur (Austin 
 Flint type) was heard at the apex. 
 
 8. In twenty-two of twenty-eight cases a systolic murmur was 
 heard, though in four it was noted only at the apex. In eighteen it 
 was loudest at the base of the heart, but not always on the right side. 
 
 g. As to a thrill at the base of the heart, one of the crucial points 
 in the diagnosis of aortic stenosis, our records are defective in seven- 
 teen out of twenty-eight cases. In eight cases a basic thrill is 
 recorded. In two it is definitely stated to be absent. In another 
 only an apical presystolic thrill is mentioned. From these very 
 meagre data we may say that the characteristic thrill was present in 
 four-fifths of the cases in which a definite record was made. But the 
 cases are too few to have value. 
 
 to. Another vital point in the diagnosis of aortic stenosis is the 
 diminution or absence of the aortic second sound. Here again 
 
220 FACTS ON THE HEART 
 
 unfortunately our records are worthless in fifteen out of twenty-eight 
 cases. Out of thirteen cases with a definite record, nine showed 
 absence and two more showed diminution of the aortic second sound. 
 In one case it is noted as normal and in one accented,—a strange 
 phenomenon with a rigidly calcified aortic valve! 
 
 t1. The pulse is chiefly notable for the absence of any “ Corri- 
 gan” shape in sixteen out of twenty-two cases definitely recorded. 
 
 Since we must suppose that regurgitation as well as stenosis is 
 
 present in these cases, the absence of the collapsing pulse is a point 
 favoring the diagnosis of stenosis. 
 
 In six cases the classical flat-topped or plateau pulse-wave is 
 recorded. 
 
 On the other hand it is notable that a “‘Corrigan pulse” was 
 definitely recorded in six cases and was accompanied by a capillary 
 pulsation in four and by a “‘pistol-shot sound”’ over the brachial in 
 one. 
 
 Here we may conjecture that the regurgitation was more marked 
 than the stenosis, but the explanation is rather lame. 7 
 
 12. It is a notable fact that despite an aortic stenosis which 
 reduced the aortic opening to a mere slit (Necropsy 3320) a blood 
 pressure of 160/110 is recorded. It would seem that such a stenosis 
 would make it impossible for such a blood pressure to be maintained. 
 This case seems to prove the contrary. 
 
 13. Nephritis of some type was found at necropsy in ten out of 
 twenty-eight, a surprisingly large proportion. One case was “‘acute,”’ 
 two “‘subacute,”’ the rest chronic. , 
 
 14. Three patients suffered from angina pectoris. In one of 
 these, a negro of forty-nine, a chronic interstitial orchitis and 
 chronic perisplenitis were found, but no aortitis or coronary narrow- 
 ing. (The connection of angina with syphilis but not always with 
 syphilitic aortitis is noted in the chapter on Angina Pectoris.) “In 
 the other two cases there was no anatomical basis for the pain. 
 
 15. In only 1 case in the 28 was the aortic stenosis associated with 
 an old pericarditis. This is in marked contrast with all other valve 
 lesions of the rheumatic type, which frequently are associated with 
 chronic pericarditis, 23 in 198 or 1 in g—3 times as often as with aortic 
 stenosis. 
 
 16. The average duration of the disease is probably greater than 
 in any other valve lesion, as the age at death is greater and the 
 supposed etiology (rheumatism) points to an infection of the valve 
 early in life. 
 
 Pie es 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 22% 
 
 17. Death was notably sudden and unexpected in six cases. 
 One patient died in the hospital corridor. In most patients, however, 
 the ordinary congestive symptoms preceded death. 
 
 AORTIC STENOSIS. ILLUSTRATIVE CASES 
 
 I. 2558. Slit-like orifice, pulmonary arteriosclerosis. Death 
 from pneumonia. 
 
 2. 2238. Typical physical signs. Mouths of coronaries narrowed. 
 Fibrous myocarditis. 
 
 3. 2603. Angina pectoris clinically prominent. Moderate 
 coronary sclerosis. 
 
 4. 4655. Trigeminal neuralgia a major complaint. Otherwise 
 typical. 
 
 5¢ 3409. Boyaet.6. Slight acute, marked chronic endocarditis. 
 
 6. 3715. Man aet. 68. Death with pulmonary and renal 
 abscesses. , ‘ 
 
 Necropsy 2558 
 
 An English janitor of sixty-three entered March 7, 1910. He had 
 had a very severe case of scarlet fever in boyhood. Otherwise he had 
 been very well. He had had gonorrhea twice when young. 
 
 Five years ago, when walking in a parade, he was suddenly seized 
 with severe dyspnea and cough with frothy sputum. Ever since then 
 he had had considerable dyspnea on exertion. For several years he 
 has urinated six or eight times at night. Four weeks ago the dyspnea 
 became much more severe, and he developed a cough and orthopnea. 
 Two days ago these symptoms became much worse, and his legs sud- 
 denly became edematous. A few hours ago he began to raise red 
 muco-purulent sputum. 
 
 Physical examination showed a ruddy-faced old man breathing 
 very rapidly, with marked tracheal rattles. The apex impulse of the 
 heart was in the sixth space, not very forcible, 15.5 cm. from mid- 
 sternum, 3 cm. outside the nipple. The right border was at the ster- 
 nal margin. At the aortic area a loud, rough systolic murmur 
 
 accompanied by a thrill. The aortic second was not heard. At 
 the apex a systolic murmur of higher pitch and different quality. 
 The pulses were of very small volume and low tension, irregular, 
 with many extra systoles. At the apex there were 96 beats, at the 
 wrists 60. The pulse was feeble. The lungs were hyperresonant 
 and full of sonorous rales. Expiration was very prolonged, with 
 loud wheezes and crackles. At the bases some dullness, with great 
 showers of fine crackles. The abdomen was obese, thick. The 
 
222 FACTS ON THE HEART 
 
 liver dullness extended from the sixth rib to three fingers below 
 the costal margin, where an indefinite edge was felt.” A tremendous 
 inguinal hernia was found. The genitals and pupils were normal. 
 There was very marked brawny edema of the legs and ankles. The 
 fundi showed no abnormalities. 
 
 Temperature 97.3 to 103.8 to 99.7, the pulse 71 to 131, respira- 
 tions 23 to 34. The amount of urine was 31 to 21 ounces. The 
 specific gravity was 1030 to 1025. It was pink at one of twoexamina- 
 tions, showed albumin and granular and hyalin casts at both, many 
 leucocytes at the first. The hemoglobin was 90%. There were 
 24,000 leucocytes and 9o% of polynuclears. Blood culture was nega- 
 tive. The sputum was at first brick red, slightly foul; within twenty- 
 four hours green, with some odor. . No tubercle bacilli were found. 
 
 The heart action became more rapid, and at the same time the 
 systolic murmur became less marked. On the evening of March 7 
 expiration became very difficult, respiration periodic, and the patient 
 became comatose and almost pulseless. He responded well to medica- 
 tion and had a fairly comfortable night. The evening of March 9 
 he had the same symptoms. The veins of the neck distended upon 
 pressure over the liver, which was definitely enlarged but not pulsating. 
 After the withdrawal of 18 ounces of blood he was more comfortable. 
 He afterwards spent most of the time in a chair, with much respira- 
 tory difficulty and a loose cough. March 11 the pulse suddenly 
 failed, and he died. 
 
 Clinical Diagnosis. —Aortic stenosis. 
 
 Broken compensation. 
 
 Bronchopneumonia? 
 
 Emphysema and chronic bronchitis. 
 
 Chronic passive congestion. 
 
 Edema. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Aortic stenosis and regurgita- 
 tion. 
 
 Chronic passive congestion of the liver. 
 
 Terminal infection. 
 
 Anatomical Diagnosis——Chronic endocarditis of the aortic valve; 
 stenosis. 
 
 Arteriosclerosis of the aorta, the coronary arteries, and the pul- 
 monary artery and its branches. 
 
 Hypertrophy and dilatation of the heart. 
 
 Bronchopneumonia, right lung. 
 
 Focal pneumonia, superior lobe of left lung. 
 
 Purulent bronchitis. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 223 
 
 Fibrinous pleuritis, left. 
 
 Chronic passive congestion, general. 
 
 Edema of the lower extremities. 
 
 Slight fibrous endocarditis of the mitral valve. 
 
 Chronic pleuritis, right. 
 
 Right inguinal hernia. 
 
 Dr. OSCAR RICHARDSON: We were not permitted to examine the 
 head. 
 
 There was edema of the lower extremities. We found no fluid in 
 the peritoneal cavity. He had a right inguinal hernia. The dia- 
 phragm in this case was at the fifth rib on the right and the fifth inter- 
 space on the left. There was no fluid in the right pleural cavity and 
 only a slight amount in the left, with a few fibrinous shreds,—chronic 
 pleuritis on the right side and fibrinous pleuritis, left. The trachea 
 and bronchi contained considerable muco-pus, a purulent bronchitis. 
 In the right lung there was bronchopneumonia and in the left lung a 
 few focal areas of pneumonia. In addition to that, chronic passive 
 congestion. | 
 
 In a passively congested lung it is sometimes very difficult to tell 
 whether there is any pneumonia present or not. JI remember a case 
 in which I returned lobar pneumonia and it was chronic passive con- 
 gestion. One has to be careful. In this particular case there were 
 definite islands of consolidation and purulent bronchitis, and the 
 picture was quite evident. Microscopic evidence showed that there 
 was bronchopneumonia and a few scattered areas of focal pneumonia. 
 
 The pulmonary artery in this case showed considerable sclerosis. 
 It isnot very common. We may get a few yellowish plaques in any 
 case at this age; but this was definite sclerosis. A curious thing was 
 that at the junction where the ascending portion of the thoracic 
 aorta and the pulmonary artery come together there was a fibrocal- 
 careous plaque which extended through the conjoined walls so that 
 we had a rough surface on the intima of the pulmonary artery and 
 along the intima of the aorta, but the wall was essentially intact. 
 
 The heart weighed 548 grams, an enlarged heart. (Normally 280 
 to 300 grams.) The right ventricle wall was six mm. thick and the 
 left thirteen mm. The columnae were hypertrophied. The mitral 
 valve measured ten cm. and the aortic hardly anything, a slit-like 
 orifice admitting the tip of the little finger. (See Fig. 39.) The 
 tricuspid was thirteen and a half cm., the pulmonary nine. We 
 cannot always believe what we see in pathological reports as to the 
 amount of sclerosis. In this case there was moderate sclerosis of 
 
224 FACTS ON THE HEART * 
 
 the aorta, considerable of the pulmonary artery, and only a little of the 
 coronaries. There was of course frank aortic stenosis of the rheuma- 
 tic type. In this case we made very sure that the bundle of His was 
 not impinged upon by the process in the aortic valve. 
 
 fe its SST Be 
 
 Fic. 39.—Necropsy 2558. Plate I.—Heart in aortic stenosis and regurgitation 
 with arteriosclerosis of the aorta, the coronary arteries and the pulmonary artery and its 
 branches. The heart weighed 548 grams. Shows the fish-mouth aortic valve—aortic 
 stenosis. A little less than three-quarters actual size. (Photograph by John W. 
 Barry. Dr. Oscar Richardson.) . 
 
 The liver showed the nutmeg markings. Of course that is stasis, 
 the blood coming back through the hepatic veins to the central veins, 
 then into the portal system, and forming a network of distended 
 vessels containing brown-red blood. The liver cells may show some 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 225 
 
 fatty degeneration or become atrophied and show a pale grayish 
 brown color, and the whole thing looks like the cross section of a 
 nutmeg. It is a convenient term for chronic passive congestion. 
 
 The spleen weighed 116 grams (normally 80 to 180), and curiously 
 enough in this case the tissue was a little mushy, possibly on account 
 
 Fic. 40.—Necropsy 2558. Another illustration of the same condition. (Photograph 
 by John W. Barry. Dr. Oscar Richardson.) 
 
 of the infection. It was rather small for a spleen in a case of chronic 
 passive congestion. 
 
 The kidneys weighed 275 grams (normally 200 to 400), and were 
 in good condition. They showed of course some chronic passive 
 
 15 
 
226 FACTS ON THE HEART 
 
 congestion. I notice that the kidneys seem to stand wear and tear 
 about as well as any organ in the body. The genito-urinary tract 
 was out of the picture. The gastro-intestinal tract showed chronic 
 passive congestion. 
 
 There was no growth from the heart blood. But the microscope 
 confirmed the gross picture of the pneumonia in the lungs and the 
 negative appearance of the kidneys. 
 
 Necropsy 2238 
 
 An American night watchman of sixty-two entered May 14. 
 His father died of ‘‘shock,”’ his mother of cancer. Except for the 
 diseases of childhood he had practically never been ill before. He 
 occasionally drank a glass of beer. 
 
 December 13 he stopped work because of a heavy “cold” and 
 periods of dyspnea with dizziness which prevented any exertion. 
 The attacks lasted five minutes or less. Since December he had 
 slept in a chair. Lying flat always brought on an attack. He had 
 
 vi 
 \V 
 
 My 
 aye 
 
 NS 
 pi 
 
 dshed. Voice sound elightly Zz 
 diminished. Tactile fremitus.)—~—j 
 Marked tenderness over lower 
 
 Dull. Breath sound dimin- | 
 ribs. 
 
 FiG.jAt. 
 
 troublesome cough, constipation, and urination once or twice at 
 night. 
 
 Examination showed a senile man with slight cyanosis and 
 evidence of loss of weight. Only a few carious teeth remained. 
 There was marked pyorrhea. The apex impulse of the heart was in 
 the fifth space 12.5 cm. to the left of the midsternum, 2 cm. outside 
 the nipple line, corresponding with the left border of dullness. The 
 right border of dullness was at the right edge of the sternum. The 
 acion was irregular. The first sound was long andloud. The second 
 sounds were not heard. Starting in the third left interspace and 
 transmitted down to the apex, entirely replacing the second sound, 
 was a blowing diastolic murmur. Over the whole precordia was a 
 loud systolic murmur transmitted to the vessels of the neck, with 
 a corresponding thrill. At the apex and transmitted to the axilla 
 and back was a blowing musical systolic murmur. To the right of 
 the sternum in the fourth interspace and transmitted to the right was 
 a systolic murmur of a higher pitch. The pulses were slightly irregu- 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 227 
 
 lar, of fair tension and long sustained plateau type. The arteries 
 were palpable and tortuous. The systolic blood pressure was 135. 
 The lung signs were as shown in Fig. 41. The abdomen was tym- 
 panitic throughout except in the flanks. The upper border of the 
 liver was obscured by chest dullness. There was slight edema of 
 the genitals and marked soft edema of the legs and lower back. 
 The pupils and reflexes were normal. 
 
 The temperature was 96.5° to 99.4°, with one rise to 101.4° two 
 days before death. The pulse was 55 to 94. The respirations were 
 20 to 30. The output of urine was 5 to 61 ounces, the specific 
 gravity I.010 to 1.030. The hemoglobin was 85%, the leucocytes 
 8400. 
 
 By May io the rough systolic murmur had extended from the base 
 more toward the apex. ‘The systolic murmur at the apex was blow- 
 ing and higher in pitch. There wasa systolic thrill in the second right 
 interspace. The edema diminished under a course of magnesium 
 sulphate. The patient lost strength. He dropped asleep for a few 
 minutes at a time while sitting in his chair, and slept more and more. 
 May 25 digitalis was begun. In three days the heart sounds were 
 slightly stronger and the amount of urine increasing. With the rise 
 in temperature June 2 he had a large pustule which cleared up 
 quickly after an injection of staphylococcus vaccine. June 4 he 
 seemed stronger and was discharged relieved, weighing 122 pounds, 
 22 pounds less than at admission. 
 
 After leaving the hospital he did no work, kept rather quiet and 
 got along well until the following February, when the dyspnea became 
 much worse. Two weeks later he had cough with yellowish sputum. 
 He always slept in a chair on account of orthopnea. His bowels 
 were very constipated. His urine was rather scanty. He passed 
 it twice at night. There was much edema of the legs. For two 
 months before his readmission, March to, he had been taking 
 strophanthus. 
 
 Upon examination he weighed 13214 pounds. The mucous mem- 
 branes were slightly pale. The apex impulse and the left border of 
 the heart were in the fifth space 2 cm. outside the nipple line, 12.8 
 cm. to the left of midsternum. The right border was just outside 
 the right sternal margin. The action was irregular in force and 
 rhythm, the sounds indistinct, the pulmonic second sound not strong, 
 the aortic second absent. A coarse discordant musical systolic mur- 
 mur was heard at the apex, transmitted to the axilla. At the base 
 was a rough systolic murmur, not transmitted. Along the left 
 
228 FACTS ON THE HEART 
 
 border of the sternum were a low systolic and a low diastolic. There 
 was a systolic thrill in the third right interspace close to the sternum. 
 The pulses were irregular, corresponding to the apex beat, of small 
 volume and low tension. The blood pressure is not recorded. There 
 was faint lateral excursion of the brachials. There were medium 
 moist rales scattered throughout both lungs, and dullness with dimin- 
 ished respiration and fremitus at both bases posteriorly. The liver 
 dullness extended from the fifth rib to three inches below the costal 
 margin. The edge was not distinctly felt. There was shifting dull- 
 ness in the flanks. The feet were cold and livid. The skin over the 
 lower legs was reddened and wrinkled. 
 
 The temperature was 95.8° to 99-, the pulse 80 to 103, the respira- 
 tion 20 to 31. The specific gravity of the urine was 1.011 to 1.019; 
 otherwise the urine was negative. The blood was normal. 
 
 The patient made marked improvement with rest in bed, digitalis 
 and purging. By March 21 he was about the ward all day, though a 
 Jittle weak and with a rasping cough. The heart sounds were slow 
 and strong. The digitalis was omitted. He continued to do well 
 without it, though he felt a litile faint when he first got up or on sud- 
 den exertion. March 31 he was discharged relieved, weighing 11914 
 pounds. 
 
 He was fairly comfortable until November 10, was outdoors 
 daily, and walked at times. He had more or less constant edema of 
 the legs, when prone marked dyspnea, and some cough with whitish 
 sputum. During the week before his readmission to the hospital 
 November 17 the dyspnea was very marked, he slept poorly, passed 
 much less urine, and felt weak. 
 
 Upon examination he was emaciated. The impulse of the heart 
 was best felt and its sounds best heard in the fifth space, nipple line, 
 tr cm. to the left of midsternum. The right border was at the right 
 border of the sternum. The sounds were entirely replaced by mur- 
 murs. A systolic thrill was felt all over the precordium, best in the 
 second space just to the right of the sternum. A harsh systolic 
 murmur, at times musical, was heard al] over the precordium, loud- 
 est at the aortic area, transmitted into the neck, axilla and back. 
 Both second sounds were replaced by soft diastolic murmurs, loudest 
 over the aortic area. The pulses were irregular in force and rhythm. 
 The systolic blood pressure was go. The arteries were calcareous. 
 The lungs showed dullness, diminished breathing and voice sounds 
 and a few fine crackling rales on inspiration at both bases, at the 
 side and back. ‘The liver edge was felt 7.5 cm. below the right costal 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 229 
 
 margin. There was slight edema of the ankles and over the shins, 
 and marked discoloration and pigmentation of the skin over the 
 feet and the lower half of the legs. 
 
 The temperature was 95.8° to 97.8°, the pulse 74 to go, the res- 
 piration 20 to 32. The specific gravity of the urine was 1.019. The 
 sediment showed an occasional hyalin cast. The hemoglobin was 
 90%, the leucocytes 17,000. There was polynuclear leucocytosis. 
 
 The patient seemed fairly comfortable except for a good deal of 
 dyspnea. Early in the morning of the 18th he had a sudden attack 
 of dyspnea and became pulseless. In an hour he died. ' 
 
 Clinical Diagnosis (from Hospital Record)—(Probably copied 
 from the necropsy record.) Aortic stenosis with regurgitation and 
 broken compensation. 
 
 Arteriosclerosis. 
 
 Cardiac hypertrophy and dilatation. 
 
 Chronic adhesive pleuritis, left. 
 
 Encapsulated hydrothorax. 
 
 Dr. Richard C. Cabot’s Diagnosis —Aortic stenosis and regurgita- 
 tion, rheumatic type. 
 
 Chronic endocarditis of the mitral valve (with some stenosis?) 
 
 Hypertrophy and dilatation of the heart. 
 
 Arteriosclerosis. 
 
 Edema of the lungs. 
 
 Ascites. 
 
 Anasarca. 
 
 Passive congestion of all the organs. 
 
 Streptococcus septicemia. 
 
 Acute pericarditis? 
 
 Anatomical Diagnosis —Fibrocalcareous endocarditis of the aortic 
 valve with stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic interstitial myocarditis. 
 
 Arteriosclerosis. 
 
 Slight hydropericardium. 
 
 Double hydrothorax. 
 
 Compression atelectasis of the lower lobes of the lungs. 
 
 Slight chronic passive congestion. 
 
 Chronic pleuritis. 
 
 Cholelithiasis. 
 
 Old infarct of the kidney. 
 
230 FACTS ON THE HEART 
 
 Dr. RicHarDson: The original anatomical diagnosis, chronic 
 endocarditis of the aortic valve with stenosis, was replaced later by 
 ‘‘fibrocalcareous endocarditis of the aortic valve with stenosis,” 
 because they did not wish to commit themselves. Now I think that 
 the original diagnosis was right. I believe it was rheumatic. 
 
 They never say “regurgitation”? in these reports. That is 
 assumed, since if he had stenosis he had regurgitation. All they put 
 down is what they can see, stenosis. 
 
 An interesting thing is an old infarct in one of the kidneys. It 
 dates back to the point of time, probably, which Dr. Cabot referred 
 to saying he thought there was an acute on top of a chronic condition. 
 The infarct bears that out. It is now an old infarct. There was no 
 acute endocarditis in this case at the time of necropsy. The other 
 valves were negative. 
 
 The case is a pure case of chronic endocarditis at the aortic valve, 
 rheumatic in origin. He also had some arteriosclerosis, which is to 
 be expected at sixty-five years. 
 
 An interesting thing in regard to the aortic valve in this case is 
 that this old material was piled up in an irregular stony mass. The 
 upper part encroached on the sinuses of Valsalva and further upon 
 the orifices of the coronary arteries, partially occluding them, though 
 not altogether. As a result we find scattered through the heart 
 areas of chronic interstitial myocarditis. One would naturally 
 say, How about his coronary arteries? They were pretty good except 
 that the orifices where the blood flows into them were decreased to 
 such an extent as to interfere considerably with the blood supply to 
 the myocardium. 
 
 The hydrothorax was so extensive as to cause compression atelec- 
 tasis of the lungs. 
 
 The chronic passive congestion, in this as in many other aortic 
 cases, does not seem to be so extensive as in the mitral cases. 
 
 Another thing of interest is that he had cholelithiasis. There 
 were nine stones, but the gall-bladder and the bile ducts were 
 negative. - 
 
 The history says, ‘“‘Except for the diseases of childhood he had 
 never been ill before.’ When he came here he was at the end of 
 trouble which occurred years ago, and the reason for not calling it 
 arteriosclerosis is because the arteriosclerotic changes were far from 
 the aortic valves. There were whole patches of good aorta. If one 
 were going to demonstrate arteriosclerotic changes in the aortic cusps 
 so extensive as this, he would have quite a job on hand if he had no 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 231 
 
 arteriosclerosis in that region. Although arteriosclerosis may be 
 selective 1t does not select in such an accumulation of fibrocalcareous 
 material on the cusps and extending well down into the myocardium 
 as well as up into the sinuses of Valsalva. It is not a process that 
 erects large irregular fused masses of fibrocalcareous material on the 
 cusps. 
 
 I noted carefully its relation to the bundle of His. It approached 
 but did not quite impinge upon the bundle. 
 
 Dr. Casot: We do not need to suppose a lesion of the bundle in 
 order to account for the arrhythmia. The only thing tied up to 
 the bundle is heart block. 
 
 Necropsy 2603 
 
 An American electrical laborer of forty-nine entered July 1. 
 His mother died of tuberculosis when he was twenty-nine. One 
 son died at twenty-three of ‘‘heart trouble.” The patient had gonor- 
 rhea at seventeen and tertian malaria at twenty-five. At eighteen, 
 thirty, forty and firty-five he had attacks of rheumatic fever. Prac- 
 tically all the joints were affected at some time, but chiefly the knees 
 and ankles. The attacks lasted from a few weeks to two or three 
 months. For fifteen or twenty years he had had slight dyspnea on 
 exertion, not increasing. 
 
 While convalescent from the last attack of rheumatism four years 
 before admission he began to have attacks of sharp pain starting in 
 the left. shoulder and shooting down the extensor surface of the arm to 
 the elbow. These attacks came three times a day or oftener and 
 lasted three or four minutes, being at times severe enough to make 
 him cry out. ‘Dull soreness” was practically constant. At about 
 the same time he began to have slight soreness over the precordia 
 with the attacks. For three years he had had a cough with consider- 
 able “green’’ sputum, bloody on three occasions. For two or three 
 weeks he had had attacks of sharp pain over the precordia lasting 
 three to five minutes. This pain did not radiate from the precordia 
 to the arm, but occasionally did from the arm to the precordia, 
 although the attacks were often independent. His legs had been 
 swollen for a week. 
 
 Examination showed a rather obese man weighing 186 pounds, 
 orthopneic, with pale skin and mucosae and slightly cyanotic lips. 
 The apex impulse of the heart was in the sixth space 14 cm. to the 
 left of midsternum, 3.5 cm. outside the nipple line, corresponding 
 with the left border of dullness. The right border was 2.5 cm. 
 to the right of midsternum. The action was slightly irregular in 
 
232 : FACTS ON THE HEART 
 
 force and rhythm. No second sound was audible except in the 
 pulmonic area, where it was faint and followed by a short diastolic 
 whiff. At the apex the first sound was rather forcible, partly 
 replaced and followed by a soft blowing systolic murmur transmitted 
 to the axilla and toward the base. In the aortic area a loud, harsh, 
 rough, rumbling, systolic murmur was heard, transmitted to the neck 
 and toward the apex and heard over the carotids on both sides. At 
 times a faint thrill was felt in the second right space. ‘The pulses 
 were equal, slightly irregular in rhythm and force, of good volume, 
 slightly increased tension, suggestive of plateau. The artery walls 
 were palpable, a little thickened. The lungs showed numerous fine 
 and medium moist rales at both bases, with occasional moist rales; 
 hyperresonance throughout. The abdomen was very tympanitic 
 and was held rather rigid. There was an epigastric hernia the size 
 of a peach, with impulse on cough, half-way between the ensiform and 
 the navel. There was dullness, not shifting, in the flanks. The 
 liver dullness extended from the sixth rib to the costal margin. 
 There was moderate soft edema over the sacrum ,and considerable 
 edema of the lower legs, ankles and feet. The pupils were very 
 slightly irregular, equal. Their reactions and the other reflexes 
 were normal. ; 
 
 The temperature was 97° to 098.6°, the pulse 70 to go, the respira- 
 tions 18 to 22. The output of urine was ro to 4o ounces, the specific 
 gravity 1.015. There was a slight trace of albumin at all of three 
 examinations, many hyalin and granular casts at two, a few pus and 
 red cells at one. The hemoglobin was 80%, the leucocytes 10,000, 
 the smear normal. A Wassermann was very slightly positive. 
 
 Under treatment the edema decreased, the heart grew steadier 
 and more regular, and the. dyspnea was relieved. Compensation 
 being fairly well established, on July 15 he was discharged. 
 
 After leaving the hospital he was able to move slowly about the 
 house and to go out a few times with care. Slight exertion caused 
 cough and pain in the region of the heart and the left shoulder and 
 arm. He usually had several attacks of this pain during the day. 
 He urinated at night rarely. . 
 
 February 7 he returned because of weakness and increasing fre- 
 quency and severity of pain. He now weighed 166 pounds. 
 
 Examination showed no cyanosis. A forcible, thrusting apical 
 impulse was seen and felt in the sixth space. The left border of dull- 
 ness was 14 cm. from midsternum, 3.5 cm. outside the nipple line. 
 The right border as 2.5 cm. to the right. The supracardiac dullness 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 233 
 
 was 8cm. There was a loud rough systolic murmur, accompanied 
 by a rough thrill, all over the precordia, loudest in the aortic area, 
 transmitted to the neck and axilla, entirely replacing the first sound. 
 No second sounds were heard at the base. The action was slow, 
 with many well marked extrasystoles. The artery walls were not 
 sclerotic. The systolic blood pressure was 110 to 118. The lungs 
 showed slight dullness with diminished breathing and occasional rales 
 at the extreme bases. There was shifting dullness in the flanks. 
 The liver dullness extended from the sixth rib to a handbreadth 
 below the costal margin, where an indefinite edge was felt with a 
 rounded mass the size of an egg on it in the nipple line. There was 
 some tenderness over the liver; no pulsation. The genitals and 
 extremities were normal. : 
 
 The temperature was 97° to 99.8°, the pulse 70 to 105, the respira- 
 tion 17 to 24. The output of urine was 20 to 50 ounces, the specific 
 gravity 1.016 to1.o19. There was a slight trace to the very slightest 
 possible trace of albumin at all of three examinations, no sugar, many 
 hyalin casts with small red cells attached, occasional fine granular 
 casts and red blood corpuscles at one, rare hyalin casts at one. The 
 hemoglobin was 90%, the leucocytes 4000, the polynuclears 75%. 
 
 In the hospital the patient was able to lie almost flat in bed. 
 He had several attacks of mild cardiac pain relieved in a few minutes 
 by nitrites. On February 13 he had a chill. The next day he 
 had pain and moderate tenderness in his knees and ankles, redness 
 and swelling in the right ankle only. This was relieved by aspirin. 
 By February 20 the joints were entirely clear. He had no further 
 attacks of cardiac pain, and was discharged relieved February 22. 
 
 He was up and about feeling fairly well until April 25, when his 
 cough began to increase in severity and he raised considerable 
 frothy sputum. He became more dyspneic and orthopenic. His 
 legs swelled. April 28 he had pain across the upper abdomen, 
 relieved before his return to the hospital May 2. 
 
 Examination was as before except for the points noted. He had 
 occasional hard dry cough during which he became cyanotic. The 
 apex impulse of the heart was not seen or felt. The percussion 
 borders were 11 cm. to the left, 4 cm. to the right, 8 cm. in the 
 supracardiac region. The whole precordia moved with systole. 
 A short systolic thrill was felt in the second right space, stronger 
 during expiration. The veins of the neck were full but did not 
 pulsate. At the apex a systolic murmur replaced the first sound, 
 transmitted to the axilla and heard all over the precordia. As the 
 
234 FACTS ON THE HEART 
 
 base was approached a harsh rough systolic was heard, loudest over 
 the aortic area, transmitted to the vessels of the neck. A faint 
 diastolic murmur was heard all over the heart. The pulmonic 
 second sound was faint; comparison with the aortic second was not 
 possible. The pulses were of the plateau type, occasionally irregular. 
 The artery walls were thickened. The systolic blood pressure was 
 too. The lungs showed equal expansion and good resonance through- 
 out. There were normal breath sounds, a few inspiratory squeaks, 
 and dullness below the angles of the scapulae posteriorly, with fine 
 moist rales at both bases. The abdomen showed no masses or 
 tenderness. ‘The liver dullness extended from the fifth space to the 
 costal margin. The edge was not felt. The knee-jerks were equal, 
 lively. There was slight soft edema of the legs and ankles. 
 
 The temperature was 98.6°, the pulse 85, the respiration 22. 
 The amount of urine is not recorded. The specific gravity was 1.017. 
 There was 14% of albumin, many hyalin and granular casts, some 
 with cells and blood attached, some laden with fat, a few free cells. 
 The hemoglobin was 85%, the leucocytes 7000, the polynuclears 
 72%. 
 
 The patient voluntarily walked upstairs, was put to bed and given 
 a quarter grain of morphia. He seemed fairly comfortable except 
 for occasional attacks of vomiting. In one of these attacks the 
 morning after admission he suddenly fell back and died. 
 
 Clinical Diagnosis (from Hospital Record).—Aortic stenosis. 
 
 Slight aortic regurgitation. 
 
 Hydropericardium. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 aortic valve with stenosis and regurgitation. 
 
 Possibly slight endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of all the organs. 
 
 Possibly slight acute glomerulo-nephritis. 
 
 Anatomical Diagnosis —Chronic endocarditis of the aortic valve. 
 Stenosis. 
 
 Arteriosclerosis of the coronary arteries. : 
 
 Fibrous myocarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydropericardium. 
 
 Incarcerated hernia, peritoneal fat tissue of the anterior abdomi- 
 nal wall. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 235 
 
 Dr. Wricut: This was a case of aortic stenosis with a very 
 marked ‘“‘fish-mouth”’ aortic valve, the valve fibrocalcareous, thick- 
 ened, fused, and forming a truncated cone. It was a typical chronic 
 aortic stenosis. The mitral valve showed no evidence of primary 
 affection, but there was some extension of the fibrous process to it. 
 
 There was no arteriosclerosis of the aorta to speak of, but it was 
 well marked in the coronaries, especially the descending branch of 
 the left, with fibrosis of the myocardium, so that he had an excuse 
 for anginoid pain. ‘This fibrosis was not obvious or gross. The 
 heart was very much hypertrophied. 
 
 There was no other significant or important lesion beyond chronic 
 passive congestion. 
 
 The kidneys grossly were negative. No note was made on the 
 microscopic examination. This is one of the few cases where it has 
 been omitted. 
 
 Necropsy 4655 
 
 An American masseuse of fifty-four entered November 5, 1018, 
 for relief of trifacial neuralgia. Her father and mother died of 
 consumption, and many relatives were tuberculous. She had 
 measles, diphtheria, scarlet fever and whooping cough in childhood, 
 and frequent mild sore throats. She had been deaf in the left ear 
 since the scarlet fever and had had occasional abscesses in both ears. 
 She had not been really well since a very mild attack of influenza at 
 fifty-one. She passed the menopause the following year. For two 
 years she had had marked pyrosis and gas, ending with the onset 
 of the present illness and accompanied by severe dyspnea, cyanosis 
 and stabbing precordial pain half an hour after meals, relieved by 
 belching or passage of gas. She had lost fifty-eight pounds (230 
 to 172) in two years, probably because of lack of proper food. 
 
 Beginning six months before admission she had had increasingly 
 frequent and severe attacks of pain in the right side of the face over 
 the malar bone. Vomiting of food seemed to be an 
 occasional cause of the attacks. 
 
 Upon examination the apex impulse of the heart , | j1 | yy 
 was not found. The percussion measurements were pyc. 42.—Meas- 
 as shown in Fig. 42. The sounds were distant and Tee ore by per- 
 of fair quality, the action slow. There was a rough 
 loud musical systolic murmur at the apex, but heard best at the base 
 over the aortic area, where a diastolic was heard. The pulses were of 
 fair volume and tension. The blood pressure was 100/70 to 100/65. 
 
 5:5 
 
236 FACTS ON THE HEART 
 
 The abdomen was negative except for a possible palpable liver edge 
 at the costal margin. Genital, pelvic and rectal examinations were 
 not made. The extremities and the pupils were normal, the knee-— 
 jerks sluggish. 
 
 The temperature was 97.4° to 99.2°, the pulse 69 to 94, the 
 respiration 16 to 28. The amount of urine was normal when recorded, 
 the specific gravity 1.024 to 1.032. The urine was alkaline at 
 one of six examinations, cloudy at two and showed leucocytes at 
 two. The renal function was 40%. The blood was normal. A 
 Wassermann was negative. The stools were negative. X-ray 
 showed the heart measurements as shown in Fig. 
 43. There was a pus pocket from a bicuspid 
 supporting extensive bridge work and appar- 
 ently communicating with the antrum, which 
 was dull. 
 
 November 20 the entire bridge work was 
 
 ao removed and the abscessed tooth roots were 
 Fic. 43.—Measurements Curetted. The pain became less frequent and 
 Dy eat Boke the patient had good nights until November 
 
 30, when severe paroxysms of right supraorbital pain started. 
 
 December 3 under ether and oxygen through a small incision in 
 the right eyebrow about 2 cm. of the supraorbital nerve was evulsed. 
 
 For the next four years the patient remained in a general run- 
 down nervous condition, taking care of an insane aunt, after whose 
 death she was considerably better. Eight weeks before her read- 
 mission she found that the area of anesthesia, which had gradually 
 grown less, had completely disappeared. Soon she had sharp 
 stabbing pain in the right eyebrow very similar to the pain at her 
 first entry, radiating out to the temple and to the top of her head like 
 a red-hot spray, the attacks coming twenty times a week. A week 
 before readmission she had all her upper teeth removed with only 
 partial relief. 
 
 On examination September 22, 1922, she appeared old for her — 
 age. There was evidence of loss of weight. The apex impulse of — 
 the heart was in the fifth space well outside the nipple-line. There 
 was questionable enlargement at the base. (The measurements 
 are not recorded.) The sounds were of poor quality or replaced 
 by a prolonged soft blowing systolic murmur heard all over the 
 precordia and in the axilla, also a short diastolic murmur at the 
 aortic area. The blood pressure was 110/90. The lungs, abdomen, 
 genitals, extremities, pupils and reflexes were not remarkable. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 237 
 
 The temperature was 97° to 1o1.1°, the pulse 71 to g1, the respira- 
 tion normal. The amount of urine is not recorded. The urine was 
 cloudy at one of two examinations, the specific gravity 1.025. There 
 was a very slight trace of albumin once. The sediment showed rare 
 leucocytes at both examinations. X-ray showed the left antrum 
 distinctly less radiant than the right. The outline was practically 
 obliterated. The frontal sinus on the left was smaller than that on 
 the right, but showed no marked change in density. Plates of the 
 mastoid region showed no definite pathology. 
 
 October 2 under gas and ether careful search for the nerve was 
 made but no definite evidence of it found. Several fragments 
 of tissue looked suspicious and were excised. Pathological examina- 
 tion showed medullated nerve bundles surrounded by fibrous tissue. 
 The patient was discharged October 7. 
 
 Very little relief followed the second operation. She continued 
 to have attacks of shooting pain lasting two or three minutes, some- . 
 times none for days, sometimes throughout one or more days. 
 Talking or eating or any movement of the face tended to bring on the 
 attacks. During the attack the eyelid closed and sharp shooting 
 pains passed through it, sometimes making her cry out, always 
 making tears come, with accompanying relief of symptoms. 
 
 In October, 1922, after being hurt in a train wreck she began to 
 have pains and soreness of the chest, with extreme dyspnea and 
 orthopnea. She gradually improved after ten months. After the 
 accident she had occasional attacks of palpitation. When she lay 
 on her left side she soon became uncomfortable, felt her heart beating 
 forcibly against her ribs, and had some sense of being smothered. 
 In May, 1923, she had edema of the legs for three weeks, during which 
 time she was in a hospital. In December for about ten days she had 
 some urinary retention, dark urine, and her doctor told her 6% 
 albumin. She urinated twice at night. December 23 her legs 
 became swollen and itched. By the middle of January, 1924, she 
 was able to breathe comfortably lying down, but had dyspnea on 
 exertion. In five years she lost about 80 pounds, perhaps in part by 
 dieting. | 
 
 The hospital in which she was treated from the r4th to the 26th 
 of May, 1923, reported: ‘Heart enlarged to the left. Murmur 
 heard at aortic and mitral areas. Sounds weak. Slight edema of 
 the ankles. Dyspnea and cyanosis on slight exertion. Blood 
 pressure 140/92. Arteries thickened. During her stay in the 
 hospital she was very short of breath and quite purple on the least 
 
238 FACTS ON THE HEART 
 
 exertion. Had several severe attacks when pulse became impercepti- 
 ble and body very cyanotic. Responded well to stimulation at these 
 times. The blood pressure came down to 112/94.” 
 
 At her third admission, January 16, 1924, she gave additional 
 history of tonsillitis and of a “‘nervous breakdown” in 1916, with 
 shooting pains in both arms and weakness. 
 
 Examination showed her emaciated and _ slightly cyanotic. 
 During the examination she had a severe attack of pain lasting four 
 minutes, during which she sat up in bed, her face distorted with pain 
 and cyanotic, with distended veins. The chest expansion was some- 
 what limited. The lungs were normal. The maximum heart 
 impulse was seen and felt in the fifth space 10 cm. from midsternum 
 and 1.5 cm. outside the midclavicular line, coinciding with the left 
 border of dullness. The right border of dullness was 5 cm. from 
 midsternum. The supracardiac dullness was normal. The action 
 was regular. There was a loud rough systolic murmur, loudest in 
 the third right interspace near the sternum, transmitted to the 
 vessels of the neck and the rest of the precordium. An early diastolic 
 murmur was heard along the left sternal border, blowing, short and 
 high pitched. There was well marked thrill over the aortic area. 
 The blood pressure was 105 /80 to 90/60. To the left of the umbilicus 
 was a swelling in the abdominal wall which felt like a lipoma. The 
 liver edge was felt rather deep in at the level of the umbilicus in the 
 midclavicular line, firm. No nodules or irregularities were felt. 
 The extremities showed very slight pitting over the shins. The knee- 
 jerks were sluggish. The vessels in the fundi were varied in size in 
 different parts of their course. In the left fundus one vessel almost 
 disappeared over a short distance as though covered by edema. 
 The disc margins were clear cut. 
 
 The temperature was 96° to 99.4°, with one rise to ro1° February 
 16. The pulse was 70 to 120, the respiration 15 to 30. The amount 
 of urine was normal when recorded, the specific gravity 1.014 to 1.022. 
 The urine was cloudy at one of four examinations, showed the 
 
 slightest possible trace to a trace of albumin at three, 6 to 50 leuco- 
 
 cytes per high power field at both. The renal function was 5 to 40%. 
 The blood was normal January 16 except for slight increase in plate- 
 lets and 2% of reticulated cells. January 18 the hemoglobin was 
 95%, the reds were 4,600,000, with slight achromia, the platelets 
 normal. A Wassermann was negative. The non-protein nitrogen 
 
 was 36.3 mgm. X-ray (Fig. 44) showed the heart shadow distinctly — 
 
 enlarged both to right and left. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 239 
 
 There was no definite abnormality of the sinuses, although 
 the plates were not entirely satisfactory. 
 
 The day after admission another examiner found a low pitched 
 rumbling middiastolic murmur at the apex after exercise; the first 
 sound replaced by a systolic murmur; an aortic diastolic murmur at 
 the aortic area, the left sternal border and the apex; a faint diastolic 
 thrill at the apex; the aortic second sound absent; a loud rough sys- 
 
 Fic. 44.—Heart shadow distinctly enlarged both to right and left. Left ventricle 
 large and round. Supracardiac shadow shows moderate increase in width and is prom- 
 inent on the right side. Root glands large and show evidence of calcification. Across 
 the right chest in the region of the interlobar fissure is a dense band about a centimeter 
 wide extending from the root to the periphery. Right lung field below this considerably 
 diminished in radiance, although not dull, suggesting a loss of expansion rather than 
 consolidation. Costophrenic angles on both sides somewha nazy but not so dull as 
 to suggest fluid. Apices relatively clear. 
 
 tolic murmur and thrill at the aortic area; sustained pulse. He found 
 many loud crackling inspiratory rales at the left border of the heart 
 and in the left axilla, and noted systolic retraction of the sternum, 
 though no definite Broadbent. Dr. White noted, ‘“‘Murmurs at 
 lower end of sternum probably transmitted aortic murmurs, although 
 there is also a slight diastolic rumble there . . . Liver large. 
 Face very cyanotic. Cause of pulmonary rales in left axilla near 
 heart? Bases clear behind. Operation will probably be borne all 
 
240 FACTS ON THE HEART 
 
 right. I should advise full digitalization in any case, with mainten- 
 ance of it thereafter.” 
 
 January 25 divulsion of the posterior root of the fifth nerve, right, 
 was done under novocain. Next day she had some dyspnea and 
 marked general bodily soreness and stiffness. The right eye was 
 ecchymotic, with a corneal abrasion, and on the 28th was swollen 
 shut. There were rales at the left base. She still had some pain in 
 the right face. She was up in a chair for a few minutes at a time, 
 but was always rather dyspneic on slight exertion. She had an 
 attack or two of dyspnea, cyanosis, and slight increase in heart rate 
 lasting three hours. The morning of February 16 she had a severe 
 attack, unrelieved by adrenalin, morphia or digifolin. The cyanosis 
 was marked, the dyspnea variable. ‘There was a red area over the 
 flank and back. February 17 the general cardiac storm continued 
 unrelieved by vagal pressure. The heart continued regular, the rate 
 about 120. In the attacks her breathing was shallow, rapid, and 
 slightly irregular. The pulse could not be felt at the wrist. The 
 attacks began and ended suddenly. She was drowsy during 
 them. February 17 she was irrational. The blood pressure was 
 110/70. February 22 she was discharged to the Eye and Ear 
 Infirmary for care of the eye. 
 
 During the next three weeks she Seal no definite attack of heart 
 symptoms. At times she had to sit up in bed to breathe with comfort. 
 She took one digitalis pilla day. March 10 she had ‘‘stomach ache” 
 followed by vomiting of food. 
 
 At her fourth admission, March 11, 1924, no additional examina- 
 tion is recorded except some notes upon the eye condition. The 
 corneal epithelium had broken down during the past few days. 
 
 During her two weeks in the hospital the temperature was 96.7° 
 to 99°, the pulse 80 to 102, the respiration 20 to 36. The amount of 
 urine is not recorded. The specific gravity was 1.034 to 1.028. 
 The urine was cloudy at both of two examinations, showed a slight 
 trace to a trace of albumin and 5 to 50 leucocytes at both and very 
 rare red blood cells at the second. The hemoglobin was 85%. 
 There were 14,600 to 12,500 leucocytes, 80% polynuclears. The 
 reds and platelets were normal. ; 
 
 The patient had a good deal of vomiting. She showed increasing 
 cyanosis and dyspnea, went steadily downhill, and died March 24. 
 
 Clinical Diagnosis (from Hospital Record)—Rheumatic heart 
 disease with aortic stenosis and regurgitation and congestive failure. 
 
 Operation, posterior root of fifth nerve section. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 241 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis of the 
 aortic valve, with stenosis. 
 
 Possibly chronic endocarditis of the mitral valve, with stenosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Double hydrothorax. 
 
 Ascites. 
 
 Arteriosclerosis, general, and in the aorta and great branches. 
 
 Slight arteriosclerosis of the kidneys. 
 
 Chronic pleuritis. 
 
 Anatomical Diagnosis —Chronic endocarditis of the aortic valve. 
 Stenosis. | 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Edema of the lower extremities. 
 
 Fibrous myocarditis. 
 
 Mural thrombus of left ventricle of the heart. 
 
 Chronic pleuritis. 
 
 Obsolete tuberculosis or bronchial glands. 
 
 Slight arteriosclerosis. 
 
 Cholelithiasis. 
 
 Old infarct of left kidney. 
 
 Dr. RicHAarpson: The body looked as though weight had been 
 lost. We were not permitted to examine the head. 
 
 The legs, ankles and feet were swollen and pitted on pressure. 
 The subcutaneous tissues were a little wet. 
 
 The peritoneal cavity contained a small amount of fluid, the 
 beginning of ascites. 
 
 The mucosa of the stomach and intestines was reddened, velvety, 
 juicy, weeping thin bloody fluid,—the typical picture of chronic 
 passive congestion. 
 
 The diaphragm on the left was at the sixth rib, a little low. The 
 right pleural cavity contained a small amount of thin pale fluid; 
 none on the left. The bronchial glands were slightly enlarged, and 
 several of them showed small areas of fibrocalcareous degeneration. 
 The left lung was bound down by old adhesions. The right lung 
 showed many scattered old adhesions. The lung tissue was spongy 
 to a little leathery, showing what we call varying shades of salmon 
 color, varying shades of brown and red intermingled. The tissue 
 yielded a moderate amount of thin brownish-red frothy fluid,— 
 
 chronic passive congestion. 
 16 
 
242 FACTS ON THE HEART 
 
 - 
 
 Dr. Casort: Is there nothing to say about that patch in the right 
 lung? 
 
 Dr. RIcHARDSON: The only thing of course is the pleural adhesions. 
 
 Dr. Casot: That is the sort of result that makes me cautious. 
 We cannot make anything of that X-ray shadow. 
 
 A Puysicran: Interlobar septum? 
 
 Dr. RICHARDSON: That shadow might be due to an adhesion 
 between the wall of the chest and the lung, especially after Dr. Holmes’ 
 careful demonstration of the shadows and of the different angles at 
 which he takes the picture. He might, I should think, pick up the 
 edge of an adhesion and possibly get a shadow of that. 
 
 Dr. Hormes: I‘don’t believe that you could get a picture of 
 adhesions to look like that. You could get a thick interlobar septum 
 which needs no more than the thickness of a knife-blade to show. 
 I mean a thickening of the pleura between the lobes. 
 
 A PuysictAn: Interlobar pleurisy that had healed? 
 
 Dr. Casot: But the pathologist does not find it. That is the 
 trouble. 
 
 Dr. RicHARDSON: I should have been a little more careful and 
 put down just where those scattered adhesions on the right side were; 
 but they were not of course of great extent. 
 
 She was fifty-nine, with fairly developed frame and muscles. 
 If her heart had weighed 240 to 260 grams that would have been 
 normal. It weighed 75ograms. Of course that is very great enlarge- 
 ment. The myocardium generally was thick, more especially that 
 of the left ventricle, which was 15 mm. The right ventricle wall 
 was 4 mm., slightly thickened. The marked increase was in the left 
 ventricle wall. The columnae carneae were well marked. There 
 was considerable dilatation of the left ventricle, nothing very definite 
 of the left auricle. On the right there was slight dilatation of the auri- 
 cle and the ventricle. The mitral valve measured g cm. There - 
 were no definite lesions of this valve. The orifice of the aortic valve 
 presented as a slit about 114 cm. long and 1 mm. wide. The cusps 
 were fused into a fibrocalcareous mass. ‘The tricuspid valve meas- 
 ured 13 cm., negative, the pulmonary 714 cm., negative. This is a 
 case, then, of pure aortic stenosis. The coronaries were negative. 
 The ascending thoracic aorta was negative. The descending thoracic — 
 and the abdominal portions showed a slight amount of fibrous sclero- 
 sis. That aorta at fifty-nine is a pretty good one. The great 
 branches, however, showed a slight to moderate amount of fibrous 
 sclerosis. 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 243 
 
 The liver weighed 1200 grams. The margin of the liver was 
 well down below the costal border, 614 cm. below. This liver was 
 rather small, and showed typical nutmeg markings,—chronic 
 passive congestion. 
 
 The gall-bladder was slightly distended with thin bile. It con- 
 tained nine stones which were facetted, 1 cm, in greatest dimension, 
 and crushed under the thumb, showing brownish crystalline material. 
 One of the stones obstructed the cystic duct. 
 
 The spleen weighed 150 grams. The organ generally was thick, 
 the tissue elastic, rubbery; passive congestion. 
 
 The kidneys combined weighed 315 grams. The capsules strip- 
 ped. The surfaces were dark bluish brown-red, as was the tissue. 
 In the left kidney there was a small old infarct. I should have men- 
 tioned that in the left ventricle opposite a place in the myocardium 
 where there were several areas and streaks of myocarditis there was 
 a mural thrombus. 
 
 The microscope comfirmed the presence of the fibrous myocardi- 
 tis in the ventricle wall and that of the thrombus. The examination 
 of the other tissue showed chronic passive congestion, and in the 
 case of the kidney there was some arteriosclerosis of the renal vessels. 
 There was no definite nephritis. 
 
 Dr. Casor: Dr. Richardson says this is a perfectly typical aortic 
 stenosis. There is no hole in the valve opening at all, as far as you 
 can see. The astonishing thing to me is that she lived on. 
 
 It is very common to find gall-stones with no symptoms, no harm, 
 no reason to pay any attention to them. 
 
 A PuysiciAn: For two years she had marked pyrosis and gas. 
 
 Dr. Cazsot: A surgeon of a certain type would find that evidence 
 of gall-stones. But you see it in hundreds of people with no trouble 
 in the gall-bladders. | 
 
 A PuysicraAn: Do you still think the leucocytosis came from the 
 eye? 
 
 Dr. Cazot: We have this heart clot in case there isn’t enough in 
 the eye. 
 
 Necropsy 3409 
 
 A boy of six who had been treated at the Eye and Ear Infirmary 
 for ‘‘mastoid’’ entered September 4.° The history is taken from the 
 records of the Out-Patient Department. At his first visit, March 28, 
 one brother was also being treated at the Infirmary for “‘mastoid.” 
 The patient had chicken-pox, tonsillectomy and adenoidectomy at 
 three, scarlet fever and mumps at four, measles at five. Cardiac 
 
244 FACTS ON THE HEART 
 
 symptoms followed the scarlet fever. His appetite and sleep were 
 poor, his bowels constipated. He wet the bed. During the past 
 week he had had stiff neck, better now that his ear was discharging 
 again. 
 
 Examination in the Out-Patient Department March 28 showed a 
 fairly well nourished, pale boy with torticollis and a stiffjaw. The 
 precordia bulged. The apex impulse of the heart was in the sixth 
 space. The percussion borders were ten cm. to the left of midster- 
 num, four to the right.. The action was regular, rapid, (124). There 
 was a musical systolic murmur at the base transmitted widely, and 
 a double murmur at the base. The pulmonic second sound was 
 accentuated. The pulses were Corrigan. 
 
 Under treatment in the Out-Patient Department he made con- 
 tinued improvement until the second week in May, when he had an 
 attack of dyspnea and palpitation. After a rest of five hours he 
 was as well as usual. June 12 he was, his father said, equal to any 
 game. September 4, however, he had been in bed with dyspnea 
 and edema for six weeks. 
 
 Examination in the wards showed him poorly nourished, with 
 marked pallor of the skin and mucous membranes. There was 
 marked pyorrhea. The neck was not stiff. The apex impulse of 
 the heart was in the sixth space, with visible wave-like pulsation 
 from the base toward the apex. The left border of dullness was 
 thirteen centimeters from midsternum, six centimeters outside the 
 nipple line, the right border four centimeters from midsternum. 
 At the apex a long systolic thrill was felt, and all over the precordia a 
 questionable presystolic. The action was rapid. The first sound 
 was strong at the apex, where there was a loud blowing musical sys- 
 tolic murmur, heard all over the precordia and followed by a rough 
 rolling diastolic sound which lasted up to the next systolic. The 
 diastolic (and presystolic?) were louder at the third and fourth left 
 interspaces and also up to the pulmonic area. The pulmonic second 
 sound was sharp and accentuated. The cardio-hepatic angle was 
 obtuse. The pulse was Corrigan. The blood pressure was 135 /55- 
 too /s50. The abdomen was protuberant. Theliver dullness, extended 
 from the fifth rib to three centimeters below the costal margin, where 
 the edge was indefinitely felt. The knee joints were rather 
 prominent, suggesting epiphyseal enlargement. The right ear drum 
 showed considerable cerumen which was removed in part, showing a 
 thickened drum—no landmarks—with a small patent perforation 
 in the upper portion. The right mastoid showed the scar of a fairly 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 245 
 
 recent complete mastoid operation. There as no tenderness or dis- 
 charge. 
 
 During his first eleven weeks in the hospital the boy’s temperature 
 was normal except for the period of elevation shown in Fig. 45. Dur- 
 ing the last three weeks it was usually subnormal, 95.4° to 98°, and 
 ‘““picket-fence.”’ The pulse was 90 to 155. The respiration was con- 
 stantly rapid, 25 to 40, after November 18 4o to 70. The urinary 
 output was usually twenty to fifty ounces daily until October 15, 
 
 [Deiecons allem 
 Days of Mone [1314 [15176] 7 81/9 aolay laclaclaalaslzb 
 pa soresourly a6. a¥%| snl | Cov ies Lee [kal | donde Af es bach ee 
 Ae] | 2eo[ee ew fice ou eure en chaehw ne 
 (Seb SSH fe apf aes Gn 
 | ge eG 
 
 210 
 200 
 190 
 
 igo | | orl! Lise liek 13 [is [8 hea [iealAliee heal | 
 
 AS] LS | 
 i | setabtlehoteletetelSe(rsr | 
 150 150 gi fl els! S$] s! SS) el StS = ra 
 wo | {ao [Slatslel sets SLosrssl [| 
 30 | a0 (ALSISIRIBISIA! a ASar | 7 
 
 250 |; ul 
 re deprecated a 
 erga be koe (al a Egil labo 
 200 [Slit ti | tt tt el TT 
 eee AB UA Ul A Ce eC 
 iJ 
 = 
 
 aod yo Fuld ae ESAT Das SS Na 
 to 2} of ee TT LACS VT AIA 
 ged eth as oo e EasR e B  e 
 sed Jt Sof el ese cl ua Be Plc bd Boe SB 
 
 Fic. 45. 
 
 then gradually decreasing until after December 1 it was usually five 
 to ten ounces. The specific gravity was I.o10 to 1.030. There was 
 a slight trace of albumin at three of six examinations. The renal 
 function was 55%. The hemoglobin was 60 to 75%, .the leucocyte 
 count 12,400, rising to 23,600 October 16, then falling to 11,000; 
 polynuclears 47 to 62%, red, 4,560,000 to 6,088,000, some irregularity 
 of size and shape, considerable achromia; blood culture negative. 
 By September 6 the pulse had come down from 140 to 120 and 
 was regular. The electric flash light showed capillary pulsation 
 
246 FACTS ON THE HEART 
 
 in the finger tips. The liver dullness was only 1 cm. below the costal 
 margin. The edge was not felt. The left cardiac border was now 
 11cm.from midsternum. Systolic and presystolic murmurs replaced 
 the first sound at the apex, diastolic and systolic at the base, where 
 the pulmonic second sound was much increased and the aortic second 
 sound faint. No thrill was felt. September 1o the pulse was about 
 tro, and the child looked and felt better. | 
 
 By September 18 there was marked arrhythmia. There were 
 pauses of apparently two seconds, and some extra systoles. The 
 boy was nauseated, and the digitalis was stopped. By the time a 
 machine could be got to take a heart tracing the rate was perfectly 
 regular. This was repeated for several days, the rate being irregular 
 in the morning but becoming regular again in the afternoon. No 
 tracing could be obtained. September 22 there was systolic blowing 
 at the apex, and a diastolic, rough at the fourth left space and blow- 
 ing at the pulmonic area. 
 
 October 14 the boy began to gain. There were rales at the right 
 base which persisted until October 19, when the lungs seemed clear. 
 
 October 20 he seemed well until the evening, when he showed 
 signs of distress, did not respond to questions, and coughed hard. 
 The heart borders were 4.5 cm. to the right, 15 cm. to the left. There 
 were many coarse rales in the left base, a few at the right, but no 
 dullness. The cardio-hepatic angle was normal. Two days later 
 the cough was very troublesome. The respiration was diminished 
 at the left base, and there was a suspicious spot in the right axilla 
 with harsh respiration, increased voice, and rales. That morning 
 the boy was roused with great difficulty. In the afternoon he seemed 
 bewildered. During the next few days he vomited frequently. 
 
 November 5 the temperature was 98.6°, the pulse 120, the 
 respirations 30 ever since the night before. The child was feeling 
 very well and had been sitting up on the edge of the bed and enter- 
 taining the entire ward. The right cardiac border was 4 cm., the left 
 14 cm. For the next two weeks he continued to grow stronger and 
 more talkative. 
 
 November rg the respirations shot up to 52, and he again became 
 unwilling to speak. Nothing definitely wrong appeared during the 
 next week except two attacks of vomiting and the subnormal tem- 
 perature and unsteady pulse. November 27 the respiration was 
 nearly 60 and the pulse 154. The child continued to grow weaker. 
 December 8 his face and legs showed edema and there was fluid in 
 the abdomen. He seemed to be failing very rapidly. His heart 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 247 
 
 reached the midaxillary line. No precordial or pleural fluid was 
 found. December 15 his penis and scrotum became edematous. 
 He was very restless and coughed a great deal. That night he died. 
 
 Outcome.—The clinical diagnosis was myocardial insufficiency, 
 mitral and aortic insufficiency with possible stenosis, and general 
 anasarca. ‘The anatomical diagnosis was chronic and acute endo- 
 carditis of the aortic and mitral valves, hypertrophy and dilatation 
 of the heart, slight subacute glomerulonephritis, chronic passive 
 congestion, right hydrothorax, ascites, anasarca, and streptococcus 
 septicemia. 
 
 Dr. RicHARDSON: The head was not examined. 
 
 The body was limp, the lips purplish, and the skin very pale, 
 somewhat waxen in appearance. The hands were puffy and the 
 body and extremities pitted on pressure. The left side of the anterior 
 thoracic wall protruded slightly. The subcutaneous fat was in small 
 amount, the subcutaneous tissues wet and of a dull coppery color. 
 The muscles were of fair consistence and pale brown red. 
 
 The peritoneal cavity contained about 200 c.c. of thin pale clear 
 fluid. 
 
 The stomach and intestines showed well marked chronic passive 
 congestion. 
 
 The anterior margin of the liver was four finger breadths below 
 the costal border in the right mammillary line. The diaphragm 
 was at the fifth interspace on the right, the sixth rib on the left. 
 
 The right pleural cavity was half full of thin clear pale fluid. 
 The left pleural cavity contained a few cubic centimeters of similar 
 fluid. ‘There was no pleural adhesions. 
 
 There was a small portion of the thymus gland still present. 
 
 The trachea and bronchi showed a brownish-red mucosa and 
 contained much frothy brownish-red mucus. 
 
 The apices of the lung tissue showed well marked chronic passive 
 congestion. 
 
 The pericardium contained a few cubic centimeters of thin pale 
 clear fluid. The heart weighed 473 grams, greatly enlarged. The 
 myocardium was of good consistence and pale brown-red. The right 
 ventricle wall measured 4 mm., the left to mm. The columnae 
 carneae were fairly well marked. The cavities were enlarged. The 
 mitral valves presented a moderate amount of chronic endocarditis 
 and several minute to small patches of acute endocarditis. There 
 were minute similar masses scattered along the chordae tendineae. 
 The cusps of the aortic valve showed considerable chronic endocar- 
 
248 FACTS ON THE HEART 
 
 ditis. The cusps were fused about an opening 4mm. by6mm. The 
 endocardium just below the cusps showed a few minute patches of 
 acute endocarditis. The tricuspid and pulmonary valves - were 
 negative. The coronary artery was negative. The sino-auricular 
 node was negative. The foramen ovale was closed. The auricular 
 appendices were negative. The aorta and great branches, the 
 pulmonary artery, veins, venae cavae, and the portal vein and radicles 
 were negative. 
 
 The spleen showed chronic passive congestion. 
 
 The kidneys combined weighed 152 grams. The organs showed 
 a well marked chronic passive congestion and a slight amount of 
 subacute glomerulonephritis. 
 
 The culture from the heart blood showed a growth of an organism 
 of the streptococcus-pneumococcus group. 
 
 Necropsy 3715 
 
 A man of sixty-eight, formerly a caterer, for the past six years 
 unoccupied, entered March 12. His mother and father both died 
 of consumption. He had always had good health, though he had 
 never been strong. From the age of twenty-five to forty-five he 
 had ‘‘sick headaches” every three or four weeks associated with 
 vomiting and lasting a day. For twenty-three years he had had none. 
 He used to be nervous. Four years before admission he had one 
 convulsion or “‘fit.”” His eyes were “‘perfect.’’ He denied venereal 
 disease. 
 
 Five years before admission he began to have dyspnea on exertion. 
 He also had occasional dizziness fora month. He was told he had 
 heart trouble. The dyspnea persisted, so that he had been unable 
 to do hard work. Two months before admission he was obliged to 
 use three or four pillows. He had considerable gas and gastric 
 distress. Two weeks before admission he had a severe cold with 
 exacerbation of all the symptoms, marked orthopnea, obliging him 
 to sit up all night, and frequent night attacks of inspiratory “croup,” 
 with cough and considerable sputum. March g his ankles became 
 edematous. He was very weak and tired. : 
 
 Examination showed a fairly well developed, emaciated man with 
 dry, yellow skin and slightly cyanotic mucous membranes. The 
 apex impulse of the heart was seen and felt, strong and heaving, in 
 the sixth space 13.5 cm. to the left of midsternum, 4 cm. outside the 
 nipple line. The right border of dullness was 4 cm. to the right, 
 the supracardiac dullness 4 cm. ‘The percussion measurements 
 
 we 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 249 
 
 are shown in Fig. 46. Theaction wasnormal. The pulmonic second 
 sound was faint, the aortic second was not heard. The first sound 
 was replaced by a loud low-pitched blowing systolic murmur loudest 
 at the apex and the aortic area, transmitted to the vessels of the neck 
 and slightly to the axilla. A softer diastolic was heard at the apex, 
 at the left border of the sternum, and very faintly at the aortic area. 
 There was no thrill. The pulses were normal. The blood pressure 
 was 145/65. The lungs showed a few fine crackles above the angle 
 of the left scapula. Below this and extending to the base were 
 marked dullness with diminished breathing, whisper, and tactile 
 fremitus; no rales. Near the angle of the right scapula was a small 
 area over which all signs were increased. The spine showed marked 
 left dorsal structural scoliosis. The abdomen was normal except 
 that the bladder was two finger-breadths above the symphysis and 
 a sharp liver edge was felt at the costal margin. Recta] examination 
 showed the prostate somewhat enlarged, the left lobe more than the 
 
 as 
 fe) 
 B 
 
 Was Cis 
 
 Midsternal 
 . Nipple — 
 Midsternal 
 
 4 cm. 9.5 cm. 5 cm. 4 cm. 9.8 cm, 
 
 18.5 cm. 13.8 cm. 
 Fic. 46.—Measurements by percussion. Fic. 47.—Measurements by X-ray.’ 
 
 right. The bladder was full and slightly tender. The genitals 
 were otherwise negative. The legs showed slight edema to the knees. 
 The pupils were irregular. The left was fixed; the right was con- 
 tracted, but reacted to light and distance. 
 
 The temperature was 98°, the pulse 78, the respiration 24. The 
 urine occasionally showed a little albumin. The hemoglobin was 
 80%, the leucocyte count 7700. A Wassermann was negative. 
 The stools gave a positive guaiac at one of two examinations. The 
 renal function March 14 was 10%, March 21 55%. A lumbar 
 puncture gave ro c.c. of fluid, at first slightly blood-tinged, not 
 under increased pressure; no cells. The blood nitrogen was 40 mgm. 
 per 100 c.c. of blood. X-ray showed enlargement of the left side of 
 the heart and dilatation of the arch. (See Fig. 47.) 
 
 __ The patient was put on constant drainage. He showed little 
 change except that the systolic blood pressure rose to 170 and the 
 diastolic to 70, and that he grew progressively weaker. March 30 
 his abdomen became distended and he died. 
 
250 FACTS ON THE HEART 
 
 Clinical Diagnosis (from Hospital Record).—Aortic regurgitation. 
 Hypertrophy and dilatation of the heart. 
 
 Arteriosclerosis. 
 Urethritis. 
 Cardiac failure. 
 
 > 
 
 eu ee as 
 
 (Actual size.) Aortic stenosis in a man 
 
 Fic. 48.—‘‘ Fish-mouth”’ aortic valve. 
 (Photograph by Lewis S. Brown. Dr. 
 
 of sixty-eight. No history of rheumatism. 
 Oscar Richardson.) 
 
 Epididymitis. 
 
 Dr. William H. Smith's Diagnosis Probably arteriosclerosis 
 involving the arch. 
 
 Hypertrophy of the heart. 3 
 
 Passive congestion of the liver and kidneys. , : 
 
AORTIC STENOSIS. ILLUSTRATIVE CASES 251 
 
 Arteriosclerotic degeneration of the kidneys. 
 
 Dilatation of the bladder. 
 
 Anatomical Diagnosis.—Chronic endocarditis of the aortic valve. 
 Stenosis. 
 
 Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Slight chronic interstitial myocarditis. 
 
 Slight chronic passive congestion, general. 
 
 Hydrothorax, slight. 
 
 Hydropericardium, slight. 
 
 Focal pneumonia, lower lobe of the left lung, with small abscess. 
 
 Serofibrinous pleuritis, left. 
 
 Suppurative nephritis. 
 
 Infarcts of the spleen. 
 
 Abscess of the left epididymis. 
 
 Obsolete tuberculosis, apices of lungs. 
 
 Slight chronic pleuritis. 
 
 Dr. RicHARDSON: This is a perfectly typical case of aortic stenosis, 
 the result of an infection a great many years ago. ‘The arteriosclero- 
 sis and aortic stenosis have caused the hypertrophy and dilatation 
 of the heart. The heart weighed 456 grams, (normally 200-300); 
 in other words, it was considerably enlarged for a man of his size. 
 The valve circumferences were interesting in this case. The aortic 
 was a small slit. The mitral measured 10 cm., the tricuspid 13, and 
 the pulmonary 7 cm.; all three were negative. There was some 
 arteriosclerosis of the coronary arteries, and a few small scattered 
 areas of myocarditis. By myocarditis we do not mean myocardial 
 weakness, but the definite replacement of heart muscle by fibrous 
 tissue. The aorta and the great branches showed arteriosclerosis. 
 We have, then, the old infectious process ending in stenosis, and the 
 added arteriosclerotic process. There was moderate dilatation 
 of the left ventricle and slight of the left. auricle. The right ventricle 
 was negative and the right auricle slightly dilated. The aortic orifice 
 presented as a small crevice-like slit with irregular margins, about 214 
 cm. long, what I call the fish-mouth valve. (See illustration.) 
 
 The spleen showed a few infarcts. How did these get there? 
 They seemed rather recent. I think that they were septic. 
 
 The kidneys were infected. Unfortunately our culture in this 
 case was contaminated. With suppurative processes in the kidneys 
 we are more inclined to think of the staphylococcus aureus as being 
 the organism, but sometimes the abscesses are produced by organisms 
 
252 FACTS ON THE HEART 
 
 belonging to the streptococcus-pneumococcus group or the colon 
 group. In arteriosclerotic conditions the kidneys, as a rule, are apt 
 to be rather large, and there may be more or less arteriosclerotic 
 nephritis. As a matter of fact it is often astonishing in examining 
 the kidneys of elderly men to find how good they are. The kidneys 
 in this case had fair cortex and good tissue generally, but scattered 
 through them were the abscesses which probably caused the low renal 
 function. 
 
 In the prostate, in the region of the so-called middle lobe, there 
 was a small nodule-of prostatic tissue which obstructed the urethra 
 slightly. The epididymis showed an abscess which was a part of the 
 expression of the infection. 
 
 In the region of the apex of each lung was an area of obsolete 
 tuberculosis. There was nothing in the bronchial lymphatic glands. 
 It is more common perhaps to find these obsolete areas of tuberculosis 
 in the glands than at the apices. Sometimes you find them in both 
 places, and again you find them scattered through the lungs, but as 
 a rule the preferred seat is in the bronchial lymphatic glands. The 
 right lung showed some chronic passive congestion, the area of obso- 
 lete tuberculosis, and nothing else. In the left lung the focus of 
 pheumonia was situated in the region of the lower third of the lower 
 lobe, and in one place showed a small abscess. The pleura over the 
 focus of pneumonia showed sero-fibrinous pleuritis. 
 
 This case shows very well indeed the end results of acute infections 
 occurring years ago and a terminal infection finding expression in the 
 lung, spleen, kidneys and epididymis. 
 
 PURE AORTIC REGURGITATION WITHOUT STENOSIS 
 (RHEUMATIC TYPE) 
 
 The rheumatic form of aortic disease ordinarily produces adhe- 
 sions of the cusps in such a form that s/enosts as well as insufficiency is 
 the result. This has been the case in the forty cases of combined 
 mitral-and-aortic disease and in the twenty-eight cases of pure aortic 
 disease already analyzed in Chapter II. On the other hand, syphilis 
 (in forty-four cases analyzed under Chapter III) produces aortic 
 regurgitation without stenosis, although there were also three cases in 
 
 that series of ninety-two in which syphilitic aortitis and aortic ~ 
 
 stenosis coexisted, and in which the stenosis may have been due to 
 the syphilis, though as I there point out, it is quite possible that 
 syphilitic aortitis might be engrafted upon an earlier rheumatic 
 lesion of the aortic valve, or that the reverse sequence might take 
 
PURE AORTIC REGURGITATION WITHOUT STENOSIS 253 
 
 place. But at any rate, in the overwhelming majority of cases, the 
 rule is: 
 
 Syphilis Produces Pure Aortic Regurgitation While Endocarditis 
 Produces Stenosis and Regurgitation at the Aortic Valve.—This 
 statement is contradicted by 11 cases in this series (see Table 72). 
 Seven of these are essentially of the ulcerative, acute, destructive 
 type. In only six of them a rheumatic history is clear. But as I 
 have been unable to make a clear separation between the rheumatic 
 group and the other types of infection of heart valves, there does not 
 seem any good reason for insisting upon this distinction here. All 
 that can be said is that the rule already formulated: ‘“‘rheumatism 
 produces combined aortic stenosis and regurgitation, syphilis gives 
 regurgitation alone” is contradicted by only 6 cases out of 93 in 
 this series, if we confine our attention to cases of chronic valve lesions. 
 It is chiefly when acute endocarditis 1s present that there has been an 
 exception to this rule in our series. Even including the ‘‘acute”’ 
 cases it remains true that in 87 cases out of 93, or 93%, the recogni- 
 tion of an aortic regurgitation supposedly due to endocarditis has 
 meant that we should assume the presence of stenosis as well as 
 regurgitation, whether we have the physical signs of the former or 
 not. The eleven exceptional cases I give below in detail. 
 
 These. cases do not differ in clinical essentials from the twenty- 
 eight cases of pure aortic stenosis and regurgitation just discussed. 
 There we found twenty-five men to three women. Here we find 
 eleven men and no women at all. Half of the cases in each group 
 (five of eleven and fifteen of twenty-eight) are beyond the fiftieth 
 year. There is one very large heart among the eleven (1205 grams), 
 the hypertrophy produced chiefly, I believe, by the associated 
 chronic pericarditis. One other heart in this group is also much 
 enlarged (778 grams), and all show some hypertrophy. Ten out of 
 eleven died a congestive death, associated with sepsis in six and with 
 angina in two. Angina was the sole cause of death in another case 
 free from passive congestion. 
 
 A diastolic murmur was recognized in every case but one, a 
 presystolic also in three. Systolic murmurs were invariably present. 
 Corrigan’s pulse was recorded in six cases, diminution or absence 
 of the aortic second in seven. But strange to say, an accented aortic 
 sound is recorded in three cases. In the six cases free from acute 
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256 FACTS ON THE HEART 
 
 Does Arteriosclerosis Ever Produce Aortic Regurgitation ?—In 
 the entire series of cases analyzed in this book, that is in the post- 
 mortem examinations extending from October 1896 to November 
 1919, our pathologists recorded but one case, Necropsy 1277, as 
 ‘‘atheromatous endocarditis of the aortic valve with aortic insuffi- 
 ciency.” In this case “the aortic cusps and sinuses are larger than 
 normal. ‘Two of the cusps are to some extent fused together and at 
 the point of fusion there is much thickening and some calcification. 
 These cusps also show some fibrous thickening in places, and the 
 remaining cusp shows an irregular nodular thickening.” ‘This patient 
 had no history of syphilis or of rheumatism, and showed no lesions 
 suggesting either of these diseases. He exhibited for seven weeks 
 before his death the usual evidence of decompensated heart trouble. 
 In the hospital! he lived but five days. There was an apical systolic 
 murmur; a diastolic murmur was heard all over the precordia, loud- 
 est in the fourth left interspace near the sternum. ‘The aortic and 
 pulmonic second sounds were of equal intensity. Corrigan’s pulse 
 was present. 
 
 He had a generalized arteriosclerosis and a heart weighing 870 
 grams. There was a slight chronic fibrous endocarditis of the mitral 
 valve, described as follows: ‘The valve is but a little deformed. At 
 one point near its edge there is considerable thickening and some puck- 
 ering over a restricted area. The chordae tendineae associated with 
 this are markedly thickened.” The circumference of the aortic 
 valve was 9 cm.,of the mitral 10.5cm. Theleft ventricle was 20mm., 
 the right 5. All the cavities were dilated. There was chronic fibrous 
 myocarditis, general passive congestion, and anasarca. 
 
 I follow here the practice to which I have adhered throughout 
 this book, that is, I submit to the pathologist’s judgment as the 
 fundamental basis of classification. But it is certainly striking that 
 in this whole series only one case was found by our pathologists 
 to illustrate the common belief that arteriosclerosis can produce dis- 
 ease of the aortic valve. In view of the very great commonness of 
 arteriosclerosis in our series it is strange that it should affect the 
 aortic valve so seldom, if it is capable of producing this effect at all. 
 From the description of the valves, in the absence of any microscopic 
 examination, I can quite see how a view contrary to that of our 
 pathologists might be maintained. On the records as I accept them, 
 however, the figures about aortic regurgitation stand as follows: 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 257 
 
 TABLE 73.—TyprEs oF Aortic DISEASE 
 
 CASES 
 Endocarditic type, stenosis and regurgitation................ 93 
 Endocarditic type, regurgitation alone (some acute)......... FI 
 syphilitic type, aortic regurgitation alone................... 44 
 Syphilitic type, stenosis and regurgitation................... 3 
 Arteriosclerotic type (?), regurgitation alone................ I 
 
 152 
 
 SUMMARY 
 
 t. Possibly the absence of a thrill in the aortic area may give some 
 clue to the diagnosis of this rare condition. In other respects it is 
 essentially like the usual rheumatic lesions of the aortic valve. 
 
 2. The rule borne out to some extent in all the different aortic 
 lesions—that males greatly predominate—is strikingly emphasized 
 in this small group: eleven males, no females. 
 
 3. The heart is enlarged in all the cases, markedly so in nine out of 
 eleven. 
 
 4. A diastolic murmur was heard in ten cases; a presystolic also 
 (“Flint murmur”’) in three. 
 
 5. Corrigan’s pulse was present in six, absent in three, not 
 noted in two. 
 
 6. Death was of the congestive type in ten of eleven cases. 
 But in four of these there was manifestation of general septicemia as 
 well, due to the accompanying acute endocarditis. In three other 
 cases sepsis seemed to be the main cause of death, while angina was 
 apparently the chief lethal factor in one case. 
 
 7. Blood pressure was unfortunately not recorded in eight of the 
 eleven cases. In all the rest, systolic pressure was high and in two 
 of these three the diastolic was also high. No reason for this is 
 apparent. 
 
 8. A single case of aortic regurgitation is recorded by the patholo- 
 gist as apparently of arteriosclerotic origin, though he does not 
 feel quite certain of this. Against this we have 104 cases of aortic 
 regurgitation due to endocarditis, and forty-seven due to syphilis, 
 so that the arteriosclerotic (?) case is in a minority of one out of 152. 
 
 PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 
 Necropsy 819 
 An engineer of fifty came to the hospital in August for relief of 
 
 hemorrhoids of twenty-five a standing. He gavea HIStory also 
 
 of painless jaundice of a year’s duration. 
 17 
 
258 FACTS ON THE HEART 
 
 Examination showed a well nourished man with dull anemic 
 yellow skin and pale mucous membranes. The apex impulse of the 
 heart was in the fifth space just outside the nipple line. . There was 
 a high pitched short musical diastolic murmur, loudest over the 
 pulmonic area, transmitted upward, across the sternum and into 
 the mitral area. The pulse was Corrigan. The liver edge was pal- 
 pable on inspiration. On deep pressure there was some tenderness 
 in the lower epigastrium in the median line. The blood showed 
 marked secondary anemia. 
 
 The hemorrhoids and prolapsed rectum were cauterized. The 
 patient made a good convalescence and was discharged eleven days 
 after operation ‘‘ well.”’ 
 
 January 16, five months later, he reentered for relief of a skin 
 _ eruption. He now gave a history of the death of a brother and a 
 sister from phthisis. He had had the diseases of childhood, scarlet 
 fever, pneumonia, gonorrhea at seventeen and three or four later 
 attacks, the last two accompanied by soft chancres and buboes in 
 each groin. He had rheumatic fever at eighteen. Two years before 
 admission he had shingles. two months before admission he had 
 nasal catarrh. He drank a glass of whiskey daily. A little over a 
 week before admission, after having a few itching pimples on his 
 chest for a few days, blisters appeared on his lips. The following day 
 blisters appeared all over the body. There was not much itching 
 except from the few lesions on the chest. His nasal catarrh became 
 worse. He had no appetite, was very thirsty, and felt sore all over. 
 For two days his legs had been very stiff. 
 
 His skin and mucous membranes were now of good quality. 
 The uvula was somewhat enlarged. The pharynx was reddened. 
 There was an expiratory rub in the left lower axilla and back. The 
 intercostal spaces were wide and separated. The apex impulse 
 of the heart was in the fifth space 414 inches from the median line. 
 The right border of relative dullness was 7% of an inch to the right of 
 the median line. The action was regular, the sounds of good quality. 
 At the apex was a systolic murmur transmitted slightly into the axilla. 
 Over the aortic area was a systolic murmur, loudest in the third left 
 interspace and transmitted down to the apex. In addition to the 
 Corrigan pulse there was visible pulsation in the brachials and caro- 
 tids, with capillary pulse in the finger nails. Nothing abnormal was 
 found in the abdomen. The under surface of the foreskin showed 
 scars. Widely distributed over the entire body, except the hands 
 and feet, was a discrete eruption of sharply defined circular lesions 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 259 
 
 varying from the size of a pinhead to an inch in diameter. In places 
 they were confluent in very large areas. Small areas were elevated 
 and hemorrhagic, firm but not painful. After reaching about a 
 quarter inch in diameter the areas became blebs in the center, 
 vesiculation spreading to the periphery, the center drying as the 
 vesiculation spread. On rupture the vesicles discharged clear sticky 
 fluid. The face was not affected, but the scalp showed many lesions 
 resembling those on the body. 
 
 During his ten days’ stay in the hospital the patient had a tem- 
 perature of 99° to 103.6° with the exception of one drop to 96.7° 
 January 21 and a terminal drop to 97°. The pulse was 88 to 110. 
 The respirations were not remarkable. The urine was smoky, 
 specific gravity 1.018-1.021, albumin 49 % to a trace at both 
 examinations, frequent fresh and decolorized red blood corpuscles, 
 occasional fine and coarsely granular casts at one, occasional fine and 
 brown granular casts and casts with adherent fat drops and blood at 
 the other. The hemoglobin was 85%, the leucocytes 23,000. 
 
 The patient felt very well for the first two days except for the 
 irritation due to the eruption, which seemed to fade in places, though 
 a few new spots appeared. He grew weaker, did not retain enemata 
 and January 26 died. His heart continued to beat for some time 
 after the respirations had ceased. 
 
 The clinical diagnosis was dermatitis multiformis. 
 
 Necropsy showed: 
 
 Extensive superficial losses in the epidermis of the head, trunk, 
 and extremities. Acute and chronic endocarditis of the aortic and 
 mitral valves. 
 
 Hypertrophy and dilatation of the heart. 
 
 Hydropericardium. 
 
 Small area of ecchymoses in the visceral pericardium. 
 
 Ecchymoses in the mucosa of the stomach. 
 
 Parenchymatous hemorrhages in the kidneys. 
 
 Hyperplasia of the spleen. 
 
 Hemorrhagic edema of the lower lobes of the lungs. 
 
 Old pleural adhesions of the left lung. 
 
 Edema piae. 
 
 Interstitial orchitis of the right testicle. 
 
 Right inguinal hernia. 
 
 Necropsy 1020 
 
 A meat cutter of forty-two entered November 11. His family 
 history was good. He had measles, mumps, scarlet fever and 
 
260 FACTS ON THE HEART 
 
 typhoid fever in childhood, and at twenty-two pneumonia and rheu- 
 matic fever of eight months’ duration and a chancre followed by 
 sore mouth and throat with loss of hair. He had gonorrhea once. 
 He drank all the gin he could get, about ten glasses daily. Fora year 
 and a half he had been troubled a good deal with gas. He was 
 almost always nauseated in the morning and occasionally vomited. 
 Six weeks before admission he became very short of breath and unable 
 to lie down, his appetite failed, and he vomited almost every morning. 
 Three weeks before admission his legs swelled, and a week later his 
 face became puffy. He coughed much, especially at night, raising a 
 good deal of white mucus. Recently he had passed little urine. 
 
 Examination showed a well nourished man with a flushed face. 
 The mucous membranes were slightly pale. The throat was reddened 
 and showed considerable mucus. There were frequent sonorous 
 and sibilant rales scattered throughout the lungs. The breathing 
 was labored. The heart sounds were best heard in the fifth space 
 in the nipple line. The left border of dullness was five inches to the 
 left of the median line, one half inch outside the nipple. The right 
 border of dullness was two inches to the right. The sounds were of 
 fair quality, the action somewhat irregular. The pulmonic second 
 sound was accentuated. There was a double first sound at the apex 
 followed by a systolic murmur heard also in the axilla. A slight 
 diastolic murmur was heard at the second and third right interspaces. 
 At the apex there was a suggestion of a presystolic roll. The pulses 
 were of rather high tension, otherwise normal. The abdomen was 
 tympanitic except for dullness in the flanks shifting with change of 
 position. A fluid wave was present. The liver dullness was from 
 the sixth rib to two inches below the costal margin in the nipple line. 
 The edge was indistinctly felt. The spleen apparently was not 
 enlarged. There was edema of the genitals and much brawny edema 
 of the feet and ankles. The right pupil was greater than the left; 
 both reacted. The knee-jerks were slight, the plantars normal. 
 The temperature was 97.2° to 103.3°, the pulse 142 to 105, the respi- 
 rations 40 to 20. The output of urine was ten to twelve ounces, the 
 specific gravity I.020-1.024. There was a large trace to a very 
 slight trace of albumin at both of two examinations. The single 
 sediment examination showed many hyalin casts with oil globules 
 adherent, numerous finely granular and occasional coarsely granular 
 casts. . 
 
 February 13 only the diastolic murmur in the aortic area remained. 
 The heart was still rapid and irregular. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 201 
 
 The night of February 14 the temperature rose to 102° with no 
 discoverable cause. At the right base there were numerous fine 
 moist rales. February 17 the heart sounds were weak, the action 
 slow. The temperature was still elevated. That day the patient 
 died. | 
 
 Clinical Diagnosis.—Aortic regurgitation. 
 
 Broken compensation. 
 
 Pneumonia. 
 
 Dr. Maurice Fremont-Smith’s Diagnosis.—Cirrhosis of the liver, 
 alcoholic or syphilitic. 
 
 Probably syphilis of the aortic valve and aorta. 
 
 Cardiac failure. 
 
 Anasarca. 
 
 Terminal pneumonia. 
 
 Possibly tuberculosis of the lungs. 
 
 Chronic passive congestion of the kidneys. 
 
 Anatomical Diagnosis.—Chronic endocarditis of the aortic valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the lungs, liver, spleen, kidneys, 
 stomach and intestines. 
 
 Hydrothorax, double. 
 
 Ascites. 
 
 Anasarca. 
 
 Chronic perihepatitis. 
 
 Chronic perisplenitis. 
 
 Anomaly of the right kidney. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 _ The muscles were pale and wet. A moderate amount of ascites was 
 present. The gastro-intestinal tract was negative except for passive 
 congestion. 
 
 There was marked chronic perisplenitis and perihepatitis, but no 
 cirrhosis of the liver. There was well marked chronic passive 
 congestion. 
 
 The aorta was smooth. 
 
 There was considerable thin brownish fluid in the pleural cavities, 
 and a few old adhesions about the right lung. The lungs were 
 rather voluminous, rather solid and spongy to leathery, showing 
 a well marked salmon color, and in the case of the right one, the 
 lower half of the upper lobe was so much firmer than usual and gray- 
 ish that I thought it was pneumonia. It was simply chronic passive 
 congestion. 
 
262 FACTS ON THE HEART 
 
 There was a slight excess of fluid in the pericardium. The heart 
 was considerably enlarged and there was considerable dilatation of 
 all the cavities. The mitral valve was negative. The aortic cusps 
 however generally showed some fibrous thickening and deformity 
 and on one of them there was a rather large thick patch, fibrous to 
 fibrocalcareous, more or less degenerated, and at one point a small 
 ulceration,—a chronic endocarditis of the aortic valve with ulceration. 
 
 The liver showed marked chronic perihepatitis and the spleen 
 marked chronic perisplenitis, otherwise they showed chronic passive 
 congestion. 
 
 Here again we find variation in the weight of the kidneys. In 
 some instances, here at least, there is considerable variation in the 
 weight of the kidneys. One can be very much smaller than the 
 other and have nothing else the matter with it. The individual was 
 born with one kidney small, the other larger. It was so in this case. 
 The right kidney was the smaller one. In addition there was some 
 arteriosclerotic degeneration, a few foci of atrophy, but other than 
 for this and the passive congestion the kidneys were negative. 
 The ureters, bladder and prostate on section were negative. ‘The 
 testes were negative. 
 
 No organism was recovered from the heart culture. 
 
 Dr. FREMONT-SMITH: Did you find any sign that he had ever had 
 syphilis? 
 
 Dr. RICHARDSON: No. 
 
 Necropsy 1107 
 
 A teamster of twenty-five entered July 24. Five years before 
 admission he had gonorrhea. Seven months before admission he had 
 pleurisy and pneumonia followed by rheumatism in the shoulder, 
 knees and feet. He was in a Boston hospital for two months. A 
 month after leaving the hospital he noticed shortness of breath, 
 palpitation, and cough with frothy sputum, occasionally accompanied 
 by attacks of vomiting. Three weeks before admission he noticed 
 swelling of the feet, two weeks later swelling of the abdomen. ‘The 
 symptoms gradually increased until the day before admission, when 
 he suddenly became much worse and on reaching home had to go to 
 bed. The chief complaint was dyspnea. He was also troubled with 
 a feeling of distension in the upper abdomen. The night before 
 admission he was not able to lie down, and slept very little. His 
 appetite was poor. In the past twenty-four hours he had taken only 
 milk. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 263 
 
 Examination showed a well nourished man with brownish-yellow 
 skin and pale mucous membranes. The apex impulse of the heart 
 was in the sixth space four and a half inches to the left of the median 
 line. The right border of dullness was two and a half inches to the 
 right. The sounds were somewhat weak, the action regular. The 
 pulmonic second sound was accentuated. In the aortic area and 
 over the third and fourth left cartilages was heard a high pitched 
 diastolic murmur. The pulse was regular, of large volume, and ill 
 sustained. There was capillary pulse. Pistol shot was heard in 
 the groin. The systolic blood pressure was 160. The lungs were 
 negative except for an occasional sonorous rale. The abdomen was 
 tensely distended in the lower portion, soft above the umbilicus. 
 There was considerable tenderness in the right upper quadrant. 
 There was a fluid wave. The liver dullness extended from the fifth 
 space to two inches below the ensiform in the median line, where the 
 edge was felt. There was considerable edema oi the legs. The 
 pupils were normal. The knee-jerks were lively. The temperature 
 was 97.9 to 102°, the pulse 81 to 130, the respirations 24 to 50. 
 There were fourteen to seventy ounces of urine daily, the specific 
 gravity 1.013—1.016, turbid at one of three examinations, high colored 
 at the other two, a slight trace to a trace of albumin atall. At the 
 single sediment examination there were a few abnormal red blood 
 corpuscles. The hemoglobin was 65%, the leucocytes 8700. The 
 fundi were normal. 
 
 The dyspnea continued severe through the day of entrance. 
 Afterwards it diminished. The fluid in the abdomen increased 
 through the day of entrance, but two days later was somewhat 
 less. The chief complaint July 26 was hemorrhoids, which were 
 tense and thrombosed. The heart action was much stronger. A 
 marked presystolic murmur was heard at the apex. July 29 the 
 hemorrhoids were incised with ethyl chlorid and clots partially 
 removed. After this the patient complained less of pain. By 
 August 1 the presystolic murmur had disappeared at the apex. 
 The diastolic persisted, and a marked systolic was heard in the aortic 
 area, transmitted to the neck. The dyspnea and cough were less. 
 The patient was constantly drowsy and complained of weakness. 
 The following night he had an attack of nausea and repeated vomit- 
 ing. The fluid in the abdomen increased. Under digitalis the condi- 
 tion rapidly improved until the night of August 10, when the dyspnea 
 became severe but was somewhat relieved by oxygen. Edema of 
 the legs and scrotum, dyspnea and malaise increased. He had dis- 
 
264 FACTS ON THE HEART 
 
 comfort in the epigastrium, pain in the left’shoulder radiating down 
 the left arm, and numbness in the left hand. August 19 Southey’s 
 tubes were inserted in the left leg. They failed to withdraw much 
 fluid. The next day the respirations became considerably more 
 rapid and the pulse and temperature rose. The patient became 
 delirious. The morning of August 21 he died. 
 
 Clinical Diagnosis (from Hospital Record) —Aortic regurgitation. 
 Hemorrhoids. 
 
 t. Anatomical Diagnosis —1. Primary fatal lesion. 
 
 Chronic endocarditis of the aortic valve (with regurgitation 
 and probably some obstruction). 
 
 2. Secondary or terminal lesions. 
 
 Hypertrophy and dilatation of the heart. 
 Septicemia (pseudopneumococcus). 
 Lobar pneumonia of upper lobe of right lung. 
 Chronic passive congestion of the lungs, liver and spleen. 
 Anasarca. 
 Ascites. 
 Hydropericardium. 
 Edema of the kidneys. 
 3. Historical landmarks. 
 Small accessory spleen. 
 Arteriosclerotic patch in aorta. 
 Infarcts of the spleen and kidneys. 
 
 Dr. RIcHARDSON: A well developed and nourished white man. 
 We were not permitted to examine the head. There was anasarca, 
 ascites, and hydropericardium, no definite hydrothorax. On the 
 left side there was a small amount of pale clear fluid in the pleural 
 cavity, on the right a small amount of cloudy fluid and fibrin and a 
 thin coating of exudate. The lungs generally showed chronic passive 
 congestion, but the upper lobe of the right Jung, about two-thirds of it, 
 showed frank pneumonia. The organism is what we called in those 
 days the pseudopneumococcus, now known as the streptococcus 
 mucosus capsulatus. This was one of the first cases in which I 
 recovered it from a case of pneumonia. 
 
 The heart weighed 778 grams,—markedly enlarged. The only 
 lesions on the valves were those of the aortic valve, where there was 
 a polypoid mass of chronic endocarditis. 
 
 In the spleen and the kidneys were infarcts. The liver showed 
 chronic passive congestion. The kidneys, although they weighed 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 265 
 
 415 grams, which of course is a considerable weight, showed nothing 
 but edema, no evidence of any glomerulo-nephritis. 
 
 I recovered from the heart blood the organism mentioned above. 
 
 Dr. CaBotT: Will you tell us a little more about the aortic valve? 
 
 Dr. RICHARDSON: In the situation of the free edges of the cusps 
 and at their points of juntion there is a row of irregularly rounded 
 yellowish tag-like masses, the largest about one cm. in greatest 
 dimension. At one point there extends down from the junction of 
 two of the cusps on to the endocardium a grayish-yellow, fibrous, 
 somewhat shaggy, firmly adherent patch of material. The material 
 of these masses in the situation of the aortic cusps'is slightly soft in 
 places, but on section it isin many places finely calcareous in character. 
 
 Dr. CasotT: So that is all chronic, no acute? 
 
 Dr. RICHARDSON: Yes, all chronic. There was some question, 
 but the histology showed the same thing. 
 
 Dr. Casor: Was there any stenosis? 
 
 Dr. RICHARDSON: The circumference was eight cm.; no stenosis 
 in one sense, but the mass when the valve closed would leave less 
 room for the blood to go through. 
 
 Dr. FREMONT-SMITH: What can we call the etiology? This is 
 not a typical rheumatic chronic endocarditis. 
 
 Dr. RicHAaRDSON: Yes, I should think it was rheumatic chronic 
 endocarditis. 
 
 Necropsy 1345 
 
 A colored houseman of thirty-three entered March 24. He gave 
 a history of boils in childhood, whooping cough, gonorrhea years 
 earlier, a sore on the penis twelve years before admission, and an 
 attack of ‘‘rheumatism”’ the previous winter. His habits were good. 
 Three months before admission he began to have heavy dull ache 
 across the upper abdomen and dyspnea on exertion. The ache 
 persisted and the dyspnea grew steadily worse until at admission it 
 was continuous and at times he had to sit up to get his breath. 
 During the past two months he had cough and raised a great deal of 
 bloody sputum. For the past month his legs had been swollen. He 
 had some palpitation, slept poorly, had little appetite, and during 
 the past week had vomited food immediately after eating. He had 
 been using salts with small movements. For four weeks he had been 
 unable to work and for three weeks had been in bed. 
 
 The examination showed a well nourished man with cyanotic 
 mucous membranes. His throat was covered with mucus. The apex 
 impulse of the heart was felt in the sixth space five inches to the left 
 
266 FACTS ON THE HEART 
 
 of the midline. The left border of dullness was four inches (?) to the 
 left. The right border of dullness was an inch and a half to the right 
 of the median line. The action was rapid. The pulmonic second 
 sound was accentuated, the aortic second sound absent. A short 
 soft systolic murmur and a soft diastolic murmur were heard at the 
 apex, a loud diastolic and a systolic all over the precordia, loudest at 
 the third left interspace. There was a diastolic murmur in the 
 aortic area and also in the back. There was Corrigan pulse, pistol 
 shot and Duroziez’s sign. ‘The lungs showed slight dullness at both 
 bases and medium moist rales throughout, more numerous at the 
 bases. Expiration was prolonged and harsh. There was slight 
 shifting dullness in the flanks and general tenderness throughout the 
 abdomen, more marked over the liver, which extended to three inches 
 below the costal margin, where the edge was felt in the mammillary 
 line. The splenic dullness was not made out. The edge was indis- 
 tinctly felt. A few bean-sized glands were felt in the axillae and 
 groins. The pupils were normal. The knee-jerks were unsatis- 
 factory, the plantars normal. There was marked edema of the 
 ankles, legs and thighs. ‘There was a subcutaneous mass, four by six 
 inches, over the lower ribs in the left back. | 
 
 During his twelve days in the hospital the temperature gradually 
 rose from 97.1° to 103.2°.. The pulse ranged from ror to 135, the 
 respirations from 16 to 39. The urine was from 34 to g2 ounces, 
 specific gravity I.012—-1.016, a slight trace to the slightest possible 
 trace of albumin at all of three examinations, a rare blood cell at one. 
 The hemoglobin was 100%, the leucocytes 14,000 to 19,300. 
 
 The patient failedfrom admission. After the first day the sputum 
 was almost pure blood. No localizing sign of an infarct could be 
 found. The edema of the legs and genitals increased. March 29 
 there was a patch of bronchial breathing just below the angle of 
 the right scapula which increased, extending to the midscapula by 
 April 3. That day, after he had been delirious for several days, 
 he died. 
 
 Clinical Diagnosis.—Aortic roughening. © 
 
 Aortic and mitral regurgitation. 
 
 Failing compensation. 
 
 Possible pericarditis. 
 
 Chronic passive congestion. 
 
 Infarcts of the lungs and bronchopneumonia. 
 
 Anatomical Diagnosis —Marked fibrous endocarditis of the aortic 
 valve and slight fibrous endocarditis of the mitral valve. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 267 
 
 Hypertrophy and dilatation of the heart. 
 
 Focal pneumonia. 
 
 Hemorrhagic edema and infarcts of the lungs. 
 General chronic passive congestion. 
 
 Anasarca. 
 
 Hydropericardium. 
 
 Ascites. 
 
 Chronic perisplenitis and hepatitis. 
 Streptococcus septicemia. 
 
 Foci of necrosis in the fat tissue of the pancreas. 
 
 Necropsy 2288 
 
 A musician of twenty-nine entered January 20, 1909. 
 
 He formerly had taken a good deal of whiskey and beer and had an 
 occasional spree. His past history was negative except for indefinite 
 rheumatic pains in the calves of his legs at times and an attack of 
 pneumonia the previous November. A week after he thought he was 
 entirely over this, a cough developed which persisted. He had 
 remained weak, tired, and unable to work, or to sleep without three or 
 four pillows, as he choked up and coughed when lying flat. 
 
 Five weeks before admission he began to be very short of breath, 
 especially on exertion. Three weeks ago he was obliged to sleep for 
 several nights in a chair, and afterwards often had to finish the night 
 inachair. Hehad very little cough. For ten days his abdomen had 
 increased steadily in size. For a week his legs had been edematous. 
 The dyspnea had now become extreme. 
 
 Examination showed a well nourished man, orthopneic, with 
 short hacking cough and husky voice. Skin pale and pasty. 
 Mucous membranes cyanotic. Fingers markedly clubbed. Nails 
 rounded and very cyanotic. Considerable throbbing of arteries in 
 supraclavicular space and in neck. Apex impulse of the heart and 
 left border of dullness in the fifth space 2! inches outside the nipple 
 line, 614 inches to left of midsternum. Right border of dullness 134 
 inches to the right. Action very irregular in force and rhythm. At 
 the apex three sounds equidistant from one another followed by a 
 pause. The P2 sharp and greater than Az. Loud harsh blowing 
 diastolic murmur heard best in third space just to left of sternal edge, 
 transmitted upward and toward the apex but not toit. At the apex 
 a soft blowing systolic murmur occupying the greater part of the first 
 two sounds at the apex and the single systole elsewhere (but to a less 
 marked degree) and transmitted to the axilla, where it was heard 
 
268 FACTS ON THE HEART 
 
 better that over the cardiac area. Pulses of fair volume, low tension, 
 Corrigan. Double sharp booming sounds heard over femorals. 
 Blood pressure not recorded. Arteries palpable and _ sclerosed. 
 Dullness, diminished respiration, voice sounds and fremitus, many 
 fine and medium moist rales at both bases posteriorly, more extensive 
 on the right. Abdomen full. A transverse ridge from the right 
 iliac crest across the umbilicus marked the lower border of the liver. 
 In the right flank was dullness, non-shifting. Liver dullness from 
 the sixth rib to four inches below the costal margin in the right nipple 
 line. Edge felt at level of umbilicus as a firm hard somewhat tender 
 body. Spleen apparently enlarged downward to precussion but 
 impossible to palpate because of tenderness. Marked soft edema of 
 everything from a point just below the knee. Temperature and 
 respiration normal. Pulse 104-115. Amount and specific gravity 
 of urine not recorded. A trace of albumin, bile, a large number of 
 red blood corpuscles, a few hyalin and finely granular casts. 
 
 The patient was very uncomfortable at admission and had a 
 good night only when being given sufficient morphia. Next day he 
 showed extreme pallor, marked distress and dyspnea. After an 
 intravenous injection of strophanthin the pale color and distress 
 remained the same, until he suddenly became livid and died at once. 
 
 Clinical Diagnosis —Aortic roughening and regurgitation (fibro- 
 calcareous endocarditis). 
 
 Hypertrophy and dilatation of the heart. 
 
 Broken compensation. 
 
 Anatomical Diagnosis.—Ulcerative polypous endocarditis of the 
 aortic valve; slight fibrous endocarditis of the mitral valve; small 
 parietal thrombi of aorta; hydropericardium; infarcts of Jungs, spleen, 
 and kidneys; obsolete tuberculosis of apex of left lung; hydrothorax, 
 slight; chronic pleuritis, left; hypertrophy and dilatation of the heart; 
 chronic passive congestion; ascites; anasarca; icterus, slight. Head 
 not examined. 
 
 The heart weighed 511 grams. The right ventricular wall 
 measured 4 mm., the left 11 mm. Valve circumferences: mitral 11 
 cm., aortic 7 cm., tricuspid 15 cm. All cavities were dilated, espe- 
 cially the left reas 
 
 Mitral Valve-—‘ The curtain at one point near the free margin 
 and at another a short distance from it shows small, circular, dis- 
 tinctly isolated fibrous-like areas. They measure about 3 mm. 
 in diameter and the auricular surface of the one nearest the free 
 margin of the valve is reddish and coated with a slight amount of 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 269 
 
 fibrin-like material. The circumference of the valve is slightly 
 increased and other than mentioned, this valve is not remarkable.”’ 
 
 Aortic Valve-—‘‘The aortic cusps are largely transformed into 
 very irregularly surfaced grayish yellow, softer and firmer polypoid 
 masses, to the surfaces of which fibrin and blood-clot-like material 
 are adherent. In places the vegetations are slightly gritty and at 
 two or three points there is a complete interruption in the continuity 
 of the masses, leaving small openings through which the cavity of 
 the sinuses of Valsalva are continuous with the cavity of the ventri- 
 cle. The endocardium just below one of the cusps and for a short 
 distance downward shows an area of slight discoloration, the surface 
 of which is slightly granular and to which a slight amount of fibrin and 
 blood-clot-liked material is adherent. 
 
 Tricuspid valve, “‘except for its edge is not remarkable.’ The 
 pulmonary valve is not mentioned. 
 
 No microscopic examination recorded. 
 
 Necropsy 2318 
 
 A clergyman and civil engineer of seventy-seven entered Feb- 
 ruary 27. His mother died of “hemorrhage from the mouth.”’ He 
 had rheumatic fever at fourteen, and was refused for the army at 
 the time of the Civil War. At thirty-one he had “country fever.” 
 At forty-four while skating he fainted and had great palpitation of 
 the heart. Since that time he had had a number of attacks of weak- 
 ness, dizziness and palpitation lasting a few hours, never laying him 
 up for more than a day. He had always led a strenuous outdoor 
 life and had done a great deal of walking. His habits were excellent. 
 In January, two months before admission, he began to be short of 
 breath, especially after exertion, and found that his heart beat fast, 
 jerkily and forcibly. He became noticeably weaker and had a little 
 cough with dark brown sputum. At the end of January his legs and. 
 feet became swollen. He would wake at two or three o’clock in the 
 morning suffocated and weak and be obliged to sit up with his 
 hands and arms resting on a table. In an hour or two he would feel 
 relieved. He had some epigastric discomfort. He had vomited a 
 few times. A month before admission he was in a hospital for nine 
 days with considerable benefit. 
 
 Physical examination showed a slight, much emaciated old man 
 with marked distension of the external jugular and the veins along 
 the left clavicle and visible bounding of the carotid, brachial and 
 femoral arteries. The left chest showed marked prominence in the 
 
270 FACTS ON THE HEART 
 
 precordial region. —The mucous membranes were very pale. Pea sized 
 glands were palpable in the axillae and groins. The apex impulse 
 of the heart was visible, beating forcibly in the fifth and sixth spaces 
 outside the nipple line, six and a quarter inches to the left of mid- 
 sternum and in the third space to the left of the sternum. The 
 impulse and dullness corresponded in the sixth space. The right 
 border was at the sternal margin. The supracardiac dullness was 
 not increased. The action was slightly irregular, chiefly in rhythm. 
 The first sound at the apex was sharp. ‘The second sound could be 
 heard only about half way toward the base, not at the apex. The 
 pulmonic second sound was accentuated. Following the sharp first 
 sound at the apex was a high pitched musical systolic murmur and a 
 diastolic murmur transmitted to the axilla. In the third space to 
 the left a harsh rough systolic was heard, and a loud blowing dias- 
 tolic murmur transmitted upward to the second space at the right 
 of the sternum, downward to the apex and into the axilla, where a 
 to-and-fro murmur was heard distinctly. The pulses were slightly 
 irregular, Corrigan. The arteries were palpable and _ tortuous. 
 Sclerosed plates were easily felt. The systolic blood pressure was 
 135 to145. The lungs showed slight dullness, diminished respiration 
 and voice sounds, with fine moist rales at both bases posteriorly, rising 
 higher on the right, and fine moist rales at the bases in front. The 
 right flank showed dullness, not shifting. The liver dullness ex- 
 tended just below the costal margin, where the edge was felt. There 
 was slight edema of the genitals and marked soft edema of the legs, 
 ankles and feet. The venules on the legs were prominent. The 
 pupils and knee-jerks were normal. 
 
 During the patient’s stay in the hospital his temperature was 
 subnormal, 98° to 94.6°, until the day of death, when it rose to ror.1°. 
 The pulse was 61 to 94 with a terminal rise to 135. The respirations 
 were 23 to 36. The daily output of urine was 10 to 28 ounces, the 
 specific gravity 1.020 to 1.022, a slight trace of albumin at one of 
 two examinations, rare pus cells at both, rare red cells at one. The 
 blood was not remarkable. 
 
 The patient was comfortable except at night, when he tended to 
 be rather delirious. At times he was very short of breath. March 
 7 he developed Cheyne-Stokes respiration. That night he gradually 
 failed. His pulse grew rapid and weak. The next morning with the 
 rise in temperature his lungs were full of moist rales. That morning 
 he died. : 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 271 
 
 Outcome.—The clinical diagnosis was aortic and mitral regurgita- 
 tion, broken cardiac compensation, arteriosclerosis, and hypertrophy 
 and dilatation of the heart. 
 
 Necropsy showed arteriosclerosis, subacute glomerulonephritis 
 with arteriosclerotic degeneration, fibrocalcareous endocarditis of 
 the aortic valve and fibrous endocarditis of the mitral valve, hyper- 
 trophy and dilatation of the heart, thrombosis of the left auricular 
 appendix, slight chronic passive congestion, papillary adenomata of 
 the kidneys, teratoma of the kidney, infarct of the kidney, general 
 peritonitis (terminal), foci of obsolete tuberculosis in the apex of the 
 left lung, chronic pleuritis, edema piae, and scoliosis. 
 
 Dr. RicHARDSON: The head in this case showed edema piae and 
 some arteriosclerosis of the vessels of Willis but was otherwise 
 negative. 
 
 The peritoneal cavity showed an acute peritonitis,—terminal. 
 Terminal infections occur in any of the cavities,—pleuritis, peri- 
 carditis, or peritonitis. In the streptococcus epidemics streptococcus 
 peritonitis is common. 
 
 The gastro-intestinal tract was negative, no perforations, no 
 ulcers or appendicitis. 
 
 The lungs showed chronic passive congestion and some obsolete 
 tuberculosis in the apex of the left Jung. 
 
 The pericardium was negative. The heart weighed 576 grams. 
 Considerable hypertrophy. ‘There was marked general arteriosclero- 
 sis. The valve measurements were, for the tricuspid 14.5 cm., the 
 pulmonary 9g, the aortic 9.5, the mitral 13.5. These valve circum- 
 ferences are all increased. On the mitral valve there was a moderate 
 amount of rather diffuse fibrous endocarditis, and on the aortic a 
 moderate amount of fibrous thickening with calcareous degeneration 
 regarded as chronic endocarditis and of the rheumatic type. In the 
 left auricular appendix there was a thrombus and in one kidney 
 an infarct. In the lower pole of the right kidney there was a 
 tumor, a small teratoma, and in each kidney some very small papil- 
 lary adenomata. The kidneys otherwise showed a combination of 
 conditions, subacute glomerulonephritis, with some arteriosclerotic 
 degeneration. 
 
 The bladder, prostate, seminal vesicles and testes were negative. 
 The gastro-intestinal tract showed passive congestion. There was 
 some curvature of the spinal column, but it was otherwise negative. 
 
 Dr. Cazot: We are sometimes asked by a patient with rheumatic 
 heart disease, ‘‘How long may I live with this?’’ We should put it 
 
272 FACTS ON THE HEART 
 
 down in the tablets of memory that we have here read a necropsy of 
 a man.who had rheumatic fever at fourteen and presumably got his 
 heart lesion then. He died at seventy-seven. He lived sixty-three 
 years with that lesion. That is a point of value in the practice of 
 medicine,—to be able to say truthfully to patients, ‘We have knowna 
 case necropsied with a rheumatic heart lesion that probably lasted 
 sixty-three years.”’ 
 
 Necropsy 2613 
 
 In September, 1905, at his first admission to the hospital, the his- 
 tory and examination of this patient, an American shopkeeper of 
 forty-five, were negative except for hemorrhoids and the heart. The 
 apex impulse was one and a half inches outside the nipple line. 
 There was a loud whistling systolic murmur transmitted to the axilla. 
 The hemorrhoids were cauterized. A year later he reported a perfect 
 result. 
 
 In May, 1906, he reentered. He now gave a history of chancres 
 two years earlier. For a week he had not felt well. For six days he 
 had had cough. Then he had severe pain in the back of the left thigh 
 and calf running up into the small of the back. Two days before 
 admission this became so severe that he had to go to bed. . He had 
 also had severe pain in the left knee-joint, and of late had had some 
 abdominal pain radiating to the back. 
 
 Examination showed a barrel-shaped chest. The apex impulse 
 of the heart was in the sixth space just outside the nipple line. There 
 was no enlargement to percussion. The action was regular, the 
 sounds of good quality, the second sound at the apex ringing. A 
 systolic murmur at the apex replaced the first sound and was trans- 
 mitted to the axilla. The aortic second sound was greater than the 
 pulmonic second. The pulses were normal, the arteries pal- 
 pable. The lungs were hyperresonant. The breath sounds were 
 loud. Expiration was prolonged. ‘There were occasional moist rales. 
 There was considerable general tenderness in the abdomen. The 
 genitals were normal. The left knee-joint contained an excess of 
 fluid, the patella floating. There was great tenderness about the 
 joint. The left leg was everted. There was much tenderness 
 over the course of the left sciatic nerve and calf. The pupils and 
 reflexes were normal except that the left knee-jerk was not obtained. 
 
 The temperature at entrance was 102.5°, after May 9 normal. 
 The pulse was 108-60. The respirations were normal. The urine 
 was normal in amount. The specific gravity ranged from 1.010 to 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 273 
 
 1.023. There was the slightest possible trace of albumin at both of 
 two examinations. The hemoglobin was 75%, the leucocytes 6600. 
 
 Under salicylates the pain and swelling of the knee-joint dis- 
 appeared. May 15 the patient was discharged ‘‘ well.” 
 
 He was admitted for the third time January 8, 1910. For the 
 past few years he had urinated four or five times at night. For two 
 months he had had considerable cough which disturbed his sleep, 
 loss of appetite, dry and slightly sore throat, and occasional vomiting. 
 He had lost some weight and strength recently. January 6 he had 
 soreness at the base of his neck, all over the chest, and along the right 
 costal margin, worse on cough or deep inspiration. For a day or two 
 he had been raising bloody sputum. 
 
 Examination showed a well nourished, full-blooded man with 
 frequent paroxysms of violent coughing, considerable dyspnea, and 
 slight periodic audible respiratory wheeze. The skin was somewhat 
 pale. The teeth were a few decayed snags, with pyorrhea. The 
 apex impulse of the heart was in the fifth space fifteen centimeters 
 from the midsternal line, five centimeters outside the nipple line, 
 corresponding with the left border of dullness. The right border of 
 dullness was four centimeters from midsternum. A systolic scratchy 
 murmur was heard at the apex. The pulmonic second sound was 
 accentuated. The pulses were normal, the artery walls moderately 
 thickened. The systolic blood pressure was 130. Expiration was 
 prolonged throughout and accompanied by many wheezes, especially 
 at the apices in front. There were a few inspiratory crackles. The 
 liver dullness extended from the sixth rib to two centimeters below 
 the costal margin; the edge was not definitely felt. The urinary 
 output was normal. The urine was light brown to black-brown at 
 the first seven of sixteen examinations, cloudy or smoky at all the 
 rest, high colored at three. The specific gravity was 1.009 to 1.013. 
 There was albumin at all but the last examination, a large trace at 
 the first six, a trace to a very slight trace later. The sediment 
 showed blood decreasing from much to rare red cells, then none; at 
 the end many red corpuscles to much free blood. The first eight 
 examinations showed many brown granular and blood casts and hya- 
 lin casts with cells and blood attached. Later there were few, and 
 the blood disappeared. At entrance the hemoglobin was 80%, the 
 leucocyte count 34,200; the reds showed slight achromia and numer- 
 ous large polychromatophilic cells. Later the leucocyte count fell, 
 
 reaching normal January 17. 
 18 
 
274 FACTS ON THE HEART 
 
 During the first week in the hospital the patient ran a tempera- 
 ture of 99.7° to 104.2°; the pulse was 71~100, the respirations 24-48. 
 During the next week the temperature was 98.2°-101°, the pulse 64-95, 
 the respirations 18-37. The third week the temperature gradually 
 reached normal and the pulse and respirations were normal through- 
 out. During the first three days the patient had violent paroxysms of 
 coughing, raising considerable thick tenacious brown sputum showing 
 some fresh blood and considerable pus; no tubercle bacilli. He had 
 slight nosebleed much of the time from entrance. A large number of 
 bloody crusts formed on the nose and upper lip. He bled easily also 
 from the ear. A purpuric spot was left after the injection of morphia. 
 After January 11 the cough was much less severe. January 14 there 
 was marked pain on inspiration and a friction rub in the left axilla. 
 He made good general improvement. The tendency to bleed 
 diminished. ‘The urine showed much less color than at first. Jan- 
 uary 18 he had a small bloody stool. January 22 there was a diastolic 
 blow transmitted down the left border of the sternum and a slightly 
 collapsing pulse. The apex impulse was localized and forcible. 
 The patient said he felt strong and well. He continued to improve 
 rapidly. January 29 his lungs were clear. That day he was 
 discharged. 
 
 After leaving the hospital he felt fairly well, though he had severe 
 paroxysms of cough. He was able to do a little work by resting every 
 few minutes to ease his dyspnea. When walking he had to rest every 
 few steps. His bowels were constipated. He slept poorly because 
 of attacks of coughing. There wasnosputum. He had much dizzi- 
 ness. In the late spring his feet and ankles began to swell at night 
 and he had severe cramps in his legs. He urinated three times at 
 night. By May g the cough had become almost incessant and dull 
 abdominal pain had developed. . 
 
 At his fourth admission to the hospital, May 12, 1910, he was 
 well nourished but looked old. He sat propped up in bed breathing 
 very rapidly, with frequent attacks of severe cough during which he 
 became cyanotic and after which he gasped for air. The skin was 
 pale and moist. Over the arms and in great numbers on the legs were 
 purpuric areas. The mucous membranes and throat were pale and 
 dry, the throat and pharynx crusted. The tongue was dry, furrowed 
 and cracked, with a brown crust. Lymph glands the size of peas 
 were felt in the neck and axillae and the size of beans in the groins. 
 The apex impulse of the heart was seen and felt in the fifth space 
 fourteen centimeters from midsternum and six and a half centimeters 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 275 
 
 outside the nipple line, corresponcing with the left border of dullness. 
 The right border was four and a half centimeters to the right. The 
 action was regular, not rapid. The sounds. were clear and of good 
 quality. At the apex was a loud harsh systolic murmur, heard also 
 over the precordia and transmitted to the axilla and back. The 
 pulmonic-second sound was slightly accentuated. There was slight 
 lateral excursion of the brachials. The systolic blood pressure was 
 105. The lungs were rather hyperresonant except at both bases 
 posteriorly, where there was slight dullness. The expiratory murmur 
 was rather prolonged. A few squeaks were heard throughout, and 
 below the angles of the scapulae numerous fine moist rales. The 
 abdomen was held rigid. The liver dullness extended from the sixth 
 rib to the costal margin. A tender edge was felt indistinctly at the 
 level of the umbilicus in the nipple line. Both shins and ankles 
 showed considerable soft edema. 
 
 During his eleven days in the hospital the patient ran an irregular 
 temperature from 97.9 to 101.6°, with two intervals of normal 
 temperature for two days and a terminal rise to 103.7°._ The pulse 
 ranged from 85 to 110, with a terminal rise to 135. The respirations 
 were 24 to 43. The output of urine was normal except on May 14, 
 whenit was 373. Theurine was smoky or cloudy at all of five exami- 
 nations, bloody at two, high colored at the other three. The specific 
 gravity was fixed at 1.o11—1.012. A trace to the slightest possible 
 trace of albumin and a few to rare red blood corpuscles were found at 
 all examinations. At one a guaiac test on the supernatant fluid was 
 strongly positive. Hyalin, granular and cellular casts were found at 
 all examinations, with blood cells attached at the first two. The 
 hemoglobin was 50 to 60%, the reds 3,000,000, showing achromia at 
 one of three examinations, macrocytosis at two, variation in size at 
 one, in shape at another. The leucocytes and differential count 
 were normal until the day of death. 
 
 The patient seemed at times rather childish. He had sudden 
 attacks of severe dyspnea which usually could be easily quieted 
 without medicine, though at times there was very marked genuine 
 dyspnea requiring morphia. This grew much worse. He _ had 
 several very severe nosebleeds. The gums and lips bled slightly 
 at times. May 1g an ulceration on the nasal septum was touched 
 with chromic acid. May 21 a localized patch of large vesicles 
 developed on the upper right eyelid. The stool was hard costive 
 pellets imbedded in a little fresh blood. May 22 the sputum was a 
 membranous looking material showing a few Gram-positive diplococcl. 
 
276 FACTS ON THE HEART 
 
 The patient was unable to swallow. A throat culture was taken. 
 The leucocyte count was 14,000. The heart was very irregular the 
 pulse was weak. May 22 he suddenly collapsed and died. 
 
 Bacteriological Report—A throat culture reported after death 
 was positive for Klebs-Loeffler bacilli. 
 
 Clinical Diagnosis.—Chronic bronchitis and emphysema. 
 
 Mitral regurgitation. 
 
 Chronic passive congestion, general. 
 
 Purpura. 
 
 Hematuria. 
 
 Secondary anemia. 
 
 Diphtheria. 
 
 Dr. Richard C. Cabol’s Diagnosis —Chronic nephritis. 
 
 Hypertrophied and dilated heart. 
 
 Acute endocarditis. 
 
 Chronic passive congestion. 
 
 Diphtheria. 
 
 Anatomical Diagnosis——Chronic fibrous and acute vegetative 
 endocarditis of the aortic and mitral valves. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the lungs and liver. 
 
 Arteriosclerosis. : 
 
 Lobar pneumonia of the upper lobe of the left lung. 
 
 Soft spleen. 
 
 Acute degeneration of the liver. 
 
 _Secondary anemia. | 
 
 Arteriosclerotic degeneration of the kidneys. 
 
 Streptococcus septicemia. 
 
 Dr. RicHarpson: The head was not examined. There is nothing 
 about diphtheria in our record here. Scattered over the lungs were 
 numerous irregular discrete and confluent purpuric-like areas. The 
 culture taken from the heart blood yielded a good growth of the 
 streptococcus. There wasa slight amount of pale fluid in each pleural 
 cavity and a few adhesions. The right lung showed chronic passive 
 congestion, no pneumonia. The lower two-thirds of the upper lobe 
 of the left lung showed frank pneumonia with the usual pleuritis. 
 
 Dr. Casot: No emphysema? 
 
 Dr. RICHARDSON: No. 
 
 Dr. Casot: You would have put it down if it had been there, 
 ' wouldn’t you? It is an obvious thing. 
 
 Dr. RICHARDSON: Yes, it is obvious. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES Zhi 
 
 Scattered along the aorta there was a slight to moderate amount 
 of fibrous sclerosis. | 
 
 The pericardium contained a slight amount of pale fluid. The 
 heart weighed 565 grams,—considerably enlarged. The myocardium 
 wasthick. The mitral valve measured 9.5 cm.,the aorticgcm. The 
 tricuspid and pulmonary valves were negative. Scattered along the 
 curtain of the mitral valve were numerous fibrous areas and nodules, 
 causing some deformity, and planted on these were smaller and larger 
 masses of soft frank spongy vegetations,—acute endocarditis on a 
 basis of chronic. 
 
 The coronaries were free, capacious, and showed only a slight 
 amount of fibrous sclerosis. 
 
 The liver and the other organs showed chronic passive congestion. 
 
 There was some question as to anemia in this case. It was 
 considered at that time that there was some anemia, but it was 
 secondary and not primary. 
 
 The kidneys weighed 345 grams. From the description there was 
 nothing but arteriosclerotic degeneration, that is, arteriosclerosis of 
 the vessels and some of the capillaries of the glomeruli and scattered 
 foci. At that particular time it was not regarded as sufficient to 
 call it arteriosclerotic nephritis. 
 
 A PuysicIAN: What about the Klebs-Loeffler? 
 
 Dr. Cazsot: It was a terminal infection. I have no doubt it con- 
 tributed to the death. But you see there is plenty more infection, 
 with the acute endocarditis throwing emboli around. I suppose it 
 perfectly might have been in the upper air passages, and if you had 
 not been told about it you would not look. 
 
 Dr. RicHArpDSON: No, but a case of Klebs-Loeffler has to be taken 
 care of in a proper fashion. 
 
 Dr Casot: One would think they would have made more of a 
 fuss about it. The chief mystery to me is that Dr. Richardson so 
 far refuses to back us up on the diagnosis of nephritis. 
 
 Necropsy 3022 
 
 An American plumber of fifty-two entered March 9g, 1912, for 
 observation. He had gonorrhea at twenty-three. He recalled no 
 illnesses until 1900, when as a soldier in the Philippines he had 
 shortness of breath and edema of the legs during forced marches. 
 A year later he had malaria. Two years after this he was discharged 
 from the army on account of ‘‘chronic dysentery, chronic gastritis, 
 heart trouble, chills and fever.’ He continued to have severe diar- 
 
278 FACTS ON THE HEART 
 
 rhea until a year before coming to the hospital, sometimes forty 
 movements a day, of late years four or five. During the past year 
 he had had only three or four short attacks. The movements were ~ 
 slimy and bloody. He drank considerable beer and whiskey until 
 five months before admission. 
 
 Eight months ago on a hot day he was “‘sunstruck,”’ was uncon- 
 scious for a few minutes, and had high fever. Ice water treatment 
 revived him. Since that time he had been in poor health. For 
 three months he did a little work. For the past five he had done 
 none. He had had marked dyspnea and at times orthopnea, con- 
 siderable precordial distress, and occasional sharp attacks of pre- 
 cordial pain lasting a few minutes. His legs and ankles had been 
 markedly edematous at times. For three days he had had moderate 
 pain. with some swelling at the base of the left thumb. 
 
 Liver edge 
 firm, rounded, 
 slightly ten- 
 der, indefin- 
 itely felt. 
 
 Examination showed a well-nourished man. The heart borders 
 are shown in Fig. 49. The action was regular, slightly rapid, the 
 sounds of good quality. Systolic and diastolic murmurs were heard | 
 over the entire precordia, the systolic short and rough, faint except 
 over the region of the apex, the diastolic long, loud, rough in the 
 aortic area and along the right sternal margin, elsewhere softer. 
 There were no thrills. The left pulse was greater than the right. 
 The artery walls were not felt. The blood pressure was 160/130- 
 110/80. The lungs showed fine crackles at both bases. There was 
 slight swelling, redness, and tenderness about the left carpophalan- 
 geal joint of the thumb. 
 
 After the day of entrance the temperature was 96° to 99°, the 
 pulse 80 to 98, the respirations 17 to 32. The urinary output was 8 
 to 27 ounces, the specific gravity 1.022-1.013. There was the 
 slightest possible trace to a very slight trace of albumin. Rare 
 granular casts were seen at both of two examinations, hyalin casts at 
 one. The hemoglobin was 85%, the leucocytes 12,000, the polynu- 
 clears 67%. The reds showed slight achromia and a number of large 
 ‘“transition-like”’ cells with nucleolae and granular pseudopodic-like 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 279 
 
 protoplasm. Two Wassermanns were negative. The fundi were 
 normal. The stools were negative. X-ray showed the heart shadow 
 symmetrically enlarged; no evidence of pathology in the lungs. 
 
 The joint condition cleared up rapidly, and the patient was com- 
 fortable until March 14, when he complained of slight sore throat 
 and weakness. Next morning he suddenly became very dyspneic. 
 His color was poor and his pulse barely felt at the wrist. He was 
 given one-thirtieth of a grain of strychnia and soon afterwards one- 
 hundredth of a grain of strophanthin intravenously. The pulse and 
 heart sounds improved markedly, and with morphia he passed a 
 fairly comfortable day. Next day the heart borders, which had gone 
 3 cm. to the left and 2 cm. to the right beyond the entrance examina- 
 tion, were back to the earlier measurements. During the night he 
 sank gradually, and the morning of March 17 died. 
 
 Clinical Diagnosis (from Hospital Record) —Chronic endocarditis, 
 aortic and mitral regurgitation. 
 
 Syphilitic aortitis? 
 
 Chronic dysentery. Amebic? 
 
 Dr. Richard C. Cabot’s Diagnosis—Acute endocarditis, aortic 
 stenosis and regurgitation. 
 
 Hypertrophied and dilated heart. 
 
 Chronic passive congestion of the liver. 
 
 Slight chronic passive congestion, general. 
 
 Anatomical Diagnosis ——Acute and chronic endocarditis of the 
 aortic valve, stenosis and regurgitation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Slight ascites. 
 
 Slight anasarca. 
 
 Septicemia, streptococcus. 
 
 Obsolete tuberculosis of a bronchial lymphatic gland. 
 
 Adenocystoma of kidney. 
 
 Dr. RicHARDSON: The patient was a well developed and fairly 
 well nourished man. He had a slight amount of ascites, and the 
 gastro-intestinal tract showed passive congestion. 
 
 There is a note that we measured the intestine; the small one was 
 twenty feet six inches, the large one five feet three inches. At that 
 time there was some talk about the varying length of intestine in 
 different individuals, and they were trying to type into groups those 
 who had a very long or a very short intestine to see if there was any 
 relationship to length of life or lability to disease. 
 
280 | FACTS ON THE HEART 
 
 The liver showed chronic passive congestion in moderate amount. 
 
 The spleen was enlarged, weighing 480 grams, and so far as we 
 could tell anatomically was like any spleen in chronic passive con- 
 gestion except that it was rather larger than they usually are. That 
 may be accounted for by his malaria. 
 
 The kidneys were large, one 214 grams and the other 190, (nor- 
 mally 200-400 grams together), but that excess in weight was due to 
 edema. There was no glomerulo-nephritis and no arteriosclerotic 
 nephritis. 
 
 The circulatory apparatus, the aorta and great branches, the 
 pulmonary artery and veins were all negative. ‘The heart weighed 
 470 grams,—moderate hypertrophy with slight dilatation. The 
 myocardium was of good consistence, with no evidence of myocarditis, 
 and the mitral, tricuspid and pulmonary valves were negative. The 
 aortic valve had the usual three cusps, two of which were larger than 
 usual, and all the cusps showed considerable fibrous deformity and 
 erected on this chronic endocarditis an acute endocarditis. So that 
 the heart valves showed acute and chronic endocarditis of the aortic 
 valve, rheumatic in type. 
 
 There was no evidence anywhere in the body of syphilis. 
 
 There was obsolete tuberculosis of one bronchial lymph node. 
 
 There was 300 c.c. of fluid in the pericardium. It was otherwise 
 negative. 
 
 In one of the kidneys was a very small tumor, an adenocystoma. 
 
 This case shows very well the anatomical basis for the rheumatic 
 picture in the aortic valve. 
 
 Dr. Casot: There was nothing to account for his dying so 
 suddenly ? 
 
 Dr. RicHARDSON: Nothing except the streptococcus infection. 
 We did not examine the head. He had a source on the aortic valve 
 from which emboli might have gone to the brain. There were 
 no infarcts elsewhere. 
 
 Necropsy 3290 
 
 A New England carpenter of thirty-one entered November 11th 
 for the relief of dyspnea and precordial pain. 
 
 The family history was good except that his mother died at 
 twenty-eight of ‘“‘brain fever.”’ 
 
 He took half a glass of whiskey, three to eight glasses of beer, and 
 two boxes of cigarettes a day until a year and a half ago. Since 
 then he had used none. He denied venereal disease. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 281 
 
 A year before entrance, following an attack of ‘‘rheumatic fever,” 
 he was obliged to give up regular work on account of dyspnea, 
 transitory edema, and sharp precordial pain. He had nycturia and 
 polyuria, which disappeared when he took to bed, as he was obliged 
 to do three weeks ago on account of aggravation of his symptoms. 
 He now has marked dyspnea on slight exertion; orthopnea, eructation 
 of gas, occasional distension of the abdomen, cough with clear, 
 watery sputum sometimes containing purulent material, cold hands 
 and feet, precordial pain at intervals, often sharp, sometimes dull, 
 a “‘leaky-pump”’ feeling over the precordia, hoarseness, and dark 
 urine. For the past three or four days he has had edema below the 
 knees. 
 
 His best weight was 172 pounds, six years ago. ‘Three months 
 ago he weighed 153. 
 
 Physical examination showed a poorly nourished man, hoarse, 
 dyspneic, and cyanotic. His skin was yellowish-pale, with many 
 papules and pustules scattered over the back, 
 chest andarms. There was also a bluish erythe- 
 ma over the lower back. The head and throat 
 were not remarkable except for some pyorrhea 
 andcaries. ‘Thechestwasbarrel-shaped. There 
 was systolic retraction of the nipple, also under 
 the ensiform and posteriorly in the tenth and eleventh spaces. 
 
 The heart did not seem to shift with change of position. The 
 precordia moved with every beat. The apex impulse was irregular, 
 diffuse and heaving, faintly felt in the seventh space, rg cm. to the 
 left of the midsternum. The maximum impulse was in the sixth 
 space, 15 cm. to the left. There was no supracardiac dullness. 
 A presystolic thrill was felt over the apex. The sounds at the apex 
 were very irregular, and not synchronous with the radial pulses. The 
 first sound was replaced everywhere by a harsh systolic murmur, 
 transmitted to the axilla and the back. There was also a short 
 blowing diastolic murmur at the apex, and a diastolic over the aortic 
 area. The aortic second was greater than the pulmonic second 
 sound, and both were greatly accentuated. At the third left space 
 the second sound was very loud and ringing, and there was also a 
 diastolic murmur. ‘The pulses were equal, irregular, not Corrigan, 
 of poor volume and fair tension, and lost many beats of the heart. 
 There was marked pulsation of the carotids and capillaries, and 
 pistol-shot sound over the femorals. 
 
 dsternal 
 Nipple 
 
 8cm |S 10cm * ocm 
 
 Fic. 50.—Borders of 
 dullness. 
 
282 FACTS ON THE HEART 
 
 The lungs showed nothing in front; slight dullness in the left 
 lower back; in the right back flatness extending from the angle of 
 the scapula downward, with diminished voice and breathing. Over 
 both backs there were medium and coarse rales, most marked on the 
 right. The abdomen showed liver dullness from the fifth rib to nine 
 cm. below the costal margin, where a smooth, rounded, tender edge 
 was felt. The spleen was barely felt. The genitals, pupils and 
 reflexes were normal. The lower extremities and the sacrum showed 
 edema. The fingers were cyanotic and slightly clubbed. 
 
 The temperature was usually 97. to 94.2. Pulse normal except 
 for drops to 40 Nov. 30 and the day of death. Respirations 30 to 20. 
 Systolic blood pressure 180 to 140, diastolic 120 to 60. Urine, 
 amount usually 9 to 17 ounces, pink at entrance, turbid. Specific 
 gravity 1026-1013. Albumin at four of five examinations, leucocytes 
 at the first, granular casts at two, hyalin at the last three. No red 
 blood corpuscles until the fifth. Renal function, in two hours, 45%. 
 Blood: hemoglobin 80%, leucocytes 12,400-8800, polynuclears 
 50%. Blood culture, no growth. Two Wassermanns negative. 
 Feces, guaiac negative. Laryngoscopic examination showed complete 
 paralysis of the left recurrent laryngeal nerve. 
 
 The heart sounds became a little more regular, and the patient 
 grew more comfortable and made a little general improvement, 
 though he was troubled by gas, vomiting, and cramp-like pain in the 
 abdomen, relieved by soda. After he had been sitting up because of 
 these symptoms his legs became badly swollen, and by Nov. 22 showed 
 peculiar reddish patches on which a skin consultant could not make 
 a definite diagnosis, but which faded in a few days. 
 
 The patient was given two digipuratum tablets daily at entrance, 
 reduced to one tablet Nov. 20. After the drop in pulse Nov. 30 this 
 was stopped, and he felt better than for some time. By Dec. 3 
 he had been worrying and was considerably worse, so weak and dysp- 
 neic that he could not be taken home. ‘The pulse was very irregular 
 and the heart action extremely arrhythmic. The digipuratum was 
 started again. The arrhythmia increased, the patient grew more and 
 more restless, the skin at the ankles broke. Dec. 5 the temperature 
 rose from 94.2 to 98.4. The murmurs were not so constant, but there 
 was no change in the size of the heart. Dec. 6 he suddenly sank back 
 and died. 
 
 Clinical Diagnosis (from Hospital Record).—Chronic and acute 
 aortic and mitral endocarditis. 
 
 Adhesive pericarditis. 
 Chronic passive congestion. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 283 
 
 Dr. Richard C. Cabot’s Diagnosis.—Chronic endocarditis of the 
 mitral valve, stenosis. 
 
 Slight if any change in the aortic valve. 
 
 Hypertrophy and dilatation of the heart. It may be due to 
 adhesive pericarditis possibly. But I think it is due to chronic 
 glomerulonephritis, because of the high blood pressure, though this 
 is a dangerous amount of weight to put on one support. 
 
 Chronic passive congestion, general. 
 
 Anatomical Diagnosis-—1. Chemical or physical origin of fatal 
 illness. 
 
 Chronic endocarditis of the mitral and aortic valves. 
 Chronic adhesive pericarditis. 
 2. Secondary or terminal lesions 
 Hypertrophy and dilatation of the heart. 
 Chronic passive congestion, general. 
 Infarct of the lower lobe of the right lung. 
 Hydrothorax. 
 Ascites. 
 Anasarca. 
 
 The heart and pericardium together weighed 1205 grams, four 
 times the normal weight. The heart alone weighed 1140 grams. 
 The myocardium was rather thick, 12 mm. on the left ventricle and 
 5 on the right. The auricular walls also were thickened. All the 
 cavities were greatly enlarged. The mitral valve measured 12 cm. 
 Its usual measurement is about 10. The aortic valve measured 8.5 
 cm. Both the tricuspid (15.5) and the pulmonary (10) were 
 increased. The mitral curtain showed considerable thickening. The 
 aortic showed considerable fibrous change in the cusps, which were 
 stiffened, giving regurgitation without stenosis. 
 
 The liver and kidneys were large, the liver nutmeg. There was 
 no nephritis. 
 
 Necropsy 3333 
 
 A teamster of forty-five came to the hospital February 24th for 
 relief of dyspnea and hemoptysis. 
 
 His family history was good. 
 
 Two children had died at birth. His wife had had two miscar- 
 riages. His wife and two children were well. 
 
 At eighteen he was in bed three weeks with ‘‘slow fever’’ accom- 
 panied by abdominal pain. He had had no chorea or tonsillitis. 
 Fourteen years ago he had ‘‘rheumatism”’ in ankle and toe-joints, 
 
284 FACTS ON THE HEART 
 
 with some fever. He was unable to work for two or three months 
 but was not sick in bed. 
 
 He drank five to seven glasses of ale daily, not much whiskey 
 during the day, occasionally one before breakfast. He had gonor- 
 rhea at twenty-two. He denied«syphilis. 
 
 Four years ago he first noticed dyspnea on carrying furniture 
 upstairs. This increased until any carrying or excitement made him 
 so weak and dyspneic that he had to stop for breath. For the past 
 year he had had occasional violent cough, with sputum. For the 
 past six months he had had palpitation. For six weeks he had been 
 so weak and dyspneic that he had worked only three days, was in 
 bed most of the time, and orthopneic. He had had edema of the 
 legs but not of the abdomen. 
 
 The night before admission he had a sense of pressure in the epi- 
 gastrium. The following morning he awoke with severe precordial 
 pain, which continued two hours. The dyspnea and palpitation were 
 worse. He had hemoptysis for the first time. 
 
 His appetite was fair. His bowels moved daily with cathartics. 
 Nycturia once. His best weight was 145 pounds; he then weighed 
 about 138. 
 
 Physical examination showed a poorly nourished man with 
 labored breathing. The skin was slightly cyanotic, the mucous mem- 
 branes pale. There was much pyorrhea. 
 
 The entire precordia pulsated. ‘The left chest was more prom- 
 inent than the right. The apex was in the sixth space. The left 
 border of dullness was 17 cm. to the left of the midsternal line in the 
 anterior axillary line. The right border of dullness was 4 cm. to 
 right of the midsternal line. In the left lateral position the apex 
 shifted 2cm. The sounds were rapid, regular, of rather poor quality 
 at the apex, where the first sound was weak and followed by a harsh 
 systolic murmur transmitted to the axilla. At the base was a dias- 
 tolic murmur loudest at the third left space, transmitted toward the 
 apex and along the sternal border. A high-pitched systolic almost 
 replaced the first sound at the lower sternum. The second sound at 
 the base was absent. ‘There was a systolic at the base transmitted 
 toward the carotids. The pulses suggested the water-hammer. 
 The vessel walls were barely palpable. 
 
 The lungs showed evidence of congestion, especially at the right 
 The abdomen was slightly rigid. There was shifting dullness in 
 both flanks, no masses, but spasm in the right upper quadrant. 
 Liver dullness was from the fifth rib to four cm. below the costal 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 285 
 
 margin. The edge was not felt (but see below), There was slight 
 varicocele on the left, where the testis was small and tender, and slight 
 edema of the scrotum. ‘There was marked edema of the lower legs. 
 Both legs showed slight varicosites. The left pupil was greater than 
 the right. The reflexes were normal. 
 
 The temperature was usually subnormal until the roth day; 
 then too-102 until death three weeks later, except for four days 
 subnormal. Pulse go-140. At times many beats did not reach the 
 wrist. Respirations 20-40. Systolic blood pressure 135-165, dias- 
 tolic 70-80. Two weeks before death, systolic 130, diastolic 65. 
 The urine was normal in amount until the roth day, then usually 6- 
 15 0z. Specific gravity 1025-1032. The slightest possible trace to 
 a trace of albumin, occasional hyalin and granular casts with cells 
 attached, and a few red blood corpuscles. Renal function, first hour 
 30%, second hour 15%. The blood showed leucocytes 12,000 to 
 78,000, polynuclears 83%. The Wassermann was negative. Luetin 
 was negative. Blood culture gave no growth. The sputum was 
 bloody at two of three examinations, showed pneumococci at three 
 examinations, also streptococci at one of these. On the 28th day 
 there was typical rusty sputum. X-ray of the chest on the ninth 
 day showed opacity at both bases, the angles between the diaphragm 
 and the chest wall obliterated. A seven-foot plate of the heart 
 showed the heart enlarged to the left, its greatest diameter 15.5 cm. 
 The greatest transverse diameter of the great vessels was five cm. 
 The apex could not be made out. X-ray on the twenty-second day 
 showed the left chest opaque throughout, especially at the base. 
 That side of the chest was contracted. The heart was displaced to 
 the left. There was considerable thickening about the right lung 
 root. The diaphragm could not be seen on the left, was indistinct 
 on the right. There was no positive evidence of tuberculosis. 
 X-ray on the following day was the same except that the opacity at 
 the left base rose as high as the middle chest. The outline of the 
 diaphragm was indistinct on both sides and the angles between it 
 and the chest wall were obliterated. No movement could be seen 
 with respiration. The heart shadow was much enlarged and tri- 
 angular in shape. The cardiohepatic angle was obliterated. Very 
 little pulsation was made out. (Evidently the radiologist suspected 
 chronic pericarditis.) The lung apices were normal. Chest tap on 
 the twentieth day gave 1200 c.c. of bloody fluid with a specific gravity 
 of tors, 2% of albumin, and abundant cells nearly all polynuclears. 
 Culture gave no growth. 
 
286 FACTS ON THE HEART 
 
 On entrance the patient was very restless and dyspneic. He was 
 put on digipuratum and much morphia. The edema disappeared 
 and the liver edge became less tender. Amyl nitrite and nitroglyc- 
 erine gave only slight and transient relief to the sudden attacks of 
 dyspnea accompanied by pain in the chest. 
 
 Under strophanthin, however, there was marked improvement. 
 The pulse and heart action steadied somewhat, and the dyspnea and 
 cyanosis became much less marked. Morphia was no longer needed. 
 The patient then began to vomit, and the diastole was seen to be 
 lengthened. The strophanthus was omitted, with cessation of vomit- 
 ing. The first sound at the apex became sharp, and there was an 
 occasional presystolicmurmur. The fluid in theright back decreased. 
 
 On the eighteenth day the temperature began to rise. Dullness 
 increased in the left lower back, where there was faint bronchial 
 breathing, many fine rales, and egophony. ‘The chest tap on the 
 twentieth day gave much relief. On the twenty-third day hemopty- 
 sis began. | 
 
 During the next week the temperature remained elevated. The 
 signs in the left back were essentially the same, and there seems to 
 have been only slight accumulation of fluid. The heart sounds 
 became much more distant, except the first, which was lost. The 
 murmurs became variable, with a presystolic at the apex. There 
 were many extra systoles. The patient raised large amounts of 
 sputum showing blood and pus. The urine output was very low, 
 the temperature high, and the general condition poor. The patient 
 had become very pale and much thinner, although he ate and slept 
 well without morphia, and was up in a chair. 
 
 At a second chest tap on the twenty-eighth day of 200 c.c. of 
 bloody straw-colored fluid was recovered. Six days later the 
 chest was again tapped, with recovery of 30 c.c. of brownish turbid 
 fluid. A smear showed polynuclear predominating. 
 
 On the thirty-fifth day Dr. W. H. Smith’s examination of the 
 sputum showed moderate numbers of pneumococci and streptococci, 
 no tubercle bacilli. Such a sputum in Dr. Smith’s opinion would 
 correspond with chronic passive congestion or infarction. Three 
 days later the left back showed tympany at the extreme base, above 
 that flatness, egophony, faint bronchial breathing, and many fine 
 rales extending up to midscapula. The heart sounds were very faint. 
 The fluid last withdrawn from the chest showed on culture pneumo- 
 coccus. Dr. Smith considered the signs in the left back as due to a 
 septic infarct or a pneumonia with abscess. 
 
PURE AORTIC REGURGITATION. ILLUSTRATIVE CASES 287 
 
 On the fortieth day the patient died. 
 
 Clinical Diagnosis (from Hospital Record).—Chronic valvular 
 heart disease, aortic and mitral. ; 
 
 Empyema. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis with 
 aortic stenosis and regurgitation and mitral stenosis and regurgitation. 
 
 Acute endocarditis and pericarditis, with effusion. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Pneumonia. 
 
 Probably infarcts of the lungs, liver, kidneys, and spleen (but no 
 peripheral embolism). 
 
 Empyema (beginning). 
 
 Anatomical Diagnosis——Chronic endocarditis of the aortic and 
 mitral valves. The aortic measured 8.5 cm. in circumference, the 
 mitral t0.5cm. ‘The aortic showed fibrocalcareous deposit extending 
 into the mitral, reducing their opening function,—really stenosis, 
 despite normal measurements. 
 
 Acute endocarditis of the aortic valve, slight. 
 
 Hypertrophy and dilatation of the heart. (Weight 595 grams.) 
 
 Serofibrinous pleuritis, right. 
 
 Empyema, left. (S500 c.c. at base and in the interlobar fissure.) 
 
 Chronic passive congestion, general. Ascites. Anasarca. 
 
 Small infarct of the right kidney. 
 
 Infarcts of the right lung. 
 
 Compression atelectasis of the left lung. (500 c.c. of pus.) 
 
 Defective closure of the foramen ovale. 
 
 Chronic pleuritis. 
 
 Diverticulum of the esophagus (congenital). 
 
 Arteriosclerotic degeneration of the kidneys (i.e. foci of arterio- 
 sclerosis. Together they weighed 350 grams.) 
 
 Necropsy 3527 
 
 An Irishman of seventy-four entered December 4 for relief of a 
 skin condition. 
 
 His family history was good so far as known. 
 
 He had had “smallpox,” “scrofula,” and whooping cough in 
 childhood. Fifty years ago the lens of his right eye was injured by 
 a blow. For a year he had been slightly deaf. For three weeks he 
 had had edema of the feet. 
 
 His habits were good, except for nycturia one to two. He used 
 no alcohol or tobacco, and denied venereal disease. 
 
288 FACTS ON THE HEART 
 
 Two years before entering the hospital a small itchy, scaling area 
 appeared on his left instep, called eczema by his doctor. It remained 
 confined to this area for a year. Then it appeared on both upper 
 arms. Local treatment was ineffectual. Two months ago his whole 
 body became involved in the scaling. The itching, however, had 
 become much less intense. For two weeks he had had alternate 
 periods of three or four days of improvement and relapse. 
 
 Physical examination showed a fairly nourished old man, slightly 
 dyspneic. The skin of the face, neck and scalp was slightly red and 
 infiltrated, and was desquamating large flakes. On the left side of 
 the neck was a crusted lesion the size of a twenty-five cent piece. 
 The borders were pearly and indurated. (This lesion was of a year’s 
 duration.) The skin of the rest of the body was dark red, of porky 
 consistency. On the abdomen and chest it was moist and oozing, 
 with several small scattered vesicles. On the 
 
 F2)) em. 
 Supra E cardiac back it was infiltrated, but showed less redness 
 8 and oozing. Over the left clavicle was an irregu- 
 As : : 
 “ lar scar three inches long (remains of scrofula). 
 6 cm. T4 cm. 
 
 At the level of the fifth thoracic spinous process 
 Fic. 51.—Dullness. was attached a pedunculated cyst the size of a 
 walnut. The skin of the legs was infiltrated, red 
 and scaling. On the dorsum of the right foot was an old scar an 
 inch long. The apex impulse of the heart was in the fifth space. 
 At the apex was a loud, rough, systolic murmur, transmitted to the 
 axilla; also a short, rough presystolic murmur. In the fourth space — 
 was a loud, blowing, diastolic murmur. The aortic second sound 
 was slightly accentuated. The rate was normal, but there were 
 occasional extra systoles. The lungs were normal except for slight 
 dullness at the left space. The liver dullness extended from the fifth 
 rib to the costal margin. The edge was felt two finger-breadths 
 below the costal margin on deep inspiration. The genitals were 
 negative. There was slight hard edema of the lower legs and feet. 
 The pupils were equal, regular, reacted slowly. The knee-jerks were 
 equal and active. 
 
 Temperature normal. Pulse too to 118. Respiration 19 to 28. — 
 Blood pressure not recorded. The amount of urine was not recorded. 
 The specific gravity was 1o15, the findings negative. The blood 
 showed hemoglobin 80%, leucocytes 19,800, polynuclears 72%. The 
 reds showed considerable achromia. 
 
 On the night of December 5 the patient was slightly dyspneic and 
 complained of some abdominal distress, which was attributed to 
 
 ‘ 
 
MITRAL REGURGITATION 289 
 
 the skin condition. At one a.m. he had an attack of sharp pain in 
 the heart region. Half an hour later he was in intense agony, with 
 P. r40, R. 50. He was given morphia gr. 1@ and nitroglycerin gr. 
 Woo. The attack continued until 5:40, when morphia gr. 16 was 
 again given. On being questioned he now said he had had attacks 
 of this sort, but much less severe, for the past four or five weeks. 
 A medical consultant advised giving nitroglycerin gr. 1499 or 1409 
 every hour or two for the attacks, increasing dosage and frequency 
 for acute pain; if still uncontrolled, morphia. The prognosis he 
 considered entirely uncertain. 
 
 December 6 the patient vomited clear greenish fluid at intervals 
 all day and all night. He became semi-conscious and irrational, 
 later restless and dyspneic, requiring morphia. Then the breathing 
 became Cheyne-Stokes, and in ten minutes he died. 
 
 Clinical Diagnosis( from Hospital Record) Dermatitis exfoliativa. 
 
 Angina pectoris. 
 
 Toxemia. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Incompetent aortic valve. 
 
 Coronary sclerosis, plugging one or more coronary arteries. 
 
 Anatomical Diagnosis —Dermatitis exfoliativa. 
 
 Fatty metamorphosis and siderosis of the liver. 
 
 Fibrous and verrucose endocarditis of the aortic valve with some 
 deformity. 
 
 Hypertrophy and dilatation of the heart. (Weight 368 grams.) 
 
 Hydropericardium. 
 
 Edema of the lungs. 
 
 Chronic peritonitis (diffuse). 
 
 Chronic perihepatitis. 
 
 Chronic perisplenitis. 
 
 Healed appendicitis. 
 
 Chronic pleuritis. 
 
 Slight arteriosclerotic degeneration of the kidneys. 
 
 Small accessory spleen. 
 
 The coronary arteries were free. The aortic valve measured 7.5 
 cm. There was no general arteriosclerosis. The aorta above the 
 cusps was smooth. The anginoid attacks were not explained. 
 
 MITRAL REGURGITATION 
 
 Does It Exist?—The commonest of all diagnoses in the field of | 
 
 heart disease is mitral regurgitation. This statement can be easily 
 19 
 
290 FACTS ON THE HEART 
 
 verified by reference to the reports of any hospital that lists the dis- 
 eases treated there, or to almost any statistical record dealing with 
 the different varieties of heart disease. Yet most of these diagnoses 
 are not in my opinion justified for it is a lesion almost never to be 
 verified post-mortem. In our 4ooo necropsies we have been able to 
 find but seven cases, three of which are more or less doubtful. 
 
 What is the reason of this astonishing discrepancy? (1) The chief 
 reason is, I think, that physicians. diagnose mitral regurgitation 
 when they hear loud apical systolic murmurs, which are extraordi- 
 narily common in all sorts of non-cardiac disease as well as in health. 
 Thus in Roger I. Lee’s experience, gained by examining healthy 
 Harvard students over a considerable period of years, 70% of 
 unselected normal individuals showed a definite systolic murmur 
 over the heart in the recumbent position after strong expiration. 
 In children the percentage of such murmurs is I believe even greater. 
 
 (2) When a systolic apical murmur happens to be associated with 
 pain about the heart, with breathlessness, fainting spells, or with 
 any of the various nervous manifestations summed up under the 
 term of ‘“‘the effort syndrome,” a diagnosis of mitral regurgitation is 
 very likely to be made by the incautious, even though it can be 
 proved beyond all question that the heart is in fact sound. 
 
 (3) In elderly people systolic murmurs are also very frequent and 
 are sometimes heard best at the apex of the heart, though usually 
 loudest at the base. It is impossible to say how far these murmurs 
 may be related to arteriosclerosis or to stretching of the aortic arch, 
 which is usually sclerotic in the elderly. But at any rate there is 
 no good reason to suppose that these systolic murmurs indicate any 
 insufficiency of the mitral valve. 
 
 (4) Besides these conditions in which systolic murmurs with nor- 
 mal valves are so common, it is well known that a great variety of 
 physiological or pathological states such as fever, anemia, muscular. 
 exertion, nervousness, are also associated with the transient appear- 
 ance of systolic murmurs or with an increase of intensity in murmurs 
 already present. 
 
 The pernicious habit of diagnosing mitral regurgitation in people 
 with sound hearts became of great importance during the war of 1914- 
 1918. In the early years of that conflict large numbers of men were 
 rejected, especially in England, because a systolic murmur was heard 
 over the heart, a murmur often associated with pain, breathlessness, 
 tachycardia, or something else which misled the examiner. Such 
 exemptions became so frequent as to constitute a serious handicap 
 to a country needing all her healthy young men in the crisis of war. 
 
MITRAL REGURGITATION 291 
 
 Fortunately the mistake was discovered, and before long the rule 
 was put into effect that no man should be rejected merely on account 
 of a systolic murmur, no matter how loud it might be. Diastolic or 
 presystolic murmurs were still considered proper grounds for rejec- 
 tion. But these, on account of their relative rarity, made no serious 
 inroad upon the body of available recruits. When America at last 
 entered the war the special cardiac examiners appointed in the 
 United States to judge the American draft army, were able to profit 
 by the experience of the English examiners and to avoid the bugaboo 
 of ‘“‘mitral regurgitation”’ as a cause for rejection. So far as [know 
 no bad results have been reported as a result of carrying out this 
 policy either in England or the United States. 
 
 Similar conclusions have been arrived at by competent physicians 
 who have been called upon to judge the fitness of athletes for competi- 
 tive contests. The presence of a systolic murmur without other 
 evidence of cardiac disease has been found to involve no functional 
 weakening of the heart, no lessening of the athlete’s powers, and no 
 evil results either immediately after the contest or in later years. 
 Judged by these most searching and practical tests—war and athletic 
 contests—which certainly bring upon the heart as great a strain as 
 any of life’s exigencies, it is now clear that systolic murmurs without 
 other signs of cardiac disease are of no importance as evidence of valve 
 lesions. They may of course be helpful auxiliary evidence of 
 hypertension, or of arteriosclerosis. 
 
 It is easier to settle this point than it is to decide beyond perad- 
 venture what zs the cause of these murmurs, or whether they are 
 ever associated with a genuine regurgitation through the mitral valve. 
 On this point the evidence may be summed up as follows: 
 
 (1) Post-mortem findings show that the scarring and deformity 
 produced by endocarditis on the mitral valve leads almost invariably 
 to stenosis of that valve, and only in the rarest instances to regurgi- 
 tation without stenosis. : 
 
 (2) Relative mitral insufficiency due to stretching of the valve ori- 
 fices from muscular weakness or other causes remains a possibility 
 which even post-mortem examination cannot exclude,—a hypothesis 
 which can never be proved or disproved. But against it one may say: 
 
 ' (a) That many cases of enlargement of the mitral orifice are 
 demonstrated post-mortem when no murmur or arrhythmia has been 
 detected during life and no cardiac enlargement, passive congestion, 
 or other evidence of poor heart function is found after death. 
 
 (b) That in many cases a loud apical systolic murmur, even 
 though transmitted to the axilla and back and occasionally even 
 
292 FACTS ON THE HEART 
 
 musical in quality, goes along with a mitral valve orifice of normal 
 size, with an absolutely sound valve and no passive congestion as 
 revealed at post-mortem examination. ‘This does not disprove the 
 possibility of a temporary stretching of this valve with transient regur- 
 gitation during life. This could never be disproved so far as I see 
 unless one could somehow visualize the movements of the cardiac 
 blood during life. But I think it can be asserted that there is no 
 evidence for such relative and temporary insufficiency, and that 
 even if it exists there is no reason to believe that it does any harm. 
 
 It is really astonishing how long the legends about mitral regur- 
 gitation have persisted and on what good authority they have rested. 
 Thus in Osler’s textbook of medicine we find the following descrip- 
 tion of the post-mortem lesions believed by him to underlie mitral 
 regurgitation: 
 
 ‘The common lesions producing (mitral) insufficiency result from 
 endocarditis, which causes a gradual thickening at the edges of the 
 valves, contraction of the chordae tendineae, and the union of the 
 edges of the segments, so that in a majority of the instances there is not 
 only insufficiency but some grade of narrowing as well. Except in 
 children we rarely see the mitral leaflets curled and puckered without 
 narrowing of the orifice . . . In longstanding cases the entire mitral 
 structures are converted into a firm calcareousring.’’* (Italics mine.) 
 
 For these “mitral leaflets curled and puckered without narrowing 
 at the orifice,” I have been searching for the last twenty years (a) 
 at necropsies, (b) in the records of necropsies which I have not 
 myself seen, and (c) by questioning various pathologists. Osler’s 
 description aroused a vivid picture in my mind. But I have rarely 
 if ever found it, and know of no one else who has seen a reality corre- 
 sponding to it except in the rarest instances. Perhaps in ulcerative 
 endocarditis such a state of things may occasionally exist. But im 
 chronic non-ulcerative heart disease itt 1s certainly so rare as to be 
 negligible clinically. 
 
 One may inquire why it is that as a matter of observation in any 
 series like the present, mitral endocarditis leads so commonly to 
 stenosis of the valve and so rarely if ever to regurgitation. The 
 reason appears to be that most of the bacteria and platelet 
 thrombi, in other words the soft vegetations, in which endocarditis 
 begins, are deposited near the free margin of the valve. When these 
 vegetations become organized and healed into scar tissue, the traction 
 of the adhesions so produced, pulls together the contiguous parts 
 
 * Osler and McCrae: The Principles and Practice of Medicine, p. 810 (1923). 
 
MITRAL REGURGITATION 293 
 
 of the mitral orifice like a purse-string, and so produces, not pure 
 regurgitation but stenosis with (presumably) regurgitation as well. 
 
 In many cases there are also small vegetations and scars upon the 
 papillary muscles and upon the tendinous cords as well as upon the 
 valve curtains. If mitral regurgitation ever exists it is probably in 
 the rare cases when the endocardial vegetations are confined largely 
 or wholly to the papillary muscles, so that in the end we get no adhesion 
 of the cusps to each other, but only a shortening and thickening of 
 these-muscles and of their tendinous cords. Such a change would 
 pull the mitral curtains back towards the ventricular wall, so that 
 they could not rise up to close. Yet it would produce no stenosis in 
 them. 
 
 Something of this kind was probably present in Necropsy 2341, 
 possibly in 3320 of our series (see below). I have myself seen one 
 case (not in the Massachusetts Hospital series) in which almost exactly 
 the conditions above described were fulfilled. There was no ulcera- 
 tion and almost no thickening of the mitral curtains, but the papillary 
 muscles and tendinous cords were so much shortened and thickened 
 that the valve could hardly float out from the heart wall. In 
 Necropsy 3092 the pathologist evidently believed that a similar 
 condition was present. In Necropsy 2825 the lesion was distinctly 
 different from that which I have described and represents a very 
 peculiar, perhaps unique, state of things. (See below.) 
 
 Can Mitral Regurgitation Be Diagnosed in Life?—But granting 
 that mitral regurgitation probably exists as a great rarity, it is not 
 a clinical entity, for it cannot, so far as I see, be recognized in life. 
 The classical trio of signs (systolic murmur widely transmitted from 
 the apex, accented pulmonic second sound, enlarged heart) which 
 have been supposed to point to mitral regurgitation, have occurred 
 many times in this series without any evidence post-mortem that the 
 mitral valve was diseased or incompetent. In most of the cases 
 just referred to, necropsy showed a hypertrophied and dilated heart, 
 often associated with arteriosclerosis or chronic nephritis, but with a 
 normal mitral valve and no dilatation of its ring. 
 
 Mackenzie has told us how he gradually came to recognize that no 
 one ever died of mitral regurgitation. Even if one admits that there 
 may be in many cases a relative mitral reflux by muscular relaxation 
 around a sound mitral valve, even then the main cause of death will 
 usually be found to lie in the nephritis, the hypertension, the general 
 infection, or the anemia which brought about this relaxation. 
 
 The old point of differentiation between functional and organic 
 murmurs heard best at the cardiac apex, namely the transmission of 
 
294 FACTS ON THE HEART 
 
 the supposedly organic murmurs to the left axilla and back, has been 
 proved to my satisfaction, in the necropsies on which this book is 
 based, to be false. I have heard many such murmurs which showed 
 nothing particular to account for them at necropsy, not even cardiac 
 enlargement, no increase of the valve circumference, and no disease 
 of the valve itself. Indeed the wide transmission of a murmur is 
 merely an evidence of its loudness. All loud murmurs are widely 
 transmitted. Some of the murmurs in congenital heart disease can 
 be heard over the extremities and even on the top of the head. A 
 few of them can be heard at a distance from the patient. Yet such 
 murmurs may have very little effect upon the cardiac function and 
 be therefore of very little practical importance. On the other hand, 
 some very faint diastolic murmurs are evidence of crippling heart 
 disease. The worse the heart grows the fainter, in many cases, the 
 murmur, while if improvement occurs one may watch the murmur 
 grow louder and louder as the patient regains his powers. (In all 
 probability this means that a faster and stronger current of blood will 
 make more noise than the feeble current in an exhausted heart, just 
 as a powerful river current makes more noise than a feeble one.) 
 
 In a recent article by Breed and White* organic mitral regurgita- 
 tion is considered the proper diagnosis when one hears ‘‘a loud sys- 
 tolic murmur at the apex masking the first sound.” To this belief I 
 see the following objections: 
 
 (1) Most if not all cases of mitral stenosis must be conceived as 
 having regurgitation also. But they often have clear, or even 
 exaggerated, first sounds. Hence mitral regurgitation under the 
 only circumstances wherein we can often feel reasonably certain 
 that it exists, usually does not abolish the first sound. 
 
 (2) In many cases of this same group the systolic murmur referred 
 to by Breed and White is not loud but is faint or absent. 
 
 (3) In our rare proved or suspected cases of mitral regurgitation 
 the first sound was sharp in one, poor (like the second sound) in two, 
 not definitely recorded but probably present in two and definitely 
 replaced by the murmur in only one out of seven. 
 
 (4) In many of our cases proved post-mortem to have normal 
 heart valves and normal valve orifices, there has been heard in life 
 a loud apical systolic masking the first sound. 
 
 (5) In many cases of mitral stenosis in which we find post-mortem 
 such rigidity of the half-open mitral orifice that we must believe that 
 regurgitation (as well as stenosis) existed in life, no systolic murmur 
 
 * Boston Medical and Surgical Journal, June 21, 1923. 
 
SUMMARY AND CONCLUSIONS 295 
 
 has been audible in life though it is the murmur most eagerly sought 
 for and most easily recognized by most examiners. 
 
 I have gone over these points at considerable length and in detail 
 because I know nothing of greater practical importance in the field 
 of cardiac diagnosis than to diminish, as far and as fast as we can, 
 that very considerable number of persons whose lives are now 
 rendered ineffective and miserable by a false diagnosis of heart 
 disease, usually of mitral regurgitation, when in fact their hearts 
 are perfectly sound. I believe such false diagnoses to be extremely 
 common. I know that they produce great mental torture and bodily 
 discomfort. Out of eighteen successive cases coming under my 
 observation recently with a diagnosis of heart disease, only four had, 
 in my opinion, any good evidence of such disease. The other four- 
 teen had systolic murmurs or cardio-respiratory murmurs, systolic in 
 time, with no history of rheumatism, no enlargement of the heart, 
 no hypertension, no arrhythmia, no thrill, and no evidence of passive 
 congestion either in the history or in the physical examination. 
 
 In life insurance examinations this certainly is a point of real 
 importance. It is a serious thing to be refused life insurance because 
 of the false interpretation of a systolic murmur. It is also serious 
 for a growing boy to be refused permission to enter athletics and to 
 gain aJl the advantages, mental, moral, and physical, which athletics 
 may bring. All this boys often lose now because an athletic instruc- 
 tor or an ill-trained physician has told them that their hearts are 
 diseased. Nearly 10% of a recent freshman class at Harvard 
 College was composed of men who believed themselves, quite falsely, 
 to be suffering from heart trouble. ‘They had been told so by their 
 physicians. Yet on careful study their hearts showed nothing signifi- 
 cant of disease, or nothing but the systolic murmurs about which so 
 much has been said in this chapter. 
 
 SUMMARY AND CONCLUSIONS 
 
 1. Mitral regurgitation without stenosis is the commonest diag- 
 nosis now made by American physicians in cases of real or suspected 
 heart disease. 
 
 2. Yet this lesion is exceedingly rare post-mortem; only 7 cases, 
 3 of them doubtful, were found in 1846 necropsied cases of heart 
 disease. In the same series there were 107 of mitral stenosis. 
 
 3. Pathologically the lesion is probably due to an endocarditis 
 confined or nearly confined to the chordae tendineae and papillary 
 muscles, 
 
2096 FACTS ON THE HEART 
 
 4. Even in rare cases wherein mitral regurgitation without 
 stenosis does exist, there are no physical signs by which it can be 
 recognized or reasoned out, so that a diagnosis of mitral eee 
 without stenosis is never justified. 
 
 5. For the proper evaluation of national strenet in time of war, 
 for the proper education and development of growing boys and girls, 
 for the fair and profitable adjustment of life insurance, and for the 
 happiness and comfort of all concerned, it is essential that we should 
 get this matter straight. JI am very glad to believe that with the 
 rapid development of cardiac clinics in many cities of this country, 
 and the better teaching of physical diagnosis which is now, I think, 
 in sight, we may see a notable improvement in this matter which will 
 date, I think, from the war of 1914-1918, and constitutes one of its 
 best results. 
 
 SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 
 
 Because of the beliefs just expressed and because I believe pure, 
 uncomplicated mitral regurgitation to be an exceedingly rare lesion, 
 if indeed it exists at all, I have given in detail all the cases of our 
 series which show any evidence of such a lesion. These cases follow 
 herewith. 
 
 Of the seven cases of this series, 5 occurred in males and two in 
 females. Five were above the thirty-sixth year. Arheumatic history 
 was obtained in only one case. The patients presented themselves 
 with the ordinary symptoms of decompensated heart trouble. 
 In the physical examination cardiac enlargement with a systolic 
 murmur were the chief data bearing upon a possible mitral lesion. 
 Two cases were thought in life to have mitral stenosis also (282, 
 2825). In one case there was another murmur referable to an 
 associated aortic stenosis. I have been interested to note that while 
 textbook descriptions—including those given in the earlier editions 
 of my own book on Physical Diagnosis—list an accentuated pulmonic 
 sound as one of the cardinal points in the diagnosis of mitral regurgi- | 
 tation, this sign was present in only three cases of our series and one 
 case observed outside the hospital. In three cases the pulmonic 
 second sound was notably weak or absent, as is often the case in 
 mitral stenosis. Possibly the explanation is the same in both groups. 
 Detailed histories of these cases follow. 
 
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 SEVEN CASES OF THAT GREAT RARITY——MITRAL REGURGITATION 
 
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20054 FACTS ON THE HEART 
 
 Necropsy 2341 
 
 An American carpenter of forty-nine came to the Accident Room 
 of the Massachusetts General Hospital, March 31, 1909. 
 
 He had had the diseases of childhood, gonorrheal urethritis as a 
 youth, chancre followed by sore throat and eruption at twenty, 
 ‘‘inflammation of the bowels”’ with vomiting, fever and tender abdo- 
 men laying him up for two weeks at twenty-two, and ‘“‘in early life.” 
 an attack of jaundice. 
 
 Two and a half weeks before admission ne was seized with 
 general abdominal pain and diarrhea. March 25 the diarrhea was 
 “checked by blackberry wine.” Since then his bowels had had to be 
 moved by enemata. The pain had continued, not localized. For 
 forty-eight hours he had been vomiting continuously, for the last 
 twelve hours a greenish material. 7 
 
 Examination showed the apex impulse of the heart in the nipple 
 line, fifth space. At the apex was a loud systolic murmur, heard also 
 over the whole precordia and transmitted to the axilla. The second 
 sounds were not made out. The abdomen was slightly distended. 
 On the left side was some deep seated tenderness, but very little 
 spasm. On the right there was considerable rigidity of the abdomi- 
 nal wall, and tenderness which was extreme in the right lower 
 quadrant, where there was an area of dullness. The knee-jerks 
 were lively. There were varicose veins in the left leg. The rest of 
 the examination showed nothing of importance. The temperature 
 before operation was to1.4°, the pulse 102, the leucocytes 25,000. 
 
 Operation, which was immediately done, showed a great deal 
 of thin very foul-smelling pus in the peritoneal cavity. The appen- 
 dix was found buried in a mass of adhesions, perforated near its tip, 
 and very friable, as was the surrounding tissue. In removing the 
 appendix it was torn in two. In making a stab wound for drainage 
 the deep epigastric artery was cut and so tied off. The pathological 
 report on the appendix was gangrenous appendicitis. Culture of the 
 pus from the peritoneum showed a scum of growth of bacilli and 
 micrococcl. 
 
 The patient was sent to the ward in good condition and was put in 
 semi-sitting posture with rectal seepage. He spent a comfortable 
 night, but the following night became very much worse. The pulse 
 became more rapid, 122-135, poorer in quality, and intermittent. 
 The temperature rose from 99° to 104°. The respirations ranged 
 from 36 to 4o. April 3 he died. 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 299 
 
 The clinical diagnosis was appendicitis with abscess and general 
 peritonitis. 
 
 Necropsy showed 
 
 Acute diffuse fibrinopurulent peritonitis, 
 
 Acute pleuritis, 
 
 Fibrous endocarditis of the mitral valve, 
 
 Syphilitic aortitis, 
 
 Hypertrophy and dilatation of the heart, 
 
 Hypoplasia of the left kidney, 
 
 Compensatory hypertrophy of the right kidney. 
 
 The heart weighed 422 grams and showed hypertrophy especially 
 of the left ventricular wall. The four cavities were all enlarged. 
 All the valves were enlarged: tricuspid 14 cm., aortic 8 cm., pul- 
 monary, 9 cm. 
 
 The mitral vaive measured 14.5 cm. Its circumference greatly 
 enlarged, its curtains generally thickened. ‘‘ Much fibrous thicken- 
 ing produced rather marked areas of elevation and depression with 
 shortening and thickening of the chordae tendineae. (Italics mine.) 
 
 The other valves were not remarkable. 
 
 Discussion.—We have here no evidence of passive congestion 
 post-mortem and no symptoms suggesting it in life. Yet the heart is 
 enlarged and none of the ordinary extracardiac causes of hyper- 
 trophy are present. It is notable that the hypertrophy is if anything 
 more marked on the left than on the right side. Yet both ventricles 
 are thickened, and we have abundant evidence that such general 
 cardiac enlargement is often associated with mitral disease. The 
 syphilitic aortitis which was present did not involve the aortic valve 
 or produce any other change which should cause cardiac hypertrophy. 
 
 Was the mitral valve a cause of trouble in this man’s circulation? 
 It is hard to say. Since all the valve orifices probably became 
 enlarged with the terminal infection following operation, the cardiac 
 murmur may have been produced at one of the other orifices and 
 may have had no connection with the demonstrated fibrous endo- 
 carditis of the mitral. The latter may belong with our series of non- 
 deforming valve thickenings (Chapter VIII). 
 
 Yet on the whole and especially in view of the lesions in the 
 chordae tendineae, it seems to me that this may be a genuine case of 
 mitral regurgitation, though slight in degree. 
 
 Necropsy 3092 
 
 An American railway engineer of forty-eight entered August 21, 
 1912. His father died with dropsy of unknown origin. The 
 
300 FACTS ON THE HEART 
 
 patient had gonorrhea at nineteen, double pneumonia in 1808, 
 measles, mumps, and chicken-pox between the ages of thirty and 
 forty. Until eight months before admission he was a heavy smoker. 
 He alsochewed tobacco. Heoccasionally drank beer. Heslept poorly. 
 
 Ever since his pneumonia in 1898 he had had slight edema of the 
 ankles at night, some cough with a little yellowish sputum, and had 
 slept on four pillows. For the past four years he had had some 
 dyspnea on exertion. For two years he had urinated twice at night. 
 A year and a half before admission he began to have edema of the 
 legs. He stopped work for two weeks. The swelling gradually 
 subsided and he was able to resume work. Beginning in December, 
 tg1i, he was laid up for three months with a return of the edema. 
 After working again for a few days the swelling returned and had 
 persisted, growing more extensive and brawny. His hands had been 
 slightly swollen for six weeks. He had been in bed most of the time 
 for the past five weeks. The least exertion caused dyspnea. He 
 belched considerable gas. The morning of admission he noticed 
 cyanosis. In 1900 he weighed 185 pounds, five months before 
 admission 146. 
 
 Examination showed a very poorly nourished man with cyanotic 
 skin and mucous membranes. The respiration was somewhat 
 labored, with both expiratory and inspiratory dyspnea. There was 
 some pyorrhea. The apex impulse of the heart was faintly felt in 
 the fifth space 12 cm. to the left of the midsternal line, one cm. outside 
 the nipple line. There was no enlargement to the right. The action 
 was regular. The first sound at the apex was replaced by a loud 
 blowing systolic murmur heard over the entire precordia, loudest 
 at the apex, transmitted to the axilla. There was slight dullness 
 above the precordia on both sides of midsternum. ‘The sounds at 
 the base were very distant, the pulmonic second sound accentuated. 
 The pulses were of fair volume and low tension. The artery walls 
 were not felt. The blood pressure was 100/80. The expansion of 
 the lungs was poor but equal. ‘There was marked retraction of the 
 interspaces with inspiration. The accessory muscles of respiration 
 were employed. There was hyperresonance throughout, with dimin- — 
 ished ‘‘emphysematous” breathing. Fine to coarse moist rales, pip- 
 ing and squeaking rales were heard throughout. The abdomen was 
 full, distended. There was marked ascites. (See Fig. 52.) In the 
 flanks was shifting flatness and a fluid wave. The liver dullness 
 extended from the sixth space to 4 cm. below the costal margin. A 
 non-tender edge was indefinitely felt. There was great edema of the 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 301 
 
 scrotum, slight edema of the penis, very marked brawny edema of 
 the upper and lower legs, slight soft edema of the hands, wrists, and 
 abdominal wall, moderate soft edema of the lower back. The fingers 
 were clubbed, thenailscyanotic. Thepupilsand reflexes were normal. 
 
 Indefinite)] { 
 liver edge Su 
 
 Tympany 
 
 Shifting 
 dulness } 
 
 Fic. 52.—Dullness, abdominal and thoracic, in case 3092. 
 
 Duration 
 of Disease 
 
 Dejections 
 
 So 
 a 
 
 reall (rs od ick ee ed dee GU a 
 210 e 100° Hae Scena me 
 seb ek Ed Sis BO VN ES Ka ld Wd 
 ne eee eee 
 
 25 PF EE a 
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 ff 
 0H yes i al 
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 ea [ea | nS 
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 ood A A A 
 Peles te ane Fe 
 AV Gol a es ed 
 22 ra en Pas 
 7 da a 
 
 Fic. 53. 
 
 The temperature and pulse were as shown in Fig. 53. The res- 
 pirations were 20 to 33. The amount of urine was 10 to 33 ounces, 
 the specific gravity 1.014 to 1.022. There were slight traces of 
 albumin at five of six examinations, occasional hyalin casts at three. 
 
302 FACTS ON THE HEART 
 
 The hemoglobin was 100%. The other blood findings were normal. 
 A Wassermann was negative. 
 
 The abdomen was tapped the day of entrance and a quart of clear 
 straw-colored fluid removed before the cannula was shut off. The 
 specific gravity of the fluid was 1.012. The sediment showed 6% 
 polynuclears, 94% lymphocytes. A culture was negative. 
 
 The patient did not respond to stimulation or diuresis. Vene- 
 section was also tried with no benefit. He failed and September 
 2 died. 
 
 Clinical Diagnosis (from Hospital Record).—Chronic bronchitis 
 with emphysema. 
 
 Mitral regurgitation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Decompensation. 
 
 Anasarca. 
 
 Ascites. 
 
 Chronic passive congestion of all the organs. | 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic broncho-pulmonary 
 infection. 
 
 Bronchitis. 
 
 Cirrhosis of the lung. 
 
 Arterlosclerosis. 
 
 Myocardial weakness. 
 
 Hypertrophy and diltation of the heart. 
 
 Passive congestion. 
 
 Anatomical Diagnosis (Dr. Oscar Richardson).—1. Chemical or 
 
 physical origin of fatal illness. | Chronic bronchitis. 
 ' Focal pneumonia. 
 
 Focus of chronic interstitial 
 pneumonitis, inferior lobe 
 of left lung. 
 
 Edema of the lungs. 
 
 2. Secondary or terminal lesions ; Mitral insufficiency. 
 
 Hypertrophy and dilatation 
 of the heart. - 
 
 Chronic passive congestion, 
 general. 
 
 Hydropericardium. 
 
 Ascites. 
 
 | Anasarca. 
 3. Historical landmarks. Chronic pleuritis. 
 
bi 
 
 SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 303 
 
 The mitral valve was 12 cm. in circumference (normally 1o cm.). 
 Except for the increase of circumference the valve was not remarkable. 
 
 The hypertrophy of the cardiac walls was more marked on the 
 right side. The organ was enlarged. Its cavities were enlarged. 
 
 There was no emphysema. There is a possibility that the 
 chronic interstitial pneumonitis was much more extensive in this 
 case than is indicated, as it may have been disguised in the section 
 surface by the chronic passive congestion. 
 
 The case is instructive in several ways as we look back upon it 
 with the wisdom of hindsight. In the first place it is a good example 
 of the heart lesion often diagnosed simply as mitral regurgitation. 
 The true diagnosis was cardiac hypertrophy, especially of the right 
 side, from overwork in overcoming the pulmonary obstruction due to 
 chronic pneumonitis or cirrhosis of the lung. As a minor feature of 
 this cardiac dilatation we have a mitral orifice measuring 12 cm. 
 instead of to cm., and perhaps somewhat incompetent. 
 
 A second point of interest is the absence of any pulmonary emphy- 
 sema post-mortem, despite the fact that he had during life hyper- 
 resonance, a breathing of the type usually associated with emphysema, 
 and rales such as usually go with that disease. This proves 
 that the physical signs often supposed to be diagnostic of emphysema 
 may accompany either that disease or other diseased conditions, 
 among which passive congestion from cardiac weakness in a barrel- 
 chested individual is perhaps the commonest. 
 
 The valves were all enlarged in this case (tricuspid 13 cm., aortic 
 8, mitral 12) but the pathologist definitely calls attention in his 
 diagnosis to mitral regurgitation and to the congested lungs, so much 
 engorged that other and more chronic changes were masked. 
 
 There is evidently more hypertrophy of the right ventricle than 
 of the left, though both sides are dilated. (Right ventricle 7 cm., | 
 left ventricle ro.) 
 
 In the absence of hypertension, nephritis and arteriosclerosis I 
 think we must say that this is one of the cases of true chronic bronchitis 
 with broncho-pulmonary infection and chronic pneumonitis gradually 
 developing after an (imperfectly resolved?) pneumonia and that as 
 part of the cardiac hypertrophy due to this cause the mitral valve 
 orifice was enlarged and very possibly incompetent. But the 
 systolic murmur might also be explained as due to incompetency of 
 the tricuspid valve especially as the pulmonary disease must have 
 brought unusual strain upon the right ventricle. 
 
304 FACTS ON THE HEART 
 
 Necropsy 2825 
 
 An American motorman of thirty-seven entered March 30, rort. 
 His past history was negative except for dyspnea on considerable 
 exertion for fourteen years. He had had his present trouble for four 
 years and a half and was refused admission to the police department 
 because of it. Six weeks before admission he became very dyspneic 
 on running for a car, and felt very cold all day. For the next five 
 days he had dyspnea on slight exertion and pain in the left shoulder. 
 Medical treatment gave relief. Since the acute onset he had had 
 cough and edema of the legs. His dyspnea, palpitation, and edema 
 had grown gradually worse unless he stayed in bed. He gave up 
 work three weeks before admission, and had been most of the time in 
 bed. The cough was now hacking, occasionally with white sputum. 
 For two days his trousers had felt too tight. He slept poorly with 
 two pillows because of dyspnea and nervousness. Cold affected 
 him unfavorably. Two days before entrance he vomited. He had 
 lost flesh, but thought he had gained weight. 
 
 Examination: showed a fairly well nourished man, tired-looking 
 and dyspneic. The mucous membranes were slightly pale and 
 cyanotic. The teeth showed many carious stumps. The apex 
 impulse of the heart was diffusely seen and felt as far down as the 
 fifth space and as far out as the border of dullness, 15 cm. to the 
 left of the midsternum and 4 cm. outside the nipple line. The right 
 border of dullness was 4.5 cm. from midsternum. The sounds were 
 irregular in force and frequency, fair in quality. The first sound at 
 the apex was rather sharp. There was a slight systolic, possibly 
 presystolic, thrill at the apex. A blowing rough systolic murmur 
 -was heard all over the precordia and in the axilla and both backs, 
 loudest over the apex. The aortic second sound was scarcely audible. 
 The pulses were irregular in force and frequency, fair in volume 
 _and tension. The blood pressure was 195/90 to 115/90. The lungs 
 were negative. The liver dullness extended from the fifth rib to 5 
 cm. below the costal margin. ‘The edge was indistinctly felt. There 
 was great soft edema of both legs and slight edema of the sacral 
 region. ‘The genitals, pupils, and reflexes were normal. 
 
 The temperature was 96.4° to 98.5°, the pulse 59 to 120, the 
 respiration 26 to 31. The amount of urine was 4 to 71 ounces. 
 The urine was turbid, the specific gravity 1.034 to 1.020. There was 
 the slightest possible trace of albumin at two of three examina- 
 tions, a few hyalin casts at all, fatty casts at one. The hemoglobin 
 
 was 95%. There were 14,000 leucocytes. The smear showed ~ 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 305 
 
 polynuclear leucocytosis. A Wassermann and a throat culture 
 were negative. 
 
 The patient was restless and dyspneic, requiring morphia and 
 atropin. ‘Tracings of the jugular vein and the apex showed auricular 
 and ventricular waves occurring synchronously, i.e. nodal rhythm. 
 He grew steadily worse, vomiting everything. All medication except 
 strychnia was omitted, and he was given intravenous strophanthin 
 
 14 to 19 mg. on April 4, 5, and 6, with temporary slowing of the 
 ae He continued to fail steadily, and April 6 died. 
 
 Clinical Diagnosis (from Hospital Record).—Mitral insufficiency. 
 
 Dilated heart. 
 
 Infarction of lung. 
 
 Dr. W. H. Smith’s Diagnosis —Mitral stenosis and regurgitation. 
 
 Probably aortic stenosis and regurgitation. 
 
 Possibly adhesive pericarditis. 
 
 Acute glomerulonephritis. 
 
 Anatomical Diagnosis——Chronic fibrocalcareous endocarditis 
 of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 - Septicemia, streptococcus. 
 
 Thrombosis of the right auricular appendix. 
 
 Thrombosis of branches of the right pulmonary artery. 
 
 Infarct of the right lung. 
 
 Septic staining of intima of all the great blood vessels. 
 
 Chronic passive congestion, general. 
 
 Slight hydropericardium, hydrothorax, and ascites. 
 
 Anasarca. 
 
 Dr. RicHarpson: The heart weighed 660 grams,—considerably 
 enlarged and all its cavities markedly dilated. (Normal weight 
 200-300 grams). The right ventricle wall measured 3 mm., the left 
 11mm. The heart muscle was thin, flabby, dirty brownish-red,— 
 anatomically a wall in harmony with the marked dilatation. The 
 dominant feature at necropsy was the dilatation of the heart. The 
 right auricular appendage was occluded by a mural thrombotic 
 mass, a typical source for the embolic thrombosis of the branches of 
 the right pulmonary artery and the infarct of the right lung. The 
 mitral valve measured 1714 cm. (normally 10)—nearly twice the 
 normal circumference. The valve was the seat of what was called 
 chronic endocarditis. The mitral valve has two cusps. Along the 
 entire length of the insertion of the posterior cusp was a. fibro- 
 
 calcareous columnar mass, its surface irregular, nodular, and fibrous. 
 20 : 
 
306 FACTS ON THE HEART 
 
 This mass ceased abruptly in the region of the anterior cusp and 
 was 6 cm. long, 1.5 cm. wide and 1.2 cm. thick. The small strip of 
 curtain of the posterior cusp which lay anterior to the mass and 
 included the free portion of the cusp showed little if any fibrous 
 change. The chordae tendineae showed little if any thickening. The 
 remaining 1114 cm. of the valve curtain was negative. One portion 
 of the valve showed chronic fibrous deformity, and the rest was so 
 stretched that between the two the valve was almost twice its 
 normal circumference. One would expect to find hypertrophy of 
 the myocardium of the right ventricle, yet it was only 3 mm.; but 
 probably it was once thicker, and had stretched. 
 
 The other valves were negative, except that their circumferences 
 were increased, especially the tricuspid, which was 16 cm. (normally 
 12-13) aortic 8.5, pulmonic 10.5; of course in association with the 
 dilatation of the heart. The rest of the circulatory apparatus was 
 negative except for deep purplish staining of the endocardium and the 
 intima of the great vessels which is found at times in association with 
 streptococcus septicemias. 
 
 The liver, spleen, etc., showed chronic passive congestion, and the 
 gastro-intestinal tract some swelling and reddening of the mucosa 
 associated with the chronic passive congestion. 
 
 Culture from the heart blood showed a good growth of streptococci. 
 
 This was a very unusual lesion of the mitral valve. The only 
 other lesion I have seen like it was in a heart in which there was found 
 in the same cusp a similar mass, which had extended across into the 
 region of the bundle of His, giving a typical picture anatomically of 
 Stokes-Adams disease. The clinical diagnosis also was Stokes- 
 Adams disease. 
 
 A Puysictan: Would the valve close? 
 
 Dr. RicHarpson: I do not know what a valve like that would do 
 under pressure. Under the anatomical condition present in the 
 valve at necropsy it would seem probable that regurgitation would 
 be more or less marked. 
 
 Necropsy 3320 
 
 A machinist of seventy-four entered the Mass. General Hospital 
 February 28, 1914. 
 
 ‘His past history was excellent except for gonorrhea thirty years 
 ago. 
 
 Four years ago he had to give up work for seven months on 
 account of dyspnea, weakness and swelling of the feet. He then had 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 307 
 
 a sore on the right leg for five months, but was not confined to bed. 
 Since then he had been well and working every day until seven months 
 ago, when he was waked one night by dyspnea. Next day he felt 
 weak and noticed that his feet were swollen. He soon began to cough 
 and raise a little frothy sputum. He has not worked since then; 
 he tried it but found that he was too weak. Sleep, appetite and 
 bowels were normal. He has urinated two or three times at night 
 for several months, and has had a little dribbling recently, but no 
 polyuria. He has not been confined to bed. — 
 
 On examination he was well developed and poorly nourished. 
 Respiration rapid, shallow. The skin showed many papules on 
 chest and some looseness. Head not remarkable. Throat reddened. 
 Much yellow exudate. Apex impulse of heart in the fifth space 1.5 
 cm. outside nipple line. No increased supracardiac dullness. 
 Action slow; occasional extrasystole. A loud musical systolic mur- 
 mur was heard at the mitral area referred to axilla and audible faintly 
 all over the precordia. No diastolic heard. Az2 not heard. Pa2 
 faint. Pulses slow, occasional extrasystole. Arterial walls tortuous 
 and hard. The lungs showed slight dullness at the right apex and 
 dullness at the right base with diminished breathing, high-pitched 
 inspiration and prolonged expiration, many coarse rales and dimin- 
 ished voice sounds. Signs in left not so marked. Abdomen 
 slightly resistant. Slight shifting dullness in flanks. No spasm or 
 masses. Slight edema of the abdominal wall in flanks. Genitals 
 negative. Hands slightly cyanotic. Skin over shins and ankles 
 raw, reddened, scaling, brawny, loose. Slight edema of ankles. 
 Pupils and reflexes negative. 
 
 Temperature 99°—-101.5° until the day of death, then falling to 
 97.8°. Pulse 99-81. Respiration 25-45. Blood pressure 160/r10. 
 Urine, 36-34. Specific gravity 1.024-1.020. A slight trace of 
 albumin at both examinations. A rare red blood corpuscle. Blood: 
 Hemoglobin 95%. Leucocytes 34,600-24,000. Polynuclears 91%. 
 
 Much morphia was used to give rest. The patient had Cheyne- 
 Stokes breathing almost constantly. March 4 a reddened, brawny, 
 tender area had appeared at the inner right thigh, pronounced by a 
 surgical consultant streptococcus lymphangitis. The general condi- 
 tion was worse, the patient almost comatose at times. The following 
 day he was weaker, with very feeble and irregular heart action and 
 very poor pulse. March 6 he died. 
 
 The clinical diagnosis reads ‘“‘chronic endocarditis of the aortic 
 and mitral valves. Arteriosclerosis.”’ 
 
308 | FACTS ON THE HEART 
 
 Anatomical Diagnosis —I. Chronic fibrinocalcareous endocarditis 
 of the aortic valve, stenosis. 
 
 Fibrous sclerosis of the mitral valve. 
 Arteriosclerosis. 
 Hypertrophy and dilatation of the heart: (558 grams.) 
 II. Septicemia, streptococcus. (Terminal.) 
 
 Erysipelas of the right thigh. 
 Hydrothorax, double. 
 
 III. Ulcers of the legs. 
 Slight arteriosclerotic nephritis. 
 Slight chronic pleuritis, right. 
 Obsolete tuberculosis of the apices of the lungs. 
 Chronic perisplenitis. 
 Hypertrophy of the middle lobe of the prostate. 
 Hypertrophy of the trabeculae of the bladder. 
 
 The aortic valve was reduced to a slit like orifice 2 cm. X 6 cm. 
 The tricuspid 13.5. Pulmonary 8. 
 
 “The mitral valve measures 9.5 cm. Its curtains present a 
 moderate amount of diffuse fibrous thickening which is slightly 
 nodular along the free margins. The chordae tendineae are slightly 
 thickened and the upper portions of the papillary muscles show small 
 yellowish fibrous areas. 
 
 “The heart weighs 558 grams. The organ is considerably 
 enlarged. On section the myocardium generally is thick and pale 
 brown red. Right ventricle wall 5 mm., left ventricle wall 13 mm. 
 The columnae carneae are thick and prominent on each side. The 
 auricular walls are thickened. The cavities of the ventricles are but 
 little enlarged, if any. The auricular cavities are enlarged.” 
 
 Comment.—Obviously aortic stenosis with regurgitation is the 
 main lesion. There may have been some mitral regurgitation also 
 though this is by no means certain. 
 
 A 17-year-old-housewife was seen March 13, 1922, complaining of 
 ‘cough and breathlessness.’ 
 
 Had childrens’ diseases and frequent tonsillitis until tonsillectomy 
 and adenoidectomy 5 years ago. Severe attacks of rheumatic fever 
 frequently (every 2-3 years) until three years before admission. 
 Nycturia, lately 2-3 times a night. 
 
 Twelve years before admission, after an attack of acute rheumatic 
 fever complicated by chorea, the patient noticed breathlessness and 
 swelling of legs. Four years later it was necessary for her to go to 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 309 
 
 bed for three months because of an increase in breathlessness and 
 swelling of legs with substernal pain. Since then she has spent about 
 a half of each year in bed because of these symptoms, up to the pres- 
 ent time. One year ago she was married and immediately became 
 pregnant. Her symptoms grew worse until she had a miscarriage 
 at five months, since which her condition has been much worse. 
 She has been in bed, suffering with a persistent cough, dyspnea, 
 orthopnea, palpitation, and substernal pain. 
 
 On examination the patient was poorly developed and poorly 
 nourished, in extreme discomfort, markedly orthopneic and coughing 
 almost incessantly. Heari: The apex impulse was diffuse; pulsations 
 were palpable in the midaxillary line 18 cm. from mid-sternal line. 
 Percussion note dull to flat over base of left lung. Absolute 
 arrhythmia. Heart rate 142 with a pulse deficit of 60. The sounds 
 were poor in quality, the 1st sound approaching the second in char- 
 acter. Soft blowing diastolic and systolic murmurs were heard over 
 entire precordium. P2 was greater than A2 and was accentuated. 
 No thrills. Blood pressure 92/54. Evidence of left hydrothorax. 
 Abdomen showed a fluid wave and shifting dullness. The liver 
 edge, firm, smooth and tender, was palpable 8 cm. below the costal 
 margin. ‘There was marked edema of the legs. 
 
 The blood Wassermann was positive on two tests. Renal Func- 
 tion 39%. Urine 1022 and 1014 in two specimens with traces of 
 albumin, rare red cells and a few hyaline and granular casts. Leu- 
 cocytes 12,000 to 16,000. Temperature 100 to 102. Pulse averaged 
 go. 
 
 Six days after admission the dullness at both bases disappeared 
 and only a few crackling rales could be heard. On the twelfth day 
 after admission the temperature rose to 104, the patient became 
 weaker, with increased edema and dullness at lung bases. She died 
 on March 25th. 
 
 Necropsy.—Heart 500 grams. 250 c.c. in pericardium. Mitral 
 13 cm., tricuspid 12, pulmonic 7.5, aortic 7.5. Left auricle big and 
 stretched. Mitral curtain and its tendinous chords thickened. 
 Aortic valve normal except for acute endocarditis. No stenosis. 
 Acute endocarditis on aortic valve (streptococci). Patchy fibrosis 
 in myocardium. ; 
 
 Lungs normal except for chronic passive congestion with infarcts 
 and thrombosed vascular branches. 
 
 Liver and spleen showed chronic passive conjestion. 
 
 Calcified (Tb.) mesenteric nodes. 
 
310 FACTS ON THE HEART 
 
 Calcified nodes (Tb.) in liver and spleen. 
 Kidneys normal. 
 Pure mitral regurgitation with acute aortic endocarditts. 
 
 Necropsy 797 
 
 A woman of 37 was in the ward from December 16th to December 
 24th with what appeared to be pneumonia. She had been ill 15 days 
 with dyspnea and fever beginning witha chill. The pulse was regu- 
 lar at 120 to 160, finally 220. The leucocytes were 16,000, 21,000, 
 24,000, the temperature 101 to 105°. The heart’s action was regular. 
 There was a slight systolic murmur at the apex. The pulmonic 
 second was slightly accentuated. . 
 
 Post-mortem the heart weighed only 360 but considering the size 
 of the individual was hypertrophied and dilated. The aortic valve 
 though quite normal measured only five cm. in circumference. The 
 mitral circumference was ten cm. The cordae tendineae leading to 
 the curtain were shortened and thickened. The free edge of its cur- 
 tain presented a row of irregular nodular masses fibrous and gray- 
 white. A soft, gray-red, shaggy, mushy mass, two cm. in diameter, 
 extended from the curtain of the valve up on to the wall of the left 
 auricle where it was weakly adherent. There was chronic passive 
 congestion of the lungs and pneumococcus septicemia. 
 
 The diagnosis was not suspected in life, but from this history and 
 symptoms, pneumonia was in all probability believed to be present, 
 and may well have been present though it was not shown at necropsy, 
 for there was a fibrinous pleurisy and a pneumococcus sepsis in addi- 
 tion to the acute and chronic endocarditis of the mitral. 
 
 Necropsy 282 
 
 A thirteen-year-old schoolboy, with good family history and past 
 history, entered June 8. 
 
 He thought he had never had any children’s diseases, rheu- 
 matism or chorea. Last October he had mumps. All winter he 
 had a cold with cough so violent that he sometimes vomited; not 
 much sputum, never blood. Two months before admission he noticed 
 a bunch on the right thigh, painful on lying down and when walking. 
 A month ago he had pain in the knee when lying down. The bunch 
 was now growing smaller. 
 
 Three years ago and a year and a quarter ago he was treated 
 in a hospital for ‘‘heart disease.”” He was not particularly short 
 of breath on going upstairs until lately. He sometimes had pain 
 
SEVEN CASES OF THAT GREAT RARITY—MITRAL REGURGITATION 3i1 
 
 over the precordia and over the left shoulder. Four days before 
 admission, after a night of hard coughing, his scrotum suddenly 
 began to swell and became bigger than his fist and painful. The 
 pain and swelling were now growing less. 
 
 A rather poorly developed and nourished, pale boy with slightly 
 cyanotic lips and fingers, breathing rapidly with effort and cough- 
 ing often and in paroxysms, more violently when lying down, 
 without much sputum. Cervical and right epitrochlear glands 
 enlarged. Apex impulse of the /eart in the sixth space (see Fig. 54), 
 strong and diffuse. Action irregular. P2 accentuated and redupli- 
 cated. At the apex a rolling presystolic, a rough systolic, and a 
 short diastolic murmur, presystolic and systolic thrills; second sound 
 audible. At the base a faint diastolic murmur. At the right border 
 of the sternum below the costal cartilage of the fifth rib a systolic 
 
 Po+ and reduplicated. 
 
 paca 
 murmur 
 
 Systolic 
 pat Naha Y) | (Marked _ 
 C41’ epigastric 
 pulsation. 
 
 murmur. Marked epigastric pulsation. A boat-shaped prominence 
 over the lower sternum. Pulse rapid, rather irregular, fair volume, 
 compressible. Lungs not recorded. Abdomen rather tense. Wall 
 edematous above the pubes. Genitals. Scrotum edematous, trans- 
 lucent, rather tender. Hvxiremities. Slight edema of the legs and 
 ankles, more on the right. Both patellae floating, the right more 
 than the left; also more tender than the left. On the right thigh was 
 an irregular, hard, slightly tender mass the size of a butternut 
 attached immovably or growing from the bone. 
 
 T.97°-102.3°. P.82-102. R.41-79. Urine. Normal amount, 
 sp. gr. not recorded, a trace of albumin. Blood. Leucocytes 18,400. 
 
 The boy coughed very hard all the afternoon, raising light bloody 
 sputum. He suffered a good deal. After being given morphia and 
 castor oil he vomited. Next day he was quieter. The temperature, 
 however, was up. He still coughed considerably. June 11 he had 
 pain over both chests and in the epigastrium, and was very restless. 
 
312 FACTS ON THE HEART 
 
 The sputum was considerably blood stained. The temperature 
 dropped to 97°, then rose to 102.3°.. The morning of June 12 he died. 
 
 Clinical Diagnosis ——Chronic and acute endocarditis. 
 
 Anatomical Diagnosis——Acute and chronic endocarditis of the 
 mitral valve. 
 
 Chronic adhesive pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the lungs, liver, spleen and kidneys. 
 
 Edema of the scrotum. 
 
 Slight double hydrothorax. 
 
 Edema of the lungs. — 
 
 The heart was large, weighing, with the pericardium adherent, 
 625 grams. The parietal pericardium was everywhere adherent to 
 the heart by old fibrous adhesions. The mitral valve was 13 cm. 
 in circumference. One half the curtain was much shortened and 
 slightly thickened. The edge of most of the valve was studded with 
 minute granulations. The left auricle was markedly dilated. The 
 left ventricle was dilated. The trabeculae were thin and flattened. 
 The thickness of the wall wast4 mm. The right auricle and ventritle 
 were somewhat dilated. The right ventricle wall was 4 mm. in thick- 
 ness. The aortic valve measured 514 cm. in circumference, the tri- 
 cuspid 13 cm., the pulmonary 6/4 cm. 
 
 A culture from the kidney showed a few bacilli. Cultures from 
 the heart blood, the liver and the spleen were sterile. | 
 
 FATAL CHOREA 
 
 Necropsies are so rare in Sydenham’s chorea that I have added 
 here the full clinical and pathological record of three fatal cases, 
 occurring in unmarried girls aged thirteen, sixteen, and twenty, 
 respectively. The duration of symptoms from the first complaint 
 until death was: eight weeks, six weeks, and four and a half weeks. 
 Two of the patients had had previous attacks of chorea. In one 
 patient there was also an acute rheumatic arthritis and tonsillitis. 
 In the others the chorea was the only obvious clinical sign, the move- 
 ments being in one case so violent as to lead to fracture of two ribs. 
 
 At necropsy all the hearts showed an acute endocarditis in the 
 form of “small, soft, grayish-yellow red-tipped vegetations”’ placed 
 in rows along the free margins of the mitral curtains; also to a less ~ 
 extent on the aortic and in one. case the tricuspid also. In two of the 
 cases there was also a chronic fibrous endocarditis on the aortic valve. 
 
FATAL CHOREA 313 
 
 In one case the heart was slightly enlarged; in two it was of normal 
 size. The myocardium showed no lesions. In one case there was 
 an acute pericarditis. 
 
 Complications of interest were: 
 
 Case 1.—Double parotitis. Slight cystitis. Slght broncho- 
 pneumonia. 
 
 Case 2—Pulmonary tuberculosis with empyema (left). Fibrin- 
 ous pleurisy (right). Fracture of 6th and 7th ribs with purulent 
 infiltration about the fractures. 
 
 Case 3.—Pulmonary tuberculosis. Serofibrinous pericarditis. 
 Status lymphaticus. 
 
 The occurrence of pulmonary tuberculosis in two of these three 
 cases is of interest, especially as it was apparently acute and gave 
 no signs or symptoms until the last few weeks of life unless we are to 
 count the rcord: ‘“‘five months ago threatened with pneumonia” as ~ 
 evidence of tuberculosis. 
 
 Necropsy 2563 
 
 An American schoolgirl of thirteen entered March 9, 1rg10. 
 Two years after her birth her mother died of tuberculosis. The 
 child was always very nervous. She had a few sore throats, with 
 removal of adenoids several years before her admission. At ten 
 she had a bad attack of chorea. ‘Three weeks before admission to 
 the “hospital she began to have twitching, which March 8 became 
 much worse and in the evening very violent. For two days she had 
 had slight cough. 
 
 Examination showed a well nourished girl unable to sit in a chair, 
 screaming at times, with violent choreiform movements of all the 
 muscles. At times she had to be held in bed. The left tonsil was 
 enlarged. The apex impulse of the heart was best felt in the fifth 
 space in the anterior axillary line 6 cm. outside the nipple, 13 cm. 
 from midsternum. There was no enlargement to the right. The 
 action was rapid. A faint systolic murmur was heard at the apex 
 transmitted to the axilla. At the base were sounds of an entirely 
 different quality. In the pulmonic area a late systolic murmur was 
 heard, with a loud sharp pulmonic second, greatly accentuated and 
 louder than the aortic second. The pulses were of fair volume and 
 tension. The lungs, abdomen, pupils and reflexes were normal. 
 The genitals and extremities are not recorded. The skin of the back 
 and the exposed areas was reddened and roughened. A skin consult- 
 ant pronounced the condition irritation due to constant movements. 
 
314 FACTS ON THE HEART 
 
 The temperature was 99.8° to 105°, with continuous general rise 
 after March 10. The pulse was 119 to 151, the respiration 29 to 58. 
 The output of urine was 9g to 29 ounces, the specific gravity 1.012 to 
 1.026, cloudy at all of four examinations, the slightest possible. trace 
 of albumin at the last, slight acetone at two. The hemoglobin was 
 75%, the leucocytes 17,000, the polynuclears 85%. 
 
 The patient continued to be very violent and was not quieted 
 except for periods of half an hour to an hour by any of the sedatives 
 used until large doses of veronal made her sleep most of the time for 
 thirty-six hours. After this the motions were easily controlled by 
 morphia. March 16 the heart seemed larger than at entrance. Dur- 
 ing the next two days the jerks increased, and the patient became 
 quite cyanotic and had a good deal of cough and painin the chest. A 
 pleural rub developed over the left chest and also a to-and-fro cardiac 
 rub loudest over the area of relative dullness and hardly heard over 
 the area of flatness. March 19 there was some dullness in the middle 
 of the left back, with a moderate number of fine respiratory crackles 
 and a dry rub over the right back. The heart’s apex impulse became 
 more forcible and localized, now in the fifth space as far out as the 
 anterior axillary line. The pulmonic second sound seemed louder. 
 
 March 1g the patient became suddenly worse and died. 
 
 Clinical Diagnosis (from Hospital Record)—Acute chorea. 
 
 Acute endocarditis. 
 
 Acute pericarditis. 
 
 Mitral regurgitation. 
 
 Dry pleurisy 
 
 Bronchopneumonia (?) 
 
 Dr. Richard C. Cabot’s Diagnosis. 
 
 Chorea. 
 
 Acute endocarditis. 
 
 Acute pericarditis (?) 
 
 Acute pleuritis (?) 
 
 Bronchopneumonia or tuberculosis of the left lung. 
 
 Anatomical Diagnosis —(Acute chorea.) 
 
 Chronic and acute endocarditis of the aortic valve. 
 
 Acute endocarditis of the mitral valve. 
 
 Serofibrinous pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, double. 
 
 Tuberculosis of the upper lobe of the left lung. 
 
FATAL CHOREA 315 
 
 Status lymphaticus. 
 
 Foci of obsolete tuberculosis in the bronchial lymphatic glands 
 and lungs. 
 
 Chronic pleuritis. 
 
 Chronic appendicitis. 
 
 Dr. RIcHARDSON: We were not permitted to examine the head. 
 
 The appendix showed a well-marked stage of chronic appendicitis. 
 
 Each pleural cavity was half full of thin, pale fluid. 
 
 The right lung was bound down generally by old adhesions, and 
 the left lung presented a few scattered old adhesions, some in the 
 region of the apex. The trachea and bronchi contained a moderate 
 amount of dirty yellowish mucopurulent material. 
 
 The thymus gland was still present and weighed 12 grams. The 
 bronchial and mediastinal glands, generally, were more or less 
 enlarged and pigmented, and three of the bronchial glands on section 
 showed small fibrocalcareous masses. 
 
 The tissue of the nght lung generally was rather leathery, dark 
 salmon red, and yielded a moderate amount of dark red, frothy fluid. 
 In the substance of the middle portion of the upper lobe there was a 
 small fibrocalcareous mass situated just beneath the pleura, which 
 was slightly retracted over it. In this lung elsewhere there was no 
 good evidence of tuberculosis of any sort. The upper two-thirds of 
 the upper lobe of the left lung was resistant and lumpy to the touch. 
 In the substance of the upper part of this lobe there was a small cavity 
 2 cm. in diameter lined with a grayish yellow membrane 1 mm. thick 
 and contained a small amount of caseo-purulent material. At one 
 point in the wall of the cavity a small bronchus opened into it. The 
 lung tissue about the cavity showed fibrosis and induration, and 
 within it were several small fibrocaseous and fibrocalcareous masses, 
 and in their region were numerous minute to small discrete and con- 
 fluent tubercles. These tubercles extended pretty well down into 
 the substance of the middle portion of the lobe. Just beneath the 
 pleura on the upper part of the anterior lobe there was a very small 
 fibrocalcareous nodule. ‘The tissue of this lung elsewhere was gen- 
 erally leathery, dark red, and yielded a moderate amount of dark 
 reddish, frothy fluid. 
 
 The pericardium contained a considerable amount of pale, 
 cloudy fluid supporting fibrinous shreds and masses. ‘The vascular 
 and parietal layers were coated with a thin layer of membranous 
 fibrinous material which weakly bound the two layers together. 
 Here and there on the pericardium there were discrete and conflu- 
 ent dark reddish hemorrhagic spots and areas. 
 
316 FACTS ON THE HEART 
 
 _ The heart weighed 257 grams, enlarged. The myocardium was 
 negative. The cavities showed some enlargement. The valve cir- 
 cumferences were: mitral 9 cm., aortic 6 cm., tricuspid 1014 cm., 
 pulmonary 644 cm. The mitral curtain showed scattered along its 
 free margin an irregular row of reddish coxcomb-like granulations. 
 The curtain elsewhere showed but little if any fibrous thickening. 
 The aortic cusps presented a moderate amount of diffuse fibrous 
 thickening which slightly contracted and deformed at least two of 
 the cusps. Along the free margin of the cusps there was an irregular 
 band of grayish granulations. The other valves were not remarkable. 
 The coronaries were free and negative. The aorta, however, showed 
 in a few places fibrous streaks and areas in an extent not to be 
 expected at this age. The great branches were not remarkable. 
 
 The spleen showed a dark red, elastic tissue with prominent 
 follicles. 
 
 The kidneys weighed 252 grams and showed passive congestion. 
 The gastro-intestinal tract was negative except that the solitary and 
 agminated follicles showed marked prominence. 
 
 The retroperitoneal and mesenteric lymphatic glands were mod- 
 erately enlarged, up to 2 cm. in greatest dimension. 
 
 Dr. Casort: It is of interest to note that there was a fibrous and 
 therefore chronic endocarditis on the aortic valve in addition to the 
 
 acute process there and on the mitral. This means that at previous 
 time, very possibly in the attack of chorea three years ago, the 
 aortic valve was involved. ‘The chronic pleuritis also gives us rea- 
 son to believe that the tuberculous process had extended beyond the 
 bronchial lymphatics at an earlier time. Indeed this seems to be 
 proved by the presence of obsolete foci of tuberculosis in the lungs 
 themselves. 
 
 One may speculate a little perhaps upon the question whether 
 this old tuberculosis, presumably acquired in her second year, was 
 lighted up by the attack of chorea, or whether the chorea itself repre- 
 sents an infection made possible by diminished resistance, itself a 
 result of tuberculosis. It would be interesting to collect cases of this 
 association and trace the order of development so as to determine 
 whether the chorea determines the out-break of tuberculosis, or vice 
 versa. 
 
 What relation, if any, has the condition of status lymphaticus 
 found here at necropsy to the rest of the lesions? We have ordinarily 
 supposed, on rather insufficient evidence, I think, that the presence 
 of status lymphaticus makes any other disease or injury, such as 
 
FATAL CHOREA ce 
 
 operative insult, much more serious. But one needs to trace further 
 the relation between this mysterious condition and the two infections 
 which were present in this case. 
 
 Since no organisms were demonstrated in this case except those of 
 tuberculosis in the lung, it might be argued that the lesions in the 
 heart and pericardium were really manifestations of tuberculosis. 
 Against that we can merely say that from their morphology it is 
 reasonable to suppose that they represent another infection, since we 
 often see such lesions in connection with rheumatic disease, and 
 do not so far as I know ever see them demonstrated to be of tubercu- 
 _ lous origin. That is, we never find tubercle bacilli in the vegetations 
 on the valves in such case. Until such are demonstrated we may well 
 refuse to believe that tuberculosis is ever a cause of endocarditis. 
 
 Necropsy 2564 
 
 A schoolgirl of sixteen entered March 13, r910. She had had an 
 attack similar to the present illness at the age of twelve. She had 
 been ailing since she had a streptococcus sore throat five weeks before 
 admission. ‘Three weeks before admission she had rheumatism in 
 her feet, ankles, hip, and wrist. Two weeks later her face began to 
 twitch. She left school five days before admission, four days before 
 began to have trouble with her speech, three days before began to 
 throw her head from side to side. The following night she was found 
 in her nightclothes squatting on the register talking to herself about 
 being chilly. Her bed was pulled to pieces and the room generally 
 torn up. She talked incoherently and later could not speak. She 
 had not slept for five or six nights, and the night before entrance 
 was very restless in spite of chloral and the care of a nurse. Her 
 bowels were regular, her appetite poor. Catamenia were regular as 
 arule. She had had no Fowler’s solution. : 
 
 Examination showed a well developed and nourished girl with 
 flushed skin and mucous membranes. ‘There was marked reddening, 
 not decolorizing on pressure, in the form of discrete and confluent 
 papules of the skin over all prominences and convex surfaces of the 
 body. The skin was dry and harsh. The lymph nodes were not 
 enlarged. The apex impulse of the heart was felt in the fifth space, 
 eight cm. from midsternum. The sounds were rapid, regular, of 
 fair quality. No murmurs were heard. At the base the pulmonic 
 second was greater than the aortic second and accentuated. The 
 lungs showed good resonance, normal breathing, no rales. The 
 abdomen was held rigid, and was tympanitic. No masses were felt. 
 
318 FACTS ON THE HEART 
 
 The knee-jerks were not obtained. The plantars were normal. 
 There was no edema. ‘There were marked incoordinate movements 
 of the entire body, requiring forcible restraint to keep the patient in 
 bed. She did not speak when questioned. No Kernig, abdominal, 
 wrist or elbow reflexes obtained. 
 
 The temperature was 100° to 102° or 103° daily until March 19 
 when there was a steady rise to 108°. The pulse was 108 to 160, 
 the respirations 15 to 28. ‘The urine was cloudy at one of two exam- 
 inations, slightly alkaline at two, the specific gravity was 1022. 
 There was a very slight to the slightest possible trace of albumin, no 
 sugar, and acetone present at one. The hemoglobin was 85%, the 
 leucocytes 14,000 to 19,000. Smear showed polynuclear leucocytosis. 
 Lumbar puncture gave fifteen c.c. of fluid, part of which was very 
 bloody, part nearly clear, and which reduced Fehling’s solution 
 slightly. The sediment from the clearer tube was mostly blood cor- 
 puscles. The cell count showed 80% polynuclears, 20% mono- 
 nuclears. ‘‘The number of these cells seems to be no more than the 
 white cells to be expected with the amount of blood present.” 
 
 The patient’s movements were only partially controlled by chloral 
 and an occasional dose of morphia. On March 18 a high-pitched 
 systolic murmur appeared at the apex. The temperature began to 
 rise. ‘The patient grew weaker, the choreiform movements subsiding 
 as her strength failed. On March 20 strophanthin was given with- 
 out response and the patient died without developing any new 
 symptoms except those of double parotitis. 
 
 Clinical Diagnosis —Chorea major. 
 
 Endocarditis. 
 
 Anatomical Diagnosis.—(Acute chorea.) 
 
 Verrucose endocarditis of the aortic and mitral valves. 
 
 Hemorrhagic areas of the lungs. | 
 
 Slight bronchopneumonia. 
 
 Fatty metamorphosis of the liver. 
 
 Slight cystitis. 
 
 Parotitis. 
 
 The pericardium was not remarkable. The heart weighed 247 
 grams. The myocardium was pale, slightly yellowish and a little 
 lax. The right ventricle wall measured three mm., the left twelve 
 mm. ‘The columnae carneae were fairly marked. ‘The mitral valve 
 measured nine cm., the aortic five and a half, the tricuspid eleven and 
 a half, the pulmonary six and a half. The mitral curtain showed 
 along its free margins in two or three places small short rows of 
 
FATAL CHOREA 319 
 
 minute reddish granulations. The valve was otherwise not remark- 
 able. The aortic cusps showed stretching across the cusps from side 
 to side, a little below the upper margins, a narrow band of fine, 
 minute, rather smooth reddish granulations. The cusps were other- 
 wise negative. ‘The tricuspid and pulmonary valves were negative. 
 The coronaries were free. The intima of each artery showed scat- 
 tered along its course a few very minute yellowish plaques, and simi- 
 lar plaques were found in the intima of the great branches. 
 Blood cultures from the heart and spleen gave no growth. 
 
 Necropsy 2260 
 
 An unmarried American girl of twenty was sent from the Out- 
 Patient Department for “‘chorea”’ and entered November 23, 1908. 
 
 Her father had died of pneumonia. There as no family history 
 of tuberculosis. She had had mumps. She had not had rheumatic 
 temple. Five months ago she received a severe blow on the right 
 temple. Five months before admission the patient was ‘“‘threat- 
 ened with pneumonia.”’ | 
 
 Five weeks before entrance, ‘‘nervousness’’ was first noticed. She 
 went to bed four weeks before and had shown some improvement, 
 at the time of entrance lying more quietly and feeling better. Since 
 the blow on her head the patient thought she had lost in weight, 
 color, and strength. 
 
 Examination showed her to be well developed and nourished, with 
 skin and mucous membranes of good color, showing some loss of 
 weight. The pupils were equal, regular, reacted normally. There 
 was slight bilateral enlargement of the inguinal glands. The apex 
 impulse of the heart was in the fifth space, eight and a half cm. from 
 midsternum in the nipple line. There was no enlargement to the 
 right. The sounds were regular, forcible. At the apex a soft sys- 
 tolic murmur was heard. The pulmonic second was greater than the 
 aortic second but not accentuated. The pulses were synchronous, 
 equal, regular, of fair volume and tension. There was slight prom- 
 inence of the sternal articulation of the clavicles. 
 
 There was dullness throughout the left lung, marked above the 
 fifth rib, with many consonating rales, bronchial breathing and some- 
 what increased voice sounds. The left back was dull throughout, 
 with fine and medium moist rales. At the apex behind there was 
 bronchial breathing. 
 
 The abdomen was level, soft, tympanitic throughout. The liver 
 extended from the sixth rib to the costal margin. The spleen was not 
 
320 FACTS ON THE HEART 
 
 felt. The right kidney was palpable zm toto. The knee-jerks were 
 present but slight, the plantar reflexes normal. The hands showed 
 several encrusted abrasions (from hitting them on the bed before 
 entrance), and small traumatic hemorrhages beneath the nails. 
 Choreiform movements were marked, especially of the fingers and 
 arms, but also involving the legs, neck, and other muscles. There 
 was a slight cough without sputum. 
 
 The temperature was tor falling gradually to 908, rising again on 
 December 6 to 105.2. ‘The pulse was 80 to 170, the respirations 22 
 to 58. The hemoglobin was go0%, leucocytes 9,700 to 25,100. 
 The urine at two examinations was acid, cloudy, with a specific 
 gravity of 1028, noalbumin, nosugar, no pus, blood, orcasts. Sputum | 
 examination showed streptococci, a few intracellular diplococci, no 
 tubercle bacilli. Chest tap gave a small amount of bloody fluid. 
 The needle did not feel as if it were in a free space. The smear 
 showed pure blood with no excess of leucocytes. 
 
 The choreic movements were less severe on November 29. ‘There 
 was intense bronchial breathing throughout the left lung, with con- 
 sonating rales. Hot baths were tried with good result. The patient 
 was quieterand slept without bromides. On December 6 the patient 
 complained of severe pain in the region of the heart. Nothing was 
 found on physical examination to account for it. Bromides, swathe, 
 and an ice-bag gave temporary relief, but the patient again became 
 restless, tossing about violently and cryingout. During theafternoon 
 and evening three-fourths of a grain of morphia in all was given, with 
 hyoscin once a little ether and chloral by mouth, which was vomited. 
 Then chloral suppositories, after which she passed a fairly good night. 
 An area of tympany to the left of the sternum, under the clavicle, 
 discovered on December 5, had now disappeared. 3 
 
 On December 8a medical consultant wrote: ‘Left back flat 
 throughout (like front), with distant tubular breathing. The per- 
 cussion note is so woodeny that fluid is strongly suggested but with 
 the heart in normal position fluid seems impossible. No rales to-day. 
 Over the sixth right rib near the nipple there was felt some days ago 
 for the first time a hard painless enlargement, apparently the callus 
 of a rib broken in her thrashing previous to entry.”’ 
 
 On December ro the left lung showed vesicular breathing, becom- 
 ing more bronchial on the r1th, with many coarse crackling rales. 
 The temperature was very high and there was a troublesome cough. 
 The patient was unable to rest quietly even with drugs. ‘Three 
 days later there was labored breathing. An area of tympany was 
 found over the left front from the clavicle to the third rib, extending 
 
FATAL CHOREA 321 
 
 to the anterior axillary line. The heart action was irregular. On 
 December 14 she suddenly coughed up a large amount of thick yellow 
 pus, the pulse was poor, she became dyspneic and cyanotic. The 
 condition was helped by strychnia and strophanthin intravenously, 
 but the pulse remained poor and the patient was restless and at times 
 irrational. On December 15 the breathing was very difficult, her 
 color and pulse were poor, there was no response to stimulation. 
 After another attack of coughing up large amounts of pus she became 
 worse and died. 
 
 Clinical Diagnosis.—Chorea major. 
 
 Caseous pneumonia (tuberculous). 
 
 Four broken ribs, sepsis near one fracture. 
 
 Streptococcus sepsis with interlobar empyema. 
 
 Anatomical Diagnosis —(Chorea.) 
 
 Verrucose endocarditis of mitral, tricuspid and aortic valves. 
 
 Slight fibrous endocarditis of the aortic valve. 
 
 Empyema, left. 
 
 Acute pleuritis, right, 
 
 Tuberculosis of the left lung with cavity formation. 
 
 Fracture of sixth and seventh ribs on each side. 
 
 Purulent infiltrations of tissues of thoracic wall on the right side. 
 
 The head was not examined. 
 
 The heart weighed 226 grams. The myocardium was fairly good, 
 a little pale. The valve measurements were: mitral eight and a 
 half cm., aortic six cm., tricuspid eleven cm. The curtain of the 
 mitral showed scattered along its free margin several shorter and 
 longer rows of rather soft grayish-yellow granular warty material, 
 the surfaces of which were reddish-tinged. ‘Together these rows of 
 vegetations extended along nearly the entire margin of the valve. 
 The valve was otherwise negative. The aortic cusps showed a 
 moderate amount of fibrous thickening which very slightly deformed 
 the valve. At one point one of the cusps showed a minute grayish- 
 red granular adhering mass. The margin of the curtain of the 
 tricuspid valve showed in several places minute to small grayish 
 granular masses similar in character to those already described. The 
 coronary arteries and aorta were negative. 
 
 Cultures from the heart gave no growth; from the spleen, a scum 
 of growth of colon-like bacilli. 
 
 Microscopic examination of the lung showed typical tubercles, 
 discrete andconfluent. ‘‘The vegetation on the mitral valve indicates 
 an old process, for the vegetation seems to consist of more or less 
 
 degenerated fibrous tissue.’ 
 21 
 
CHAPTER III 
 
 SYPHILITIC HEART DISEASE 
 
 In the material studied for this book syphilitic heart disease means 
 essentially syphilitic aortitis and its results. I do not forget that 
 gumma of the heart is not very rare. I remember vividly the case 
 of a huge gumma of the interventricular septum demonstrated by 
 Dr. William H. Welch at the Johns Hopkins Hospital a few years 
 ago, from a case of heart-block. Nevertheless in this particular 
 group of cases, that is, in the twenty-three years from October 1896 
 to November 1919, we have had at the Massachusetts General 
 Hospital but one case of cardiacgumma. (Reported in detail on p. 
 375. See reference to one other dubious case under Myocarditis, 
 p- 496.) 
 
 Neither do I forget the studies of Warthin and the frequency with 
 which he has found the organism of syphilis in the heart muscle. As 
 we have not been able to follow his methods or to devote the generous 
 allowance of time given by him to the finding of organisms in the 
 heart, our negatives in no way contradict his positives. But I donot 
 know that he has ever been able to show that the presence of 
 syphilitic organisms in cardiac muscle proves that that muscle is 
 functionally impaired. In this, as in many other parts of the body, 
 the organisms may well be present without doing any harm. ‘Their 
 presence does not prove disease of the organ in which they are dis- 
 covered, though it certainly raises the fear that such disease if not 
 already present may be coming later. 
 
 Syphilitic myocarditis therefore may well be the end-result of 
 the triponema’s presence. Butin our necropsies there was no notably 
 frequent association of fibrous myocarditis with syphilitic aortitis 
 nor with any other demonstrable form of syphilis. What our cases 
 might have shown could we have pursued Warthin’s methods I can- 
 not say. . 
 
 Syphilitic Aortitis a Late Syphilitic Lesion.—In thirty-one cases 
 of our series we had reliable evidence as to the date when the syphi- 
 litic infection began. Seventeen of these cases were in the end of 
 the aneurismal type, and in them“the average duration of life from 
 
 322 ; 
 
ip 
 
 SYPHILITIC HEART DISEASE 323 
 
 the original syphilitic infection to death was eighteen years. Eight 
 were of the uncomplicated or latent type of aortitis, and averaged 
 twenty years of life after infection. Five were of the type first 
 manifested by aortic regurgitation and its results. In these cases 
 the average duration since the original infection was fifteen years. 
 In only one case out of 31 in our series did the serious symptom follow 
 swiftly upon the original infection, after an interval of only fourteen 
 months. 
 
 Associated Syphilitic Lesions.—Though our studies are rather 
 fragmentary and incomplete on this point, we have obtained in this 
 series but little evidence of syphilitic lesions outside the circulatory 
 system. Only six cases showed such evidence. ‘Two of these were 
 tabetics, three showed syphilitic orchitis accompanied in two cases 
 by syphilitic hepatitis and amyloid disease, and in another case by 
 syphilis of the kidney and lung. I recognize; however, that with our 
 methods of examination we cannot challenge such evidence as War- 
 thin has brought to light. | 
 
 Four Types of Syphilitic Aortitis—Our 92 necropsied cases of 
 syphilitic aortitis are divisible into four groups: (1) Aneurismal 
 type. In 41 cases of our series the disease produced aneurism of 
 the aorta (with or without aortic regurgitation.) 
 
 (2) In 26 cases aortic regurgitation without aneurism was the out- 
 standing feature of the syphilitic process in the aorta. 
 
 (3) In 22 cases the disease was latent; that is, it had involved the 
 aortic arch or other portions of the aorta without producing aneurism, 
 aortic regurgitation, aortic stenosis or angina pectoris. I shall call 
 this group latent or uncomplicated aortitis. 
 
 (4) Finally, in three cases the aortitis was associated with aortic 
 stenosis, whether as cause or concomitant will be discussed later. 
 
 There is some reason to believe that at any one time the largest 
 number of cases of syphilitic aortitis is of the uncomplicated or unman- 
 ifested type. In the very numerous necropsies on young negro sol- 
 
 _ diers which I saw in France during 1918 a small patch of syphilitic 
 
 aortitis was the rule. It did not involve the aortic valves or the 
 coronary arteries. It had not produced aneurism or any known 
 symptoms. Judging from the age of these men, one may suppose 
 that it represented the earlier portion of that long period of develop- 
 ment which I have already referred to as characterizing syphilitic 
 aortitis.. Presumably the natural history of syphilitic aortitis is 
 represented by fifteen to twenty years of silent, symptomless prog- 
 ress or regress during which it may well happen that the patient 
 
324 FACTS ON THE HEART 
 
 dies of some other disease, so that for him syphilitic aortitis is appar- 
 ently a harmless as well as a symptomless malady. Manifest syphi- 
 litic aortitis, on the other hand, represents probably the terminal 
 stages of this long latent disease. 
 
 When once the disease becomes known tt kills in most cases within 
 iwo years from the firstsymptom. Thusinthe 41 cases of the aneurismal 
 type, the course of the manzfest disease from the first symptom to 
 death was under two years in all but three cases. In the 26 cases 
 associated with aortic regurgitation all but seven had less than two 
 years of life after their disease became manifest. In the cases of 
 uncomplicated aortitis we can say nothing as to duration, since there 
 were no symptoms clearly referable to the disease itself. In these 
 latent cases the patients died of non-circulatory diseases such as 
 pneumonia, general peritonitis, brain tumor, etc. Hence we cannot 
 speak of the duration of the symptoms in this group. ‘There were no 
 Symptoms. 
 
 Age of Manifestation.—It has often been noted that syphilitic 
 aortitis is characterized by the appearance of heart symptoms or 
 aneurism symptoms in a middle-aged man, previously free from such 
 and not subject to rheumatism. This familiar observation is entirely 
 borne out in our series. In 30 of our 41 aneurismal cases and 13 of 
 those showing themselves by aortic regurgitation the disease 
 appeared within the years from thirty-six to forty-nine. Only in one 
 case of the entire series did the disease appear before the thirtieth 
 year, only in five cases out of g2 before the thirty-fifth year. On 
 the other hand only fourteen cases out of 92 were over fifty. Hence 
 
 TABLE 75.—AGE AT ONSET OF SYMPTOMS 
 
 Type with aortic 
 regurgitation 
 
 Aneurismal type 
 
 Unknown 
 
 29 
 39-34 
 39,39 
 40-45 
 46-50 
 DD 
 56-60 
 61-66 
 
 [Mig Prey tee boeates Matos 
 
 tS 
 Oo 
 
SYPHILITIC HEART DISEASE 325 
 
 we may say: Roughly—the disease appears between 35 and 50. A 
 more detailed picture of the age incidence is shown in Table 75. 
 
 It appears that in men the symptoms usually appear earlier than 
 they do in women. ‘Thus before the fiftieth year there are fifty-two 
 men to 10 women; after fifty, eighteen men to eight women. But 
 these figures are not of much significance, since the total number of 
 cases Is not large enough. 
 
 These ages are in manifest contrast with those of the two other 
 main groups of heart disease;—the rheumatic which appears much 
 earlier, usually before the twenty-first year, and the hypertensive 
 type, which usually shows itself much later. 
 
 Color.—Few colored patients seek the assistance in the Mas- 
 sachusetts General Hospital. Hence the small number of colored 
 patients in the aneurism series ( 5 out of 41) is not of any significance. 
 There is good reason to believe that this, like most manifestations of 
 syphilis, is decidedly commoner in negroes than in whites. 
 
 Sex.—All but six of the 41 aneurismal cases, all but 7 of the 26 
 cases of aortic regurgitation, and all but three of the uncomplicated 
 group were inmen. Of the three cases producing aortic stenosis two 
 were female and one male. From these figures it is clear that the 
 disease is six times as common in men as in women, if we leave out 
 of account the three stenoses. The fact that two of these occurred 
 in women raises a slight suspicion that in them there may be some 
 other cause at work. I shall refer to this point later. 
 
 Occasions of Discovery 
 
 The grounds of diagnosis in this disease will be discussed in detail 
 later. But here it is convenient to point out that the disease is 
 discovered: 
 
 (1) most frequently by the evidence of aneurismal pressure 
 (pain, aphonia etc.); 
 
 (2) less often by the evidence of aortic regurgitation with or with- 
 out broken compensation; 
 
 (3) by the appearance of angina pectoris in a young or middle- 
 aged syphilitic man. In the vast majority of all cases the disease will 
 be manifested, if at all, in one or more of these three fashions. 
 
 (4) Occasionally an X-ray of the chest taken for some other pur- 
 pose reveals an unsuspected aneurism. I have seen one such case. 
 Beyond this, one may say that in a known syphilitic patient the 
 appearance of any cardiac symptoms raises the suspicion, perhaps the 
 presumption, that these symptoms are syphilitic in origin. 
 
320 FACTS ON THE HEART 
 
 Position of the Disease in the Aorta.—22 of 80 cases in our series 
 affected the ascending aorta alone, 26 were confined to the region 
 of the arch, and 5 to the vicinity of the aortic valves, 16 affected 
 the whole aorta, 10 affected the whole thoracic aorta, 7 affected 
 the arch and upper thoracic aorta. Obviously the most dangerous 
 part of this disease is the part which attacks the aortic arch, where 
 it can produce aneurism, angina pectoris, and aortic regurgitation. 
 In the remainder of the aorta the disease may occasionally produce 
 aneurism, but usually produces no recognizable disturbance of any 
 sort. 
 
 Associated Arteriosclerotic Lesions.—In eight of the cases asso- 
 ciated with aortic regurgitation, in fourteen of the aneurismal cases, 
 and in nine of the uncomplicated cases—making a total of thirty- 
 one cases, 14 of all, arteriosclerosis complicated /the syphilitic process. 
 In six of these cases the sclerosis affected the aorta generally, in three 
 the aorta and its branches, in two the sclerosis is recorded as “‘gen- 
 eral.’ Besides these cases there were four cases of arteriosclerotic 
 nephritis and two of focal renal arteriosclerosis. I know no 
 reason to believe that the associated arteriosclerosis was of any 
 - importance. 
 
 DIAGNOSIS OF THE DISEASE IN LIFE 
 
 t. As already said, most cases, probably, are recognized by the 
 presence of aneurism. In 23 of the 41 aneurismal cases in this group 
 it was aneurismal symptoms which brought the disease to light. 
 Sixteen of the aneurisms were not diagnosed at all, but a study of 
 these cases shows that seven of these should have been diagnosed 
 and three more perhaps suspected, leaving only 6 out of 41 that were 
 quite impossible to reach, unless a purely fortuitous X-ray examina- 
 tion had brought them to light. In these six patients there were no 
 pressure signs, no evidences of syphilis. One of them entered the 
 hospital for general peritonitis due to perforated gastric ulcer; 
 another was seen only in his final collapse; two others met their death 
 from pneumonia, having had, so far as we can learn, no trouble from 
 their aneurism. Another case dying of pneumonia should have been 
 suspected of aneurism, however, in addition to the pneumonia, since 
 he had had dysphagia, hard dry cough, and evidences of aortic 
 regurgitation. 
 
 2. In the 26 cases manifested chiefly by aortic regurgitation the 
 diagnosis of syphilitic aortitis was made in twelve, aortic and mitral 
 endocarditis in 1, aortic and mitral insufficiency in 1, a diagnosis” 
 
DIAGNOSIS OF THE DISEASE IN LIFE 327 
 
 merely of aortic regurgitation in five, a diagnosis of aortic endo- 
 carditis in three, a diagnosis of arteriosclerosis and angina pectoris 
 in one, a diagnosis of cancer of the vagina in one, and no diagnosis 
 at all in the 2 remaining cases. Probably all but one case of this 
 group could have been diagnosed in life. 
 
 Of the 22 uncomplicated or latent cases, one was recognized in 
 life upon the evidence of a luetic history, Argyll-Robertson pupils, 
 and poor cardiac function. It is doubtful however whether in this 
 case the diagnosis was well founded, since the patient had also a 
 chronic nephritis which might have accounted for his cardiac troubles. 
 In the remaining 21 cases of this group there was nothing in the 
 patient’s history on which diagnosis could be based. 
 
 X-ray Diagnosis.—Of the 41 aneurismal cases X-ray diagnosis 
 was not attempted in 26. In the remaining 15 the disease was identi- 
 fied in seven, mistaken in five, and missed altogether inone. In two 
 cases the radiologist remained in doubt. The five mistaken X-ray 
 diagnoses predicted that a neoplasm would be found, largely, it 
 would appear, because of the absence of demonstrable pulsation in 
 the aneurismal sac. Evidently pulsation is not at all a reliable differ- 
 ential point in the distinction between neoplasm and aneurism by the 
 X-ray. : 
 
 In 24 out of the group of 26 cases manifested by aortic regurgita- 
 tion there is no record of any X-ray examination. In the remaining 
 two cases the radiologist reports enlargement of the aortic arch. But 
 as this formula is a very common one accompanying a diagnosis of 
 simple hypertrophy and dilatation of the heart (which was also pres- 
 ent in these cases) we have no reason to believe that the radiologist 
 thought these cases syphilitic. é 
 
 Of the 22 uncomplicated or latent cases of aortitis, an X-ray 
 examination is recorded in three, two of which are quite negative 
 while in the third there is recorded a slight dilatation of the aorta,— 
 a phrase which, like that just referred to in the last group, is equivocal 
 and does not indicate any clear recognition of syphilitic disease on 
 the part of the radiologist. , 
 
 Wassermann Reaction.—The Wassermann reaction began to be 
 done as a matter of routine only in the 5 year period covered by the 
 last 1000 necropsies in this series. Hence in 56 out of our 92 cases 
 no test was made. In the remaining 36 cases there were 29 positive 
 (80%) and 7 negative which is about the figure reported by other 
 observers. 
 
328 FACTS ON THE HEART 
 
 These 36 cases were divided as follows: 
 
 TABLE 76 
 Wassermann 
 Lesion 
 Positive Negative 
 
 Sypaliticaortitis with aneuristin. 0... ce he eee eee II 2 
 Syphilitic aortitis with aortic regurgitation.............. 13 I 
 
 Pure syphilitic aortitis without aneurism or aortic regur- 
 Pitation fe in Peeve eg eee eon Rites tne eee ae 5 4 
 29 | 
 
 In 19 of 29 positive cases the diagnosis was made (10 out of 13 
 with aneurism, 9 out of 11 with aortic regurgitation, none out of 5 
 “pure’”’ aortitis) doubtless in part on the basis of the reaction. In 
 some of the cases the details are of interest. 
 
 (a) Aneurism Cases.—In No. 3038 the diagnosis was suspected but 
 not positively made. ‘There was a syphilitic history 14 years ago, 
 a recurrens paralysis, a suspicion of tracheal tug, sluggish and irregu- 
 lar pupils, a failing heart with a basal systolic murmur. Here the 
 presence of a positive Wasserman was undoubtedly of value in sup- 
 porting the diagnosis. 
 
 In No. 3369 a man of 38, with syphilitic history 22 years ago, with 
 signs of a failing heart for a year, an apical systolic murmur, an unex- 
 plained cough and edema of the left arm, was apparently not suspected 
 of aortitis in life. The positive Wassermann might have aroused 
 such a suspicion. 
 
 In No. 3469 a man of 59, dying of prostatic obstruction in a surgical 
 ward, had apparently very little cardiovascular examination. The 
 aneurism was not suspected. Possibly the indication of the positive 
 Wassermann might have led to some suspicion, as he had previously 
 had cough and substernal oppression. 
 
 (b) Cases with Aortic Regurgitation—In No. 2982 no diagnosis of 
 syphilitic aortitis was made though there was a diastolic murmur 
 along the right sternal margin with a Corrigan pulse. There had been 
 definite symptoms of congestive failure at intervals for three years. 
 
DIAGNOSIS OF THE DISEASE IN LIFE 329 
 
 The Wassermann certainly should have suggested the diagnosis. In 
 No. 3033 and in No. 3557 the conditions are essentially the same. 
 
 In No. 3499 the diagnosis was simply cancer of the vagina, but 
 there was ample evidence of aortic regurgitation as well and the pres- 
 ence of a Wassermann should have clinched the diagnosis of aortic 
 syphilis. 
 
 In No. 3748 the Wassermann was negative and there was good 
 evidence of aortic regurgitation but without any proof of a syphilitic 
 origin. ‘There had been decompensation for a year with pain sug- 
 gesting angina pectoris, which in a woman of 42 who had been 
 divorced from one husband and deserted by another (one miscar- 
 riage, no children) is certainly enough to suggest syphilis strongly. 
 But the absence of the Wassermann reaction probably led to the ward 
 diagnosis of aortic regurgitation and stenosis, without syphilis. 
 
 (c) “Pure” Cases —No. 3759. Clinical diagnosis: ‘‘ femoral embo- 
 lism, myocardial weakness, fibrillation. Wassermann-+-+. Chancre 
 25 years ago. Probably syphilis somewhere. Heart weak.’’ Aor- 
 titis might have been suspected, I think. 
 
 No. 3619. Colored, female, 60. Died of acute pericarditis and 
 chronic nephritis after an operation for cancer of cervix. Wasser- 
 mann +-++. Aortitis, as one of the commonest sites for syphilis, 
 might have been suspected. 
 
 No. 3607. Male, 36, died of post-operative hemorrhage after an 
 operation for intestinal obstruction. X-ray recorded “slight dilata- 
 tion of arch.” Wassermann suspicious. At 36 these two facts 
 might have led to a suspicion of aortitis. 
 
 No. 3526. Male, 35. Aneurysm of superior mesenteric with 
 syphilitic aortitis. Diagnosis made in life apparently from dias- 
 tolic thrill at the base (no murmur recorded). Suspicious Wasser- 
 mann. At necropsy no aortic valve involvement. Wassermann 
 may have helped here. 
 
 Cardiac Hypertrophy in Syphilitic Aortitis 
 
 In the aneurismal group there was no record of cardiac hypertrophy 
 in 28 out of 39. The heart weights were recorded as normal in five 
 cases and under 290 gramsin five more. In six cases the weights were 
 between 300 and 400 grams; in eleven the weights were from 400 to 
 1000 grams; in two the only record is “slightly hypertrophied,”’ and 
 in 12 we have no definite figures. 
 
 It is of interest to seek the cause of hypertrophy in the group of 
 11 out of 39 aneurismal cases in which it was marked. 8 of I1 cases 
 are accounted for by aortic regurgitation. Of the remaining three 
 
330 FACTS ON THE HEART 
 
 TABLE 77.—HEART WEIGHTS 
 
 EMF tat Aortitis with b 
 Aortitis with Uncomplicated 
 
 : aortic regur- 4 
 aneurism at Minne aortitis 
 gitation 
 
 Under “oo gratis. 5. een te 
 300-320 grams 
 340-400 grams 
 400-450 grams 
 450-500 grams 
 500-600 grams 
 600-700 grams 
 700-800 grams 
 800-1000 
 “Slight” 
 
 Not recorded 
 
 oO 0O O NFP OH NHN HPW O 
 
 I 
 fe) 
 fe) 
 I 
 I 
 I 
 5 
 7 
 5 
 3 
 fe) 
 fe) 
 26 
 
 cases, two show only moderate enlargement, 402 and 450 grams 
 respectively. One of these patients died after an operation, without 
 cardiac symptoms. The other had had dyspnea for two years and 
 died with evidences of passive congestion. The third case had also 
 had dyspnea for six months and died of passive congestion. In this 
 case the heart weighed 553 grams. In none of these cases, tt seems to 
 me, do we need to suppose that there was any connection between the 
 aneurism and the cardiac hypertrophy. Aortic regurgitation accounts 
 for most of them, and in the rest the hypertrophy may well have been 
 associated with a previous hypertension. All the heaviest hearts— 
 Io0oo grams, 950 grams, 940 grams—were associated with aortic 
 regurgitation in addition to the aneurism. 
 
 Of the 26 cases manifested chiefly by aortic regurgitation, all showed, 
 according to the pathologist, a greater or less degree of hypertrophy. 
 In 20 cases this produced hearts weighing more than 500 grams, 
 and of these 20, 5 weighed more than 600 grams. 
 
 Of the 22 cases of uncomplicated or latent aortitis, 17 showed 
 hypertrophy, though in only six did this hypertrophy produce a weight 
 of more than 500 grams. In the cases with hypertrophy there was, we 
 may assume, a hypertension, since all showed an associated arterio- 
 sclerosis or nephritis, the latter accounting for three of the six cases 
 with hearts weighing more than 500 grams. 
 
GENERAL CARDIAC SYMPTOMS OF SYPHILITIC AORTITIS 331 
 
 From the whole group of cases studied in this chapter, then, we 
 may conclude that syphilitic aortitis does not produce cardiac hyper- 
 trophy unless it involves the aortic valves, producing regurgitation or, 
 rarely, stenosis. Aneurism does not produce hypertrophy of the heart, 
 nor does uncomplicated aortitis. But of course these diseases do not 
 inhibit the action of the commonest of all causes for cardiac hyper- 
 trophy, namely hypertension with or without nephritis. 
 
 GENERAL CARDIAC SYMPTOMS OF SYPHILITIC AORTITIS 
 
 (1) Dyspnea, the commonest of all heart symptoms, was present 
 in most of these cases except in the “‘uncomplicated”’ group. Of the 
 AI aneurismal cases 31 showed more or less dyspnea. This was 
 apparently of the cardiac type in 18 cases and due to local pressure in 
 to. In 14 0f these 18, aortic regurgitation was present, in the rest only 
 hypertrophy and dilatation of the heart. Dyspnea was due to aneuris- 
 mal pressure or obstruction in ten cases. Seven of these included 
 paralysis of the recurrent laryngeal nerve. This pressure-dyspnea 
 was usually of the “asthmatic”? type, that is, it produced wheezing 
 and difficult expiration. In three cases this was definitely paroxys- 
 mal and had been diagnosed as asthma over a considerable period of 
 years. In one, the “asthma” showed (naturally) a considerable 
 improvement under iodide of potash, which fact was considered dur- 
 ing life a proof that the diagnosis of asthma was correct. 
 
 In two case dyspnea had lasted but a few days and was due pre- 
 sumably to the pneumonia with which the patient died. 
 
 These three causes: pneumonia, pressure on respiratory structures, 
 and cardiac failure, account for the dyspnea in all the cases except 
 one, in which a man of forty-five died with symptoms of passive con- 
 gestion, although the heart weighed but 286 grams and showed no 
 hypertrophy. He had complained of dyspnea for twelve months 
 and no explanation for this was found after death. 
 
 In the 23 cases associated with aortic regurgitation dyspnea was 
 absent in only four cases, doubtful in one. All the others showed it 
 for varying periods, but in 16 out of 20 cases this period of dyspnea— 
 coinciding with the patient’s awareness that he was ill—was two years 
 or less, and in only three of the cases did it extend beyond one year. 
 In contrast to this, one case gave a history of dyspnea for five years 
 and one for eight years. In this type of the disease the dyspnea was 
 ordinarily the first symptom, though it was preceded in five cases by 
 other symptoms; by angina in two, palpitation in one, edema, in one, 
 and cough in one. 
 
332 FACTS ON THE HEART 
 
 In the uncomplicated or latent cases dyspnea was present only 
 when an associated hypertrophy and dilatation had weakened the 
 heart. Only in one case of this group was there death from passive 
 congestion. The other causes of death will be mentioned later. 
 
 (2) Angina.—Pain of the.anginoid type was present in five of 41 
 aneurismal cases, in two of the uncomplicated cases, and in 8 of 
 those associated with aortic regurgitation, making a fotal of 15 cases 
 out of 92. Yet evidently this was not the revealing symptom which 
 brought the disease to light in most cases of this series. 
 
 The coronary arteries were blocked either at their mouths or in 
 their course in five of the regurgitant cases. In the uncomplicated 
 cases the coronaries were normal except in two. In other words, in 
 this relatively early or mild form of the disease the coronaries 
 ordinarily escaped, as they did in all the aneurismal cases. 
 
 These cases bring out a fact elsewhere noted, that angina pectoris 
 is prone to be associated with syphilitic aortitis, whether there is any 
 coronary blocking or not. 
 
 The ages and the sex in these 15 cases of syphilitic angina were as 
 follows: 
 
 TABLE 78 
 
 Necropsy 
 No. 
 
 Type of aortitis 
 
 With aortic regurgitation 
 With aortic regurgitation 
 With aortic regurgitation 
 With aortic regurgitation 
 Uncomplicated 
 With aneurism 
 With aneurism 
 With aneurism 
 With aneurism 
 Uncomplicated 
 With aortic regurgitation 
 With aortic regurgitation 
 With aneurism 
 With aortic regurgitation 
 With aortic regurgitation 
 
 In 8 of these 15 cases, the angina comes at a relatively early age. 
 One notices, however, that 3 of the 4 females in this list are from 50 
 to 57 years old. 
 
SPECIAL SYMPTOMS OF ANEURISM 333 
 
 CAUSE OF DEATH 
 
 Naturally, in the cases with aortic regurgitation, that lesion and 
 its results usually led to death from passive congestion. Only in 
 two was angina undoubtedly the lethal event. In two others it 
 was associated and perhaps dominant, though passive congestion was 
 also well marked. 
 
 In the aneurismal group 14 died apparently of cardiac failure see 
 above), though in fourof these there is somedoubt. Only 6 out of 41 
 died of rupture of the aneurism. Four were post-operative deaths; 
 four died of respiratory failure (choking), three of pneumonia, three 
 of uremia, one of general peritonitis, one of intestinal obstruction, and 
 four without known cause. 
 
 Of the cases of uncomplicated or latent aortitis, four died of 
 nephritis, four of post-operative conditions, three of pneumonia, one 
 each of empyema, pulmonary cancer, brain tumor, acute pericarditis, 
 sepsis, general peritonitis and prostatic disease. In one an unex- 
 plained passive congestion was apparently the main cause of death, 
 and in another it was associated with sepsis. 
 
 The fourteen aneurismal deaths from cardiac failure seem to 
 correspond with the fourteen cases of aortic regurgitation included in 
 that group. Butasa matter of fact the two numbers do not precisely 
 correspond. In fact, eight of the aneurismal cases dying a congestive 
 death had no regurgitation. On the other hand, one of the patients 
 in whom aortic regurgitation was present died of pneumonia, two of 
 uremia, a third of rupture of the aneurism, another of respiratory 
 pressure, while in two more the nature of the death was never 
 explained. 
 
 SPECIAL SYMPTOMS OF ANEURISM 
 
 An abnormal area of pulsation was noticed in fourteen out of 41 
 cases, not counting pulsation seen in the neck or at the xyphoid. 
 The pulsation involved the left upper chest in four cases, the right 
 upper chest in four, the sternal and parasternal region in three, in 
 the rest is not clearly described. This abnormal pulsation was 
 associated with tumor in eight out of fourteen, with thrill in only 
 three—a surprising point. Of the total five cases showing thrill two 
 were not associated with any pulsation.. Percussion dullness was 
 associated with the pulsating area in only three cases, and diastolic 
 shock in three. Tracheal tug occurred in association with a pulsating 
 area in five cases and without it in three. 
 
 A systolic thrill was present in five cases only, three of them, as 
 has already been mentioned, without any abnormal area of pulsation. 
 
334 FACTS ON THE HEART 
 
 Paralysis of the recurrent laryngeal nerve was noted in twelve cases. 
 Its most common associations were with unequal pupils in six cases, 
 and with tracheal tug in five cases. 
 
 X-ray examination gave the correct diagnosis in seven cases. In 
 two of these it was the only sign of importance, and in another was 
 the only sign of importance except a diastolic murmur. 
 
 Tracheal tug was noted in eight cases. In was associated with 
 recurrens paralysis in five, with abnormal pulsation in five, with 
 unequal pupils in four, with tumor in two. 
 
 Inequality of the pupils was noted in ten cases. It was associated 
 with recurrens paralysis in six and with diastolic murmur in four. 
 
 Systolic murmurs at the base of the heart were noticed in twenty- 
 seven cases and absent in only four. Dzastolic murmurs were heard 
 in fourteen cases. 
 
 The actual association post-mortem of aortic regurgitation was | 
 fifteen cases out of 41. Thirteen of these proved cases had diastolic 
 murmurs; three others not so proved also had diastolic murmurs. If 
 we count these three cases as having aortic regurgitation we have a 
 total of 18 cases out of 41, showing regurgitation, and these with 26 
 other cases make a total of 44 cases (out of 92) in which aortic regurgi- 
 tation was also present. In the three cases of stenosis a regurgitation 
 may be assumed. 
 
 THE DIAGNOSIS OF ANEURISM 
 
 It has already been said that all but six of the 41 aneurisms either 
 were diagnosed or should have been diagnosed during life. Thirteen 
 of those which were recognized during life had no evidences of aortic 
 regurgitation. Butin the majority this lesion was present, including 
 four of those not recognized. Hence it appears that in syphilitic cases 
 with aortic regurgitation the presence of aneurism should always be 
 suspected and sought for by all the other diagnostic means at our 
 disposal. Summing up the physical signs of aneurism: 
 
 TABLE 79.—PHYSICAL SIGNS OF ANEURISM 
 
 NONE oa Fs niga tsacor RAC RIVE oa vw tap Aeste Rg SPOR RII ey enn a 5 
 SOME d sees a wepeye op Wis a's ies Lea deg Na: Ba ie Rat ete, ee 36 
 Dullareay Pears anid ale susie cae thant cemeRe Wiha etL t ties cae ea 22 
 Diastolic:murmurs, |. isi... 5 2 Paced an suey hoe oe eae 14 
 Pusatine arch aso: OTA eee ce ee 14 
 Arterial phenomena of aortic régurpitationy. 4 o7s.G,. ie eee 12 
 Recurrens’: pargly sis qcajs ...'vi- 018 din bos eat ica Ae On iced ee 12 
 Unequal pupils i233 9-05... Seis. Bias re a ee 10 
 X=TAY SVIGENCE! vse fo etic oe fk eA de a ee eee 7 
 Trachealtig..0. 05.5 sehen. Ri aia hes Ce ep eee ee 8 
 TUmor faire die ten win tog iis Pie eae oe ee oe ee 8 
 Thre ese Rake ee ae he cash 8 eae EAEE Ge ee eke oh ie an 5 
 
THE DIAGNOSIS OF ANEURISM 335 
 
 I have not mentioned here the 27 cases showing systolic murmurs, 
 because these do not seem to be of diagnostic importance. Of the 
 fourteen cases with diastolic murmurs, it may be said that this was 
 the only significant sign in two cases, that in two others this with the 
 peripheral arterial phenomena characteristic of aortic regurgitation 
 were the only striking signs, and in one other the association of dias- 
 tolic murmur and X-ray evidence was the only fact on which we had 
 to build. Arterial phenomena were associated with the diastolic 
 murmur in ten cases. A presystolic murmur was present with the 
 diastolic in two cases and without it in one, making a total of three 
 cases that can_be said to have had the ‘‘Austin Flint murmur” at 
 
 - the apex of the heart. 
 
 Pressure Signs——Eleven cases showed evidence of pressure on 
 respiratory structures. In eight of these the pressure was evidenced 
 by stridor or wheezing, in two by so-called ‘‘asthma,”’ and in one by 
 laryngeal obstruction. 
 
 Dysphagia was noted in only one case in the whole group. I think 
 this scantiness was due to insufficient questioning of the patients. 
 
 Edema in the Aneurismal Region.—One arm was swollen in three 
 cases, both arms in two cases, the face in one case, the chest and arms 
 in one, the neck and jaws in one. 
 
 Pain in Aneurism.—Excluding pain of the anginoid type we find 
 pain present as an early symptom of aneurism in seventeen cases; 
 dyspnea had preceded it in ten cases, and accompanied it in six; 
 edema, cough and hoarseness had preceded it eachin one case. Ten 
 cases were noticeably free from pain and were obviously of the type 
 due to pressure on respiratory structures, which might be called 
 “the asthmatic type.”’ One case (No. 878) occurred in a man of forty- 
 five who got his primary syphilitic infection thirteen years before we 
 saw him and began to suffer from “‘asthma”’ in the following year. 
 Post-mortem examination in this case showed that the aortic arch 
 was dilated into a huge sac of irregular shape compressing the left 
 primary bronchus, eroding the manubrium and the 2nd and 3rd ribs 
 to the left of the sternum. The bronchial stenosis had led to bronchi- 
 ectasis with chronic interstitial pneumonitis and abscesses. He had 
 no aneurismal symptoms except “‘asthma”’ until a year before death, 
 when he began to notice pain in the left chest and shoulder. 
 
 In ten cases the symptoms were those of cardiac fatlure without 
 other notable symptoms, oranything characteristic ofaneurism. Two 
 showed angina as their first symptom and might be said to belong to 
 the “angina type.” 
 
336 FACTS ON THE HEART 
 
 CARDIOVASCULAR COMPLICATIONS 
 
 TABLE 80 
 1. In 39 out of 94 cases—nearly half—there were no other cardiovascular 
 Lesions ¢ isi oe Sh Fee G Shoe bw be es Rye Wc of culo dh gongs ty Gergana 39 cases 
 2. The commonest complication was arteriosclerosis, present in ........... 23 cases 
 3. (Next comes acute (terminal) pericarditis..... 7... 4. . aes 8 cases 
 4. Next comes nephritis: \,% . to.) is hex sth 0) 2 aw eee ce 7 cases 
 5. Next comes chronic non-deforming endocarditis..................... 7 cases 
 6. Valve lesions (rheumatic type). ..<. 45... os S2 ya ue + tr 4 cases 
 7, Chronic.adhesive pericarditis... 2.520 Js... +. ap ew tee er 3 cases 
 8. Myocarditis, acute endocarditis, and arteriosclerotic degeneration of 
 the:kidnéys, each aisha ene woe alae vee > 6 ree rea ele et 3 cases 
 94 
 
 The most interesting point is the rarity of rheumatic valve lesions, 
 only four casesin g4. ‘This means that if in our diagnostic examination 
 we are convinced that any valves other than the aortic are involved, 
 the case almost certainly is not syphilitic aortitis. 
 
 CONCLUSIONS 
 
 1. So far as our studies go, cardiac syphilis means a syphilitic 
 aortitis which is usually confined to the arch of the aorta. 
 
 2. This is often, perhaps usually, harmless, a mere post-mortem 
 finding. 
 
 3. It becomes serious (a) when it produces aneurism, (b) when it 
 deforms the aortic valves and makes them leak, and (c) when it 
 obstructs the coronary orifices in the aorta so as to produce angina or 
 cardiac infarction. 
 
 4. It is recognized 
 
 (a) by the presence of aneurism, 
 (b) by evidence of aortic regurgitation appearing usually 
 in a middle-aged man with a syphilitic history. 
 
 5. It issix times ascommon in menas in women, and usually makes 
 itself felt between the 35th and the 5oth year. The aneurismal type 
 appears later in life than the type manifested by aortic regurgitation. 
 
 6. The disease appears from fifteen to twenty years after the 
 original syphilitic infection. 
 
 7. When symptoms finally appear they usually lead to death 
 within two years. 
 
 8. Enlarged heart is found only when the aortic valves are incom- 
 petent or when some complication (such as chronic nephritis) is 
 present. Aneurism does not produce cardiac hypertrophy. 
 
 9g. Rheumatic valve lesions rarely accompany syphilitic aortitis. 
 
ILLUSTRATIVE CASE OF SYPHILITIC AORTITIS 337 
 
 ro. An isolated aortic regurgitant lesion in a man under the forty- 
 fifth year is usually syphilitic. Only eleven of our 41 cases of ‘‘pure”’ 
 non-syphilitic aortic disease were in persons under forty-five years old, 
 while only 18 of 41 cases of syphilitic disease in the aortic valves 
 occurred after the forty-fifth year. 
 
 1. Pain suggesting angina pectoris in a young or middle-aged 
 man (i.e. under forty-five) is often evidence of syphilitic aortitis. 
 Severe epigastric pain (perhaps of the anginoid or infarction type) 
 is a feature of some cases. 
 
 12. Death in the cases with aortic regurgitation is usually from 
 passive congestion. In the aneurismal cases only 14% died from 
 rupture of the sac, and only in 24% (including the cases of rupture) 
 was the aneurism the main cause of death. 
 
 13. Among the physical signs of aneurism abnormal percussion 
 dullness is more often of value than any other single sign. Abnor- 
 mal pulsation or bulging is next in value, and recurrens paralysis 
 next. 
 
 14. X-ray evidence is in some cases our best help towards diag- 
 nosis, yet in five cases the radiological diagnosis was mediastinal 
 tumor, and in one case the aneurism was missed altogether. 
 
 15. Chronic aneurismal ‘‘asthma”’ may be due to compression 
 of a primary bronchus or of the trachea by an aneurism. 
 
 POINTS OF SPECIAL INTEREST TO THE WRITER 
 
 1. The frequency of syphilitic aortitis in a wholly latent and 
 apparently harmless form. 
 
 2. The infrequent association of syphilitic with rheumatic heart 
 disease. 
 
 3. The long interval between the syphilitic infection and the 
 appearance of aortic symptoms. 
 
 4. The fact that aneurism does not cause cardiac enlargement. 
 
 5. Isolated aortic disease or angina pectoris under the forty- 
 _ fifth year is generally syphilitic. 
 
 ILLUSTRATIVE CASE OF SYPHILITIC AORTITIS 
 
 Necropsy 4734 
 
 A Canadian railway engineer of thirty-nine entered September 
 3 complaining of nervousness, loss of speech and pain in the stomach. 
 His memory was very defective, especially for symptoms relating to 
 the central nervous system. ‘The story given in the wards differed 
 
 in most respects from that given in the Out-Patient Department. 
 22 
 
338 FACTS ON THE HEART 
 
 One brother died of kidney disease. 
 
 The patient’s past history was negative except for some dyspnea 
 and pain across the chest upon exertion. 
 
 For six years he had had running of the nose. At one time he 
 gave this as his chief complaint, though he said he was not troubled 
 with head colds. For eight months he had had attacks of motor 
 aphasia every week or two lasting one or two days. For three or 
 four months he had been growing weaker. His dyspnea and chest 
 pain on*exertion had increased. For six months he had had colic 
 with each stool. For three months the pain in the stomach had been 
 getting worse. It was continuous and partially relieved by food. 
 He was becoming more nervous and irritable. His sister reported 
 temporary amnesia. ‘The day before admission he was dizzy for the 
 first time. During the illness he had gained weight. 
 
 In the Out-Patient Department June 3 his blood pressure was 
 found to be 128/84. The abdominal reflexes were present but slug- 
 
 gish, especially the cremasterics. The deep reflexes of the upper 
 
 extremities and the knee and ankle reflexes were normal. Babinski 
 was present both sides. Oppenheim, Chaddock and Gordon were 
 also present. There was no ankle clonus. Finger ‘counting was 
 awkwardly done. He did not recognize the smell of acetic acid, 
 alcohol or ammonia. The skin and mucous membranes were pale. 
 The right pupil was greater than the left and did not react to 
 light. The left reacted poorly. Both reacted normally to distance. 
 The fundi were normal. August 30 the red blood corpuscles num- 
 bered 2,080,000, the polynuclears 74%, the hemoglobin 50%, the 
 platelets were somewhat decreased. There were some microcytes 
 and occasional macrocytes, not much change in the shape of the cells, 
 which were often well laden with hemoglobin. There was striking 
 sallowness and pallor of the mucousmembranes. The tongue showed 
 slight atrophy of the marginal papillae. : 
 Examination showed a well nourished, anemic looking man whose 
 mind functioned rather slowly. All the mucous membranes were 
 pale. Pus was expressed from the root of one incisor. The tonsils 
 were moderately enlarged on the left. The heart sounds were of 
 fair quality. The action was normal. ‘The apex impulse was 8 cm. 
 from midsternum in the midclavicular line, the left border of dull- 
 ness one cm. outside the midclavicular line. There was no other 
 enlargement topercussion. Thesounds were of fair quality, the action 
 normal. There were no murmurs. The blood pressure was 105/72. 
 The lungs were norma]. The abdomen showed voluntary spasm. 
 
 ae 
 
 =". 
 
ILLUSTRATIVE CASES OF SYPHILITIC AORTITIS 339 
 
 A possible liver edge was felt 744 cm. below the costal margin. The 
 bladder dullness was two finger-breadths above the symphysis. 
 The genitals and rectal examination are not recorded. The extremi- 
 ties were normal. The pupils were unequal, the right greater than 
 the left. The right reacted to distance but not to light. The right 
 knee-jerk was greater than the left. There was inconstant Oppen- 
 heim. The gait was that of a weak man rather than anything else. 
 Rectal examination showed a sphincter which seemed to have lost 
 some of its strength. The fundi showed slight arteriosclerosis. The 
 right disc showed a vein extending a short distance into it on the 
 temporal side and then seeming to disappear. 
 
 The temperature was I01.9° to 102.5° at entrance, then 98.1° 
 to 100.3° until September 8, when it rose to 103.5°; afterwards not 
 remarkable until a terminal rise beginning September 17 and reach- 
 ing 107.8°. The pulse was 78 to 104, with a terminal rise to 161. 
 The respirations were normal except for a terminal rise to 44. The 
 amount of urine is not recorded. ‘The specific gravity was 1.008 to 
 1.018. There was the slightest possible trace of albumin at both of 
 two examination, leucocytes at both, one or two red blood corpuscles 
 per high power field at the second. September 4 he was catheterized. 
 The residual urine was 32 ounces. The hemoglobin was 60 to 55%. 
 There were 6500 to 10,600 leucocytes, 75% polynuclears, 2,720,000 
 to 1,929,000 reds, some polychromatophilia and variation in size, 
 with a tendency to large cells, slight variation in shape, occasional 
 achromic cells at one of three examinations, reticulated cells 2% at 
 -another. A Wassermann in the Out-Patient Department three days 
 before admission was strongly positive. Three Wassermanns in 
 the ward were strongly positive. The bleeding time was 2 minutes, 
 coagulation time 12 minutes. Retraction was normal in one hour 
 and marked in three hours. The serum dilution was 1:20; this wasa 
 surprise. The non-protein nitrogen was 40 mgm. September 5 
 the fasting contents of the stomach were 30 c.c. of slightly blood 
 tinged white material showing no free HCl, total acid 3 c.c._ A test 
 meal gave 50 c.c. of blood tinged white material, total acid 9 c.c. 
 Both showed fresh blood and a very strongly positive guaiac. Lumbar 
 puncture September 4 showed an initial pressure of 180, oscilla- 
 tion normal, jugular compression 260, respiration 170. After with- 
 drawal of 5 c.c. the pressure was 150, after withdrawal of 5 more 
 c.c. 140. There were 6 cells. Alcohol and ammonium sulphate were 
 positive, the total protein 63, goldsol 5555553110, Wassermann 
 strongly positive. September 17 the initial pressure was 270, after 
 
340 FACTS ON THE HEART 
 
 withdrawal of 5 c.c. 210, after withdrawal of 5 c.c. more 150. The 
 jugular compression is notrecorded. There were 7 cells. Ammonium 
 sulphate and alcohol were positive, Wassermann strongly positive, 
 total protein 55, goldsol 5555542000. X-ray September 6 showed 
 the frontal sinuses practically absent; no anatomical variation. The 
 antra showed no definite evidence of pathological change, although 
 the plates were not very satisfactory. The calvarium was normal in 
 outline. ‘The sella showed no abnormalities in size or shape. ‘There 
 
 Fic. 55.—Area of diminished density in midportion of stomach suggesting a mass 
 nearly as large as the palm arising from the wall of the stomach, freely movable with 
 the stomach. 
 
 was little calcification in the region of the pineal, which was normal. 
 A plate of the chest was not entirely satisfactory. There was no 
 definite evidence of pathological change; no evidence of periostitis 
 of the clavicles. Another examination September 12 confirmed the 
 previous findings. There was an area of diminished density in the 
 midportion of the stomach suggesting a mass arising from the wall of 
 the stomach nearly as large as the palm, freely movable with the stom- 
 ach. (See Fig. 55.) There was no peristalsis over this region. 
 The shadow was constant on repeated examinations. ‘There was a 
 
ILLUSTRATIVE CASES OF SYPHILITIC AORTITIS 341 
 
 small six-hour residue. The first portion of the duodenum, the 
 pyloric sphincter, and the colon were not remarkable. 
 
 During the first two nights in the hospital the patient was dis- 
 oriented and laughed easily. He looked myxedematous. He made 
 no general improvement until the gth, when he was mentally a 
 little clearer, although still disoriented as to time and place in the 
 immediate past. He was very restless, with poor insight. 
 
 The morning of September 17 he suddenly saw double and had 
 complete disassociation of the eyes, one moving upward, the other 
 downward. The left eye showed a lateral nystagmus with quick 
 component to the right. There was no ptosis. Vomiting soon 
 started, but was not projectile in type. The vomitus contained 
 brown changed blood at first, one pint three times, and later bright 
 red blood in the stomach fluid, one pint twice. Donors were collected 
 and large doses of morphia given. The vomiting stopped and counts 
 were found to be normal, the pulse steady. The eyes were bandaged. 
 They were widely divergent and moving ceaselessly, even while he 
 was deeply asleep. The blood pressure was 140/75 all that day and 
 evening. The temperature, which had been practically normal for a 
 week, began to rise, reaching 107.7° the evening of the 18th. The 
 pulse rose to 162, the respirations to 44. Examination on the 18th 
 showed no evident paralysis, although the left arm was found spastic 
 the night before. His whole body was now flaccid. The arm reflexes 
 were active, the knee-jerk very active on the right, normal on the 
 left. . There was marked Babinski on both sides, not present the night 
 before. No clonus. The eyes were now divergent and the right 
 pupil greater than the left. The heart was very rapid. The lungs 
 were clear except for fine crackling rales in the right back between 
 the angle of the scapula and the spine. ‘The patient was in mild 
 shock, unconscious. The breathing was Cheyne-Stokes. He con- 
 tinued in coma. The left pupil was pinpoint, the right dilated. 
 The right fundus showed dilatation of the veins but no choking of the 
 discs. The eyeballs continued divergent. On the roth there was 
 edema of both bases. Bubbling rales were heard well up to both 
 angles of the scapulae. The temperature rose steadily. The breath- 
 ing was very shallow, rapid and stertorous and continued Cheyne- 
 Stokes. The breath was foul. The pulse was rapid and thready. 
 The patient sweated profusely. A soft short systolic murmur was 
 heard at the apex and the base. A: was greater than Py. The right 
 side of the heart was slightly enlarged to percussion, possibly dilata- 
 tion. The abdomen was slightly distended with gas, not relieved by 
 
342 FACTS ON THE HEART 
 
 an enema. The patient was catheterized. The Babinski persisted. 
 There was no Kernig. September 1g he died. 
 
 X-ray Interpretation September 12.—Findings probably represent 
 new growth in the wall of the stomach. 
 
 Clinical Diagnosis (from Hospital Record).—Syphilis and malig- 
 nancy of stomach. 
 
 Cerebral hemorrhage? 
 
 Syphilis, tertiary stage? 
 
 Dr. Richard C. Cabot’s Diagnosis.—Syphilis of the central nervous 
 system. 
 
 Gastric, tumor, probably benign, with hemorrhage. 
 
 Secondary anemia. 
 
 Anatomical Diagnosis——Embolism of the basilar artery. 
 
 Anemic infarction of the pons. 
 
 Adenomatous polypi and adenocarcinoma of the stomach. 
 
 Embolism of a minute branch of the left coronary artery. 
 
 Infarcts of the spleen and kidneys. 
 
 A few areas of bronchopneumonia, right. 
 
 Wet brain. 
 
 Slight chronic pleuritis, right. 
 
 Luetic aortitis with small aneurism and mural thrombus. 
 
 Dr. RICHARDSON: This was a very unusual case. 
 
 The pia was wet, infiltrated with thin pale clear fluid. The vessels 
 of Willis showed a very slight amount of sclerosis in places, nothing 
 remarkable. The basilar artery was occluded at its distal portion 
 by a frank embolic columnar mass which was prolonged a little into 
 the branches at its bifurcation. (See Fig. 56.) Practically the entire 
 pontine tissue was softened, pasty, pale and homogeneous,—frank 
 anemic infarction. ‘The brain tissue generally was a little wet. 
 
 The esophagus was negative. Hanging off from the anterior wall 
 of the stomach midway was a large adenomatous-like mass, as seen in 
 Fig. 57. Macroscopically it looked like an adenoma. ‘There were 
 several hemorrhagic areas in the peripheral portion of the mass, and 
 areas of ecchymosis in the mucosa of the stomach. Microscopic 
 examination showed at one place in this adenomatous tissue a slight 
 invasion of the wall of the stomach. That would make it of course 
 cancerous in that portion. So we have a mass the greater portion of | 
 which is adenomatous but at one place an area of cancerous 
 degeneration. 
 
 The intestines were negative save that they contained a little 
 bloody mucus and blood-like material. 
 
ILLUSTRATIVE CASES OF SYPHILITIC AORTITIS 343 
 
 The lungs were negative except that on the right side at one place 
 there were a few small areas of bronchopneumonia. 
 
 The heart weighed 370 grams, a little large, a little dilated. The 
 aorta in the region of the ascending thoracic was the seat of a definite 
 luetic aortitis. (See Fig. 58.) One of the areas of luetic aortitis was 
 capped by frank thrombotic material. Across from this larger area 
 were two or three smaller ones capped with thrombotic material. 
 
 Fic. 56.—Embolism of the basilar artery. <3. (Photograph, with enlargement, by 
 Louis M. Adams. Dr. Oscar Richardson.) 
 
 The spleen showed two or three infarcts and the kidneys showed 
 several infarcts. 
 
 Microscopic examination of the aorta showed luetic aortitis. 
 
 Every once in a while we find mural thrombi on the aorta. Some- 
 times we find infarcts associated with them. 
 
 Dr. Casot: How big was the pedicle of the stomach tumor? 
 
 Dr. RicHARDSON: The pedicle ran along the base of the mass 
 without much thickening of the wall underneath, and it was only at 
 that one point microscopically that it showed carcinoma. ‘The mass 
 was 7cm. X 414 cm. X 3)4 cm. 
 
344 FACTS ON THE HEART 
 
 Dr. Casor: It was not a papillary mass not like a papilloma of 
 the bladder? 
 
 Dr. RicHAarpson: No. It did not have a small pedicle, but a 
 pedicle running all along the base of the mass. 
 
 Fic. 57.—Adenomatous polyp of the stomach. .(Photograph by Louis M. Adams. 
 Dr. Oscar Richardson.) 
 
 These adenomatous masses along the gastrointestinal tract are not 
 uncommon. Ihave seen a stomach that was practically covered with 
 them, like the knotted fringe of a shawl. 
 
 The large intestine of one of our former cases presented in the 
 
 upper portion of the descending colon adenomatous masses while in 
 the lower part of the same colon there was frank cancer. 
 
ILLUSTRATIVE CASES OF SYPHILITIC AORTITIS 345 
 
 Dr. Casort: Is adenoma the ordinary benign tumor of the stom- 
 ach? 
 
 Dr. RIcHARDSON: Adenoma, fibroma, fibrolipoma—I should say 
 adenoma is probably the commonest. 
 
 * 
 
 Fic. 58.—Syphilitic aortitis with small aneurisms. Aortic valves stretched close 
 to aortic wall so as to be incompetent. (Photograph by Lewis S. Brown. Dr. Oscar 
 Richardson.) 
 
 The anatomy of the heart is beautifully shown in Fig. 58. There 
 was but little if any decrease in the orifices of the coronary arteries. 
 In the first portion of the aorta, just above the aortic cusps, which 
 were not invaded by the luetic process, the thrombotic caps are well 
 
346 FACTS ON THE HEART 
 
 shown. One cap was about one and a half cm. across and consisted 
 of brown soft thrombotic material. The other smaller caps are 
 apparent. The black shadow is a small aneurism. Along the aorta 
 we can see irregular streaks and areas of thickening and elevation and 
 thinning and depression, longitudinal striation, etc., characteristic 
 of luetic aortitis. 
 
 A PuysicrtAn: Do you ever find evidence of the presence of the 
 spirochetes? 
 
 Dr. RICHARDSON: Once in a while. When the process is old we do 
 not find them. But if the material was all cut up in serial sections we 
 might find a few. 
 
 A PuysiciAn: We might conclude from that that the spirochel 
 at times are floating in the blood? 
 
 Dr. RICHARDSON: Yes. It is or was a septicemia. 
 
 In this case then a bit of that material from the mural thrombus 
 of the aorta was swept up into the basilar artery, shut if off, and pro- 
 duced anemic infarction of the pons. Then bits were swept down 
 into the splenic and renal arteries and produced the infarcts of the 
 spleen and kidneys. In addition to that, in speaking of the heart I 
 forgot to mention that a very minute branch of the coronary artery 
 was also occluded by a very minute embolus. 
 
 Dr. Lincotn Davis: I should like to ask a question. Don’t 
 you think it is extraordinary that an embolus can occlude the basilar 
 artery? The basilar artery is larger than the two arteries that make 
 it up. 
 
 Dr. RicHarpson: No. The basilar artery is larger than the 
 vertebral arteries, but the basilar artery gives off branches and at 
 its distal end bifurcates into two smaller arteries, and so anatomically 
 this distal portion of the basilar is well arranged for the lodgement of 
 an embolus, as in this case. 
 
 Dr. Davis: Have you ever had an embolus of the basilar artery 
 before? 
 
 Dr. RicHarpson: I do not remember at the moment a case like 
 this one. There are those cases where there is marked arteriosclero- 
 sis of the vessel with arteriosclerotic thrombotic occlusion at the 
 site. We.must remember that this embolus in the plate looks 
 huge; it was of course roughly only twelve and a half mm. long, two 
 mm. in diameter. 
 
 Dr. Cazot: I should interpret this man as having syphilis of 
 the nervous system. I do not think Dr. Richardson would in any 
 way contradict that. He did not examine the cord, and the changes 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 347 
 
 in the cerebral arteries in a man of thirty-nine are such as we think of 
 with syphilis. ‘There is nothing in any of the findings post-mortem 
 which would account for a spinal fluid such as was found in life. 
 
 The tumor in the stomach seems to be partly benign and partly 
 malignant, so I think we did pretty well on that. Dr. Holmes said 
 malignant, I said benign. Did you look at the marrow? He had a 
 great anemia and I discussed and excluded pernicious anemia. 
 
 Dr. RicHARDSON: The vertebral marrow was negative macro- 
 scopically. 
 
 Dr. Casot: I do not believe there was any pernicious to it. 
 
 SYPHILITIC AORTITIS WITH AORTIC REGURGITATION. ILLUSTRATIVE 
 CASES 
 
 Necropsy 3912 
 
 An unoccupied negro of thirty-six entered December 27 for 
 relief of sleeplessness and nausea. His mother died of heart trouble. 
 His health had been fair. At eighteen he had typhoid fever. For 
 five years he had had hemorrhoids. At thirty-two he had acute pain 
 in the right lower quadrant. Forsixmonthshe had been very thirsty. 
 His bowels were constipated. For the past week they had been mov- 
 - ing hourly as a result of catharsis. He had a little cough with dark 
 colored sputum and occasionally hemoptysis. His best weight was 
 145, his usual weight 135. 
 
 Four months before admission he became dyspneic and had 
 increasing edema of the ankles and sleeplessness. Soon afterward he 
 began to sweat at night. In order to rest at all he required three 
 pillows. After slight exertion he had attacks of boring precordial 
 pain sometimes lasting three or four hours. For two months he had 
 been taking veronal every third night with no appreciable relief. 
 For three weeks he had had nausea and vomiting, caused he thought 
 by his medicine. He now had continual nausea, partially relieved 
 by vomiting. For ten days there had been pain localized at the 
 umbilicus. 
 
 Examination showed a well nourished man. The apex impulse of 
 the heart was seen and felt in the fifth space 14 cm. to the left of 
 midsternum. The action was rapid, the sounds of fair quality. 
 The aortic second sound was accentuated. There was a diastolic 
 murmur at the aortic area and a systolic at the apex, transmitted to 
 the axilla. The murmurs were heard in the left back. There were 
 loud sounds over the vessels in the neck. The pulses were of high 
 
348 FACTS ON THE HEART 
 
 tension, the artery walls palpable, the brachials tortuous. The 
 blood pressure was 165/55. There was a sound over the brachial 
 with no pressure. The lungs were normal. The abdomen was — 
 tympanitic except in the right upper quadrant. The liver dullness 
 extended from the fifth space to 5 cm. below the costal margin, where 
 the edge was felt. There was slight bilateral costovertebral tender- 
 ness. ‘The genitals were negative. The legs showed edema up to 
 the knees. ‘The pupils and reflexes were normal. 
 
 The temperature was 95.3° to 98.7°, the pulse 80 to 85, the res- 
 piration 20 to 49. The amount of urine is not recorded until Decem- 
 ber 30, when it was 24 ounces. The specific gravity was 1.010 
 to 1.018. ‘There was the slightest possible trace to a slight trace of 
 albumin at four examinations, rare pus cells at one, occasional to 
 many hyalin casts at the last two. The renal function was 15%. 
 The hemoglobin was 90%. There were 10,000 leucocytes, 75% 
 polynuclears. The urea nitrogen was 40 mgm. per 100 c.c. of blood. 
 A Wassermann was strongly positive 
 
 The patient was much troubled with dyspnea and epigastric dis- 
 tress and slept little. The night of December 31 the pulse began to 
 be slower and he complained of difficulty in breathing. About twelve 
 o’clock the heart rate was 50 per minute, later 40-42 per minute, 
 although still regular There appeared to be a 1-2 heart block. 
 Within two hours he died. 
 
 Discussion by Dr. Richard C. Cabot.——Sleeplessness and nausea 
 are not a usual combination in the cases coming into this hospital. 
 Very few, I should say, come in for those symptoms, and they have 
 so many causes that I do not think it is worth while to discuss them 
 at any length. Sleeplessness and nausea are caused by alcoholism, 
 general peritonitis, uremia, and psychoneurosis. But I think it is 
 unlikely that we can hit the cause in this case in our preliminary 
 consideration. , 
 
 Apparently the pain in the right lower quadrant was not serious, 
 for no further account of it is given. . 
 
 Dyspnea and edema look like cardiac trouble. We get no 
 idea from the past history as to why he had this present group of 
 symptoms. 
 
 The history of the present illness points strongly to cardiac or 
 renal trouble, and a good deal more on the whole to cardiac than to 
 renal. In cardiac trouble in a negro of thirty-six one’s snap diag- 
 nosis is syphilitic aortitis. Seeing a large number of autopsies on 
 negroes as I have in the past two years, I can say that syphilitic aorti- 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 349 
 
 tis in the American negro seemed to be almost invariable, and almost 
 every negro had a positive Wassermann. 
 
 The vomiting and the pain that this patient had I have seen a 
 number of times in connection with syphilitic aortitis. We must 
 remember that the coronary artery goes off just above the aortic 
 valve, and that syphilitic aortitis usually begins within an inch of that 
 artery. <A very slight extension will close the mouth of the artery and 
 produce just as great obstruction as if we had coronary sclerosis. 
 When one gets pain of the anginoid type in young people, especially 
 in a negro, we think of syphilitic aortitis because of the known 
 relation of anginoid pain to disease of the coronary artery, and 
 because of the position of syphilitic aortitis. 
 
 Properly speaking there are two aortic areas, the second right and 
 fourth left interspaces. JI presume this note means the second right. 
 
 The pulse pressure, 110, is such as we get in three conditions: 
 (1) aortic regurgitation, the commonest and most marked; (2) 
 arteriosclerosis without regurgitation; (3) exophthalmic goitre. 
 These are the three conditions which give the largest pulse pressure. 
 All may give rise to a capillary pulse, a phenomenon that we ordi- 
 narily associate with aortic regurgitation. 
 
 “There was a sound over the brachial with no pressure.”’ Pre- 
 sumably a systolic sound but no sufficient evidence. They were 
 looking for Duroziez’s sign, which is a diastolic murmur over the 
 peripheral arteries heard on pressure with the stethoscope. 
 
 Bilateral costovertebral tenderness under these conditions I 
 should say means nothing. It is a very hard thing to make any 
 deductions from, because it is hard to tell how sensitive the individual 
 isin that region. It is not the pleasantest place in the body to have 
 pressure exerted. It is only when a patient is very much more sensi- 
 tive on one side than the other that I get anything out of it. Do you 
 agree? 
 
 Dr. Hucu Casor: Yes, provided the examination is made at the 
 costovertebral angle; but not twenty-five out of a hundred house 
 officers know where the costovertebral angle is. The valuable point 
 of tenderness is high up, really in the angle between the rib and the 
 spine. If present, I believe it is very important evidence of trouble 
 in the kidney. In the flank it may mean anything, but usually means 
 nothing. 
 
 Dr. Ricuarp Casor: If you had this tenderness in the real costo- 
 vertebral angle on both sides, would it be important? 
 
350 FACTS ON THE HEART 
 
 Dr. Hucu Casot: I think it would. I have no idea that he had it 
 in this case. 
 
 Dr. RicHARD CaBpoTt: When we say “pupils and reflexes”’ we 
 mean that the pupils were tested for reaction to light and accom- 
 modation, their size was looked at, and their shape. By reflexes we 
 mean the knee-jerk and the plantar. There are many other reflexes 
 which are not tested as a matter of routine in this hospital, but these 
 two we do in every case, because they can be done so quickly, and if 
 anything is wrong with them, it is usually important to find it out. 
 
 I should say there is nothing important in that urinary examina- 
 tion. The renal function was 15%. Ina cardiac patient in bed with 
 
 the dropsical conditions which we find in that state of things I do 
 
 not think 15% is enough to give us any particular information about 
 
 the kidney. It shows that that kidney is not doing much work, but 
 
 a normal kidney under those conditions often will not do much work. 
 So I should conclude nothing from that examination. 
 
 _ The urea nitrogen findings are above the average, but under those 
 conditions do not seem to me significant. The blood is normal. 
 
 Differential Diagnosis—The essentials of that case, I should say, 
 are a history of cardiac trouble in a young negro who shows a dias- 
 tolic murmur, a large heart, a positive Wassermann and anginoid 
 pain. That is the typical picture of syphilitic aortitis. 
 
 I want to stress particularly the occurrence of pain and vomiting 
 in syphilitic aortitis. It is sometimes so great that we think the 
 patient must have a perforated gastric ulcer or something of that kind. 
 Why they have so much vomiting I do not know. They vomit dis- 
 tinctly more than other cardiac patients, and they suffer more. The 
 worst suffering that I have seen in cardiac patients has been in this 
 type of case. In other words, syphilitic aortitis is the worst kind of 
 cardiac trouble one can have, not merely in prognosis. It is the 
 shortest; it is the most resistant to treatment; but is also the most 
 agonizing. If anybody wants to use the end results of syphilis as a 
 terror he certainly should point out syphilitic aortitis as one of the 
 most torturing results of that disease. Few people who die of 
 syphilitic aortitis have any other than a painful death. 
 
 I have mentioned only one diagnosis; I can see only one reasonable 
 diagnosis in this case. It is perfectly true that a man who already 
 had a rheumatic type of endocarditis and a cardiac lesion resulting 
 from it, acquired in childhood, might get syphilis on top of it and have 
 a positive Wassermann for that reason. But this combination is 
 rare; experience has taught us that when we can explain all the 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 351 
 
 facts of a case by one diagnosis, we are more likely to be right than 
 if we explain them by two. There is only one diagnosis that will 
 explain all the facts in this case, and that is syphilitic aortitis. 
 
 Shall we find aneurism? That is the natural, I suppose the 
 invariable result of syphilitic aortitis if the patient lives long enough. 
 But most patients with syphilitic aortitis do not get aneurism, other- 
 wise it would be a much commoner disease than itis. We have no 
 symptoms of aneurism here that I see. He has pain which might be 
 due to aneurism, but might perfectly well be produced in other 
 ways. 
 
 There are no pressure symptoms, as differences in the pulses, 
 pupils, aphonia due to laryngeal paralysis. The majority of aneu- 
 risms show pressure symptoms unless the aortitis is very slight. 
 
 Is there anything in the lungs? Ido not see any reason to believe 
 there is anything other than passive congestion. 
 
 The liver was enlarged, presumably by passive congestion, possi- 
 bly by syphilis in that organ. But syphilis of the liver is rather rare, 
 and we do not need to suppose it. 
 
 I do not think we shall find anything in the kidneys. If that turns 
 out to be true, it will support what I have said about the functional 
 test and the urea nitrogen. 
 
 If the diagnosis is correct we should find a very large heart with 
 a so-called basin-shaped left ventricle, with an aortitis which has 
 dilated the aorta and bound back the aortic valves flat against the 
 wall in such a way that the blood regurgitates through them, but 
 without stenosis. I have no evidence that syphilitic aortitis often 
 produces aortic stenosis. If it produces any valve lesion, it usually 
 produces aortic regurgitation. The mouth of the coronary artery 
 will be wholly or partially obstructed. We say that because of the 
 pain that he had. There will probably be some arteriosclerosis. 
 Most of these cases show it, but not as a cause of death. 
 
 A PuysictAn: Do you expect to find anything corresponding to 
 heart block? 
 
 Dr. Casot: He had at the end what may have been heart block. 
 But that is always a dangerous diagnosis to make without either a 
 well-taken polygram or anelectrocardiogram. So Iam not atallsure 
 that he had heart block. If he had it, what should we find in addition 
 to what I have said? We should find a lesion in the interventricular 
 septum where the conduction fibers known as the bundle of His 
 carry the impulse from the auricle to the ventricle. Syphilis is the 
 disease which most often produces heart block. We know we have 
 
352 FACTS ON THE HEART 
 
 disease not more than an inch from the bundle of His, and it is quite 
 possible that at that point we shall have either fibrous or fibrocal- 
 careous degeneration; if so we should have heart block. 
 
 A PuysictAN: Don’t you think this was a terminal heart block? 
 
 Dr. Casort: It might perfectly well be. On the other hand the 
 existence of true heart block might have been the cause of death. 
 The lesion back of it might exist for a good while without being 
 sufficient to produce heart block. I have seen a gumma of the heart 
 as big as a man’s thumb, a real tumor, which must have been there 
 a long time, but without symptoms enough to produce heart block 
 until near death. 
 
 Heart block may be produced by rheumatism as well as by 
 syphilis. I took care of such a case in France; the patient got 
 entirely well. 
 
 A PuysiciAn: Was it rapid or merely hard breathing in this case? 
 
 Dr. Casort: I assume it was rapid, because we should have called 
 it air hunger otherwise. 
 
 A Puysictan: The sputum was not frothy? 
 
 Dr. Casot: I assume not. I assume no edema of the lungs. 
 
 A Puysictan: Why should aortic regurgitation give such a high 
 blood pressure? 
 
 Dr. Casot: High systolic pressure comes from the great power of 
 the left ventricle. The left ventricle is hypertrophied because of the 
 leak of the aortic valve. It will send a bigger volume of blood into 
 the arteries and therefore raise systolic pressure. 
 
 Dr. Hucu Casort: I think I must disagree about the kidney func- 
 tion test. If your view is sound it seriously undermines the position 
 of the functional test. When it was introduced it was believed that 
 the test would enable us to distinguish in. cardiorenal cases between 
 the cases which were primarily renal and those which were primarily 
 cardiac. In essentially cardiac cases it gives a pretty normal result, 
 30 or 40% instead of this very low %. I should be surprised if simply 
 poor general condition with more or less starvation would give this 
 result, the kidney functioning poorly simply because the body is 
 functioning poorly. Added to that there is the slightly high blood 
 nitrogen. I think there is a lesion of the kidney here. 
 
 Dr. RicHARD Casort: Other than passive congestion? 
 
 Dr. Hucu Casor: I think so. 
 
 Dr. RicHARD CaABotT: I think not. 
 
 Clinical Diagnosis (from Hospital Record).—Chronic nephritis 
 (specific?). 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 353 
 
 Endocarditis. 
 
 Myocarditis. 
 
 Heart block with coronary spasm. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Syphilitic aortitis, aortic 
 regurgitation, obstruction of coronary artery. 
 
 Passive congestion of the liver. 
 
 Hypertrophy and dilatation of the heart. 
 
 Slight arteriosclerosis. 
 
 Anatomical Diagnosis.—Syphilitic aortitis with coronary obstruc- 
 tion and involvement of the aortic valve (aortic regurgitation). 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Hydropericardium. 
 
 Ascites. 
 
 Anasarca. 
 
 Chronic pleuritis. 
 
 Obsolete tuberculosis of a bronchial lymph node. 
 
 Dr. RicHARDSON: This was a typical case of syphilitic aortitis. 
 Anatomically the picture was as follows: 
 
 The heart weighed 760 grams, very marked hypertrophy. The 
 dilatation, which was also marked, was greatest in the left ventricle, 
 the cavity of which was basin-shaped. The valves other than the 
 aortic were negative. The aortic cusps presented a certain amount 
 of fibrosis, and in the region of their contiguous margins were bound 
 down to the aortic wall by thick fibrous bands which were continuous 
 with a syphilitic process in the aorta. This same process extended 
 about the orifices of the coronary arteries, causing marked decrease in 
 their circumferences. The aorta presented an irregular luetic band 
 3 or 4 cm. wide, extending around just above the aortic cusps and 
 continuous with the process mentioned, and from that point up there 
 were scattered areas of syphilitic aortitis as far along as the arch. 
 In the descending portion of the thoracic aorta the process faded out, 
 ~ and in the abdominal portion and in the great branches there was no 
 aortitis or any definite arteriosclerosis. 
 
 Dr. RicHARD CasotT: That is in contrast with what you would 
 have found if there had been arteriosclerosis. 
 
 Dr. RicHARDSON: Yes. One of the favorite seats of arteriosclero- 
 sis is in the abdominal portion of the aorta with involvement of the 
 great branches. We seldom have an opportunity to examine the 
 
 peripheral arteries, but when we do the clinical observations of 
 23 
 
/ 45354 FACTS ON THE HEART 
 
 sclerosis in these vessels are not always borne out unless it is so 
 evident that we do not need to examine. 
 
 The liver weighed 1440 grams, the spleen 170 grams, the kidneys _ 
 295 grams. ‘These organs all showed chronic passive congestion. 
 
 So far as I could find in this case there was no other evidence of the _ 
 presence of syphilis except in the aorta and the extension to the 
 aortic cusps. 
 
 The gastro-intestinal tract showed the usual picture of chronic 
 passive congestion,—thickened, reddened, velvety, juicy mucosa. 
 
 The head was not examined. 
 
 Dr. Casor: Is there anything to explain the heart block? 
 
 Dr. RicHARDsON: No. Death would seem related to hypertrophy 
 and dilatation of the heart, with the added burden of the considerably 
 - _. obstructed coronary arteries. There was no ana- 
 tomical evidence at all of the presence of anything 
 impinging upon the bundle of His. 
 
 A PuysiIcIAN: Do you see as many aneurisms 
 as you used to? 
 
 Dr. RICHARDSON: We get them every once ina 
 
 Fic. 59.—The dark 
 narrow strip above 
 shows the _ ordinary 
 
 thickness of an artery. 
 The wide band below 
 it is the thickened wall 
 of the syphilitic aorta. 
 Natural. size: a Dr; 
 Oscar Richardson.) 
 
 while; yes. 
 
 A PuysictAn: All the old text-books seem to be 
 full of aneurisms. I have not seen any in four or 
 five years. 
 
 Dr. Casot: I get the impression that they are 
 not so common, but it is very hard to be sure. It is only an 
 impression. 
 
 Dr. RicHarDsoN: The astonishing thing to me is the absence of 
 syphilitic lesions elsewhere in the body. The man must have been 
 infected at some time, possibly unknown to himself, and syphilis is a 
 septicemia. Why the spirochetes in these cases should select the 
 first portion of the aorta as the favored seat of residence seems diff- 
 cult to explain. 
 
 Necropsy 4438 
 
 An Irish-American chauffeur of thirty-six entered November 
 20,1922. He had difficulty in seeing in the dark and stumbled easily. 
 For these conditions a physician gave him “five drops for three 
 months.” He had possibly once been jaundiced. His weight was 
 never better. 
 
 Fifteen years before admission he had a syphilitic infection. The 
 first symptom was trouble with his eyes. He also lost some hair. 
 He thought he had some 606, but “not much.” 
 
 A 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 355 
 
 Six weeks before admission he had a head cold, then a cough with 
 scanty white, sometimes brownish, tenacious sputum. Since the 
 onset he had developed dyspnea on exertion. Four weeks ago he 
 began to have edema of the ankles, disappearing at night. In the 
 past week, during which he had been in bed, he had had palpitation 
 and urination once at night. 
 
 It was learned from another hospital that since May 8, 1922, he 
 had been given weekly doses of arsphenamin at the Out-Patient 
 - Department there, o.2 grams for the first five doses, then 0.5 grams 
 for 12 doses. Between September 4 and October g he had five doses 
 of intramuscular ‘‘mercury solution,”’ ten minims each dose. Fol- 
 lowing this he had four doses of arsphenamin, each of 0.4 grams. 
 Total arsphenamin 21 doses, total 7.4 grams in seven months. 
 
 Examination showed a well nourished man with some smoothing 
 out of the nasolabial folds. The mucous membranes were slightly 
 pale. The tongue and throat were very dry. There was some pus in 
 the nasopharynx. The heart was greatly enlarged, with diffuse 
 irregular heaving impulse in the left sixth interspace 12 cm. from 
 -midsternum. The left border of dullness was 13 cm., the right 
 border 4 cm., the substernal dullness 10cm. The midclavicular line 
 . is not recorded. The sounds were mostly obscured by murmurs. 
 There were systolic and diastolic murmurs over the base, a mitral 
 diastolic over the apex. Each beat was followed by an extrasystole. 
 There was a very coarse diastolic thrill after the extrasystole at the 
 apex. There was Corrigan pulse, pistol shot, bigeminy, and visible 
 capillary pulsation. Electrocardiogram showed the rate 110, bige- 
 miny due to ventricular premature beat occurring every other beat, 
 possibly slight aberration. The blood pressure was 140/80. The 
 lungs showed many moist rales and slight dullness at both bases, 
 more on the left. (The left side was down during examination.) 
 The abdomen was slightly full, otherwise normal. The knee-jerks 
 were equal. There was no clonus or Babinski. Romberg’s sign is 
 not recorded. The right pupil was greater than the left. The right 
 was oval, the left irregular. Both reacted to distance but poorly to 
 light. 
 
 The temperature was 97.3° to 99° until November 28, 98.1° to 
 tor° until December 4, then rising, 99° to 106°. The pulse was 50 to 
 140; after November 24 only once below 100, after November 30 not 
 below 108, and after December 4 not below 120. The respirations 
 were 17 to 30. The amount of urine was 22 to 25 ounces on the 
 three occasions recorded, the specific gravity 1.020 to 1.030. The 
 
356 FACTS ON THE HEART 
 
 urine was alkaline at one of two examinations. The sediment showed 
 leucocytes at both examinations, red blood corpuscles at one, much 
 bile at two. The hemoglobin was 80%, the leucocyte count 8600 to 
 6800, the polynuclears 76 to 85%, the reds and platelets normal. 
 A Wassermann was unsatisfactory on account of the presence of bile. 
 The non-protein nitrogen was 39.3 mgm. ‘The stool was negative to 
 guaiac. Lumbar puncture gave 15 c.c. of clear fluid. The initial 
 pressure was more than 240 (the fluid rose very slowly). After the 
 withdrawal of 5 c.c. the pressure was 240, after 5 c.c. more 230, after 
 5 ¢.c. more 210. Jugular compression raised the pressure only 20 
 
 Fic. 60.—Heart shadow much enlarged in all diameters; greatest increase to the 
 left. Also marked increase in supracardiac dullness.. There is no definite tumor-like 
 formation. 
 
 mm. Cough caused no increase. Normal pulse and respiratory 
 oscillation. There were 26 cells. Alcohol was positive, ammonium 
 sulphate negative, Wassermann strongly positive, goldsol 555555- 
 3210, total protein 65. A heart consultant reported November 20, 
 ““Apparently well marked Austin-Flint murmur with mitral diastolic 
 thrill . . .” An eye consultant reported November 20. “ Appar- 
 ently beginning changes in the macular regions of both eyes. 
 Retinae show a suggestion of pigment deposits with a few vague 
 areas suggestive of involvement. The condition is slightly more 
 marked in the left eye. Pupils not dilated well enough for the best 
 view. Vitreous opacities in both eyes.” <A _ syphilis consultant 
 reported, “. . . Further antisyphilitic treatment contraindicated.” 
 X-ray November 25 (see Fig. 60) showed the outline of the various 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 357 
 
 chambers of the heart indistinct. The examination was rather 
 unsatisfactory on account of the patient’s condition. 
 
 The patient seemed to be holding his own. By December 2 the 
 jaundice was about the same (sic). The digitalis was discontinued. 
 After three days he seemed less jaundiced. The pulse was poor 
 several times on the 5th, and there was much mucus in the throat. 
 There was edema of the right forearm and hand for which no cause 
 was found, and which was much reduced by December 7. Decem- 
 ber 8 there was a great change for the better. The pulse was good, 
 the heart vigorous. The patient was restless, not stuporous, and 
 talked with his friends, though he would not answer the doctor’s 
 questions. December 1o the condition was not so good. The 
 jaundice was increased. ‘The spleen was readily palpable. Percus- 
 sion of the liver showed it to be possibly smaller than at the previous 
 examinations. December 11 the patient became comatose and died. 
 
 Clinical Diagnosis (from Hospital Record).—Syphilis. 
 
 Aortitis and acute atrophy of the liver. 
 
 Central nervous system syphilis. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Syphilis of the central nervous 
 system. 
 
 Syphilitic aortitis. 
 
 Aortic regurgitation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis ——Luetic aortitis with small aneurism. 
 
 Fibrous endocarditis of the aortic valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Thrombosis of the portal vein. 
 
 Atypical cirrhosis of the liver. 
 
 Hypertrophy of the spleen. 
 
 Icterus. 
 
 Ascites. 
 
 Decubitus. 
 
 Hemorrhagic areas in the serosa of the intestines and the 
 peritoneum. 
 
 Serofibrinous pleuritis, right. 
 
 Slightly defective closure of the foramen ovale. 
 
 Dr. RIcHARDSON: What were the clinical data as to the liver? 
 
 Dr. Casot: They do not say. They say it was enlarged and then 
 less enlarged. But we do not know any more. 
 
358 FACTS ON THE HEART 
 
 Dr. RicHarpson: It is curious, because the history given before 
 the necropsy inclined the house officers to think there was atrophy, 
 and it was so stated on the necropsy permission. 
 
 Unfortunately we were not permitted to examine the head. The 
 conjunctivae and skin showed a well marked saffron discoloration. 
 There was quite an extensive bedsore in the sacral region. 
 
 The peritoneal cavity contained 1500 c.c. of thin bile-stained 
 fluid. The appendix was negative, and the peritoneal cavity in 
 general, other than for the fluid, was negative. 
 
 The mucosa of the esophagus showed a well marked meshwork of 
 varices running up and down. ‘The stomach showed some areas of 
 reddening in the mucosa but was otherwise out of the picture. The 
 intestines were negative except as stated below, and the fecal material 
 in the large intestine brown. It is to be mentioned that scattered 
 along the mucosa of the intestine In numerous places were small 
 hemorrhagic areas, and we might as well clear that up now. The 
 portal vein at its lower end presented an area of chronic phlebitis to 
 which a long columnar thrombus was attached, extending up towards 
 the liver and in the direction of the stream. This thrombus only 
 partly occluded the portal vein, but the obstruction was sufficient to 
 produce the hemorrhagic areas in the mucosa of the intestine which 
 otherwise were unaccounted for. 
 
 The mesenteric and retroperitoneal glands were out of the picture. 
 The right pleural cavity contained about 400 c.c. of thin pale cloudy 
 fluid. On the left there were only a few c.c.—one of those not very 
 uncommon cases where we find fluid on one side and not on the other. 
 The bronchial glands were soft and juicy. The lungs showed hemor- 
 rhagic edema, and on the lower lobe of the right lung a little fibrino- 
 purulent pleuritis. On the left there was no evidence of any exudate. 
 
 The pericardium was negative. The heart weighed 645 grams,— 
 considerably enlarged. ‘The myocardium was pale brown-red and a 
 little lax, or what is called flabby, although the right ventricle 
 measured 314 and the left 14 mm., a good thickness. On the right 
 side the chordae tendineae were well marked. The left ventricle 
 showed much dilatation and was basin-shaped,—that peculiar dila- 
 tation and configuration which we associate with syphilitic aortitis. 
 The left auricle was of full size. On the right side there was moderate 
 dilatation. The valve circumferences were: mitral 12 cm., aortic 
 9g cm., tricuspid 15 cm., pulmonary 8 cm. Those were large cir- 
 cumferences, a little increased. But the valves, other than the aortic 
 valve, were out of the picture. We have a very good picture of the 
 
SYPHILITIC AORTITIS WITH AORTIC REGURGITATION 359 
 
 aortic valve here; and we shouldynote that one of the cusps is in pretty 
 good condition. The other two speak for themselves. They are 
 markedly deformed, wrinkled down, curled up, plastered back against 
 the wall. So that two of them are not cusps at all, but simply 
 flattened, wrinkled masses of fibrous tissue. 
 
 - That condition we took to be syphilitic aortitis, and it accounts 
 very well for the clinical manifestations. 
 
 We noted that the right coronary was frankly negative; the left 
 was just below a little aneurism shown very well in the picture. 
 There was no apparent obstruction to the left coronary. Of course 
 with the distension of the sac there might have been a little, but 
 nothing marked. So that we have syphilitic aortitis with extension 
 
 Fic. 61.—Syphilitic aortitis. C, fairly good aortic cusp. C’ and C”’, deformed 
 cusps. C’”, tag of C’’. A, area of aortitis. An, aneurism. I.c., beginning of left 
 coronary artery. 
 
 to the aortic valve, with deformity of the cusps and with irregular 
 luetic areas for a short distance on the aorta just above the aortic 
 cusps. Beyond that the aorta over its entire length and the great 
 branches were negative. This position just above the aortic cusps is 
 the typical zone for luetic aortitis. 
 
 Dr. Capot: How big was the aneurism? 
 
 Dr. RicHarpson: It was not bigger than the end of the little finger. 
 
 Dr. Casot: You won’t blame us for not diagnosing that. 
 
 Dr. RICHARDSON: The venae cavae were negative. The portal 
 vein we have spoken of. The liver weighed 990 grams. That means 
 some atrophy in a man such as Is described here. His liver should 
 have weighed at least 1300 or 1400 grams. There was chronic 
 passive congestion. ‘There was some sclerosis. So far as we have 
 gone there was no definite evidence of the destruction of the liver 
 tissue such as we find in some of these cases where salvarsan has been 
 
360 FACTS ON THE HEART 
 
 pushed and we get conditions which simulate acute yellow atrophy 
 of the liver. | 
 
 In association with this the spleen weighed 995 grams. Here 
 again there was chronic passive congestion and a certain amount of 
 sclerosis in the background. 
 
 The gall-bladder and bile-ducts were frankly negative, so that the 
 icterus cannot have been from obstruction unless of the very minute 
 ducts within the liver substance itself. But that is not what we 
 usually mean by obstruction, although the current belief is that 
 all icterus is mechanical obstruction of the bile-ducts somewhere. 
 
 The kidneys were a little large but showed no definite lesion. The 
 bone-marrow of the lumbar vertebrae was rather red, but was 
 negative. 
 
 Dr. Casor: Did that portal thrombus have anything to do with 
 the sclerotic process in the liver? 
 
 Dr. RicHarpson: No. There are two or three possibilities: 
 sometimes with chronic passive congestion we get a condition which 
 simulates cirrhosis; the second is a straight ordinary cirrhosis; and 
 the third is the question whether it is syphilitic or not. There was 
 chronic passive congestion in this case, which is responsible for a 
 part of the picture. The bile ducts were negative. That throws out 
 the possibility that any infection went up and produced the so-called 
 biliary infections with cirrhosis. The liver tissue finally showed no 
 such definite picture as we get in the over-salvarsanized liver cases. 
 
 Dr. CasotT: It might; however, be due to syphilis? 
 
 Dr. RicHARDSON: It might. The anatomical evidence is fibrosis 
 or sclerosis of an atypical kind. If the other things all point to that, 
 then it might be syphilitic. 
 
 ILLUSTRATIVE CASES 
 1. Syphilitic Aortitis with Aneurism 
 2. Malignant Lymphoma Simulating Aneurism 
 Case LX 
 
 A Russian Jewish court interpreter of fifty-three entered August 
 30 for relief of loss of voice, hoarseness, and “‘inability to breathe.” 
 
 Thirty years before admission he was shot in the left elbow. 
 About the same time his nose was fractured. Since that time he 
 had had almost constant catarrh and sinus involvement. A year 
 after the extraction of the bullet in his elbow he had paralysis of the 
 vocal cords and possibly syphilis, though there were no secondary 
 symptoms. While in Vienna taking a nine months’ course of treat- 
 
ILLUSTRATIVE CASES 261 
 
 ment for syphilis the elbow became intensely and increasingly painful, 
 so that large amounts of morphia had to be used. He acquired the 
 habit, and had it for a year and a half, taking eleven grains a day. 
 Then he was treated at the Mt. Sinai Hospital, New York, for numer- 
 ous boils caused by his hypodermics, and was cured of his morphin- 
 ism. For twenty-five years he had had bleeding hemorrhoids. 
 Five years before admission he had gastric distress, heartburn, gas 
 and nausea for several months, relieved by careful dieting. The 
 following year he had an attack of chills and fever followed by enlarge- 
 ment of the heart, and was laid up in bed six weeks. For six months 
 he had had a dull aching across the small of his back, not radiating, at 
 times catching him up suddenly. Two years before admission he 
 weighed 210 pounds, his best weight. His usual weight was 200, 
 
 He drank a rare glass of whiskey and smoked twenty or twenty- 
 five cigarettes a day. 
 
 The first attack of loss of voice and difficulty in breathing came on 
 suddenly over night twenty-nine years before admission. The 
 attacks previous to the present one lasted from a few hours to five 
 days, rarely over three days. Cold, dry winter air seemed to free 
 him from them. He talked in an undertone and only on forced expir- 
 ation after a very deep breath. With each attack there was increased 
 difficulty of inspiration. During the present attack, which had 
 lasted three weeks, it had seemed at times as though he could not 
 get breath, try as he might. Loss of voice had been marked, with 
 cough, sputum, and hoarseness. . Talking tired him out and caused a 
 dull pain beneath the base of the sternum. During the past few 
 weeks he had had a good many headaches, with some dizziness. His 
 appetite was poor. His bowels were constipated. At the Out- 
 Patient Department, August 23, 1915, a Wassermann was negative. 
 X-ray (Fig. 62) showed the entire right chest less radiant than the 
 left; marked peribronchial thickening; enlarged and calcified glands; 
 the aortic arch dilated; the heart shadow enlarged to the left. Exam- 
 ination in the Nerve Department was negative except that the left 
 biceps and triceps reflexes were greater than the right. In the Throat 
 Department operation was advised. The patient was unwilling to 
 have it done immediately, but agreed to consider it. 
 
 Examination showed a pale, well-nourished man, speaking 
 hoarsely. Glands were palpable in the neck and axillae. The 
 apex of the heart is not recorded. The width of the arch was 7 cm. 
 The other dimensions are shown in Figure 63. The sounds were of 
 poor quality. X-ray showed the dimensions as in Figure 64; the 
 
362 FACTS ON THE HEART 
 
 length of the heart 17.1 cm. There was a systolic murmur at 
 the apex and a faint diastolic at the second right interspace. 
 The pulses were of fair volume. The artery walls were just palpable, 
 
 the brachials slightly tortuous. The abdomen, genitals, extremities, 
 
 Fic. 62.—Hypertrophied heart in syphilitic aortitis. 
 
 and reflexes were normal. The pupils were irregular, otherwise 
 normal. 
 
 The temperature was 97. to 99.7°, the pulse 60 to 100, the respira- 
 
 tion normal except for two rises to 29. The amount of urine was 
 
 RAS AOTn y fray eR 8043 
 3 ) 
 F 2 . 
 S = Pe 
 Z 3 : 
 : a 7 
 TECM. meny2s cI. 6.8 cm. 0:3 Cine 
 
 Fic. 63.— Measurements 
 
 Fic. 64.—Measure- 
 by percussion. 
 
 ments by X-ray. 
 
 normal, the specific gravity 1.018 to 1.010. ‘There were leucocytes 
 at both examinations. The renal function was 50%, the hemoglobin 
 75%. The other blood findings were normal. A Wassermann was 
 negative. The spinal fluid gave a cell count of three lymphocytes. 
 Noguchi and Nonne were negative. A Wassermann was anti- 
 
 ee 
 
ILLUSTRATIVE CASES 363 
 
 complementary. Gold chlorid test was suspicious of syphilis. The 
 stool gave a negative guaiac. 
 
 Two throat surgeons advised tracheotomy. September 11 
 it was done. The patient was sent to the ward in good condition 
 and breathing well. Next day the tube slipped out of the trachea 
 and could not be reintroduced because of swelling around the wound. 
 The tube was too short. There was considerable.emphysema of the 
 tissues of the neck and face. The sutures were therefore removed 
 and the wound left wide open. Next day the emphysema was much 
 reduced, and the tube was reintroduced. September 14 it was 
 replaced by a longer tube after a larger opening had been made in 
 the trachea by punching out part of the rings with a tonsil punch. 
 The wound was moderately septic. This tube also slipped out, 
 but was put back a few hours later. September 15 a still 
 larger tube was put in, slipped out, and was put back. The patient 
 was much depressed, and complained a great deal. September 
 16 an extra long tube was put in, fitting better than any of the 
 others, but it also slipped out. September 17 a new, extra 
 long tube was inserted and strapped tightly to the neck with 
 adhesive. It stayed in place until next morning, and was reinserted 
 with ease. The wound was draining a little pus. After this the 
 tube remained in place. September 22 the patient was discharged, 
 feeling very comfortable, the wound granulating. 
 
 Dr. Richard C. Cabot’s Diagnosis—Syphilitic aortitis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Paralysis or syphilitic ulceration of the vocal cords. 
 
 Interpretation of X-ray, August 23.—Dilatation of the arch. 
 
 Enlargement of the heart. 
 
 Thickened pleura. 
 
 O.P. D. Throat Department Diagnosis, August 23.—Complete 
 paralysis of left vocal cord, abductor paralysis of right vocal cord. 
 
 Diagnosis in Medical Department, September 11.—The same, with 
 
 Dilated aorta. 
 
 Operation.—No pre-operative diagnosis but that above is recorded. 
 Two-inch median incision over the trachea at the upper limit of the 
 first tracheal ring. The deep tissue was infiltrated with novocain. 
 The sterno-thyroid and sterno-hyoid muscles were split and retracted, 
 the isthmus of the thyroid gland defined by powerful blunt dissection 
 and retracted upward. The trachea below this was exposed for 
 about an inch. A few drops of 10% cocain with adrenalin were 
 introduced into the lumen of the trachea by means of a hypodermic 
 
364 FACTS ON THE HEART 
 
 needle. A longitudinal incision 34 inch long was made in the 
 trachea, cutting two rings, which were found to be partially calcified. 
 A silver tracheotomy tube was inserted. 
 
 Clinical Diagnosis at Discharge (from Hospital Record)—New 
 growth of lung? 
 
 Dr. Richard C. Cabot’s Diagnosis —(See above.) 
 
 Later History (from Out-Patient Record).—September 24 the wound 
 looked well. September 29 it showed exuberant granulation, and 
 was cauterized. Oct. 4 it was again cauterized. It was doing well 
 at this and the next visits, October 18 and 29. At three later visits 
 there is no entry except that once the tube was cleaned, as it had 
 been at most previous visits. March 3, 1916, the patient was found 
 to be doing well. July 8, 1916, there was slight movement in the 
 left vocal cord. ‘There were no signs of growth. He kept the tube 
 closed but in place for emergency use. September 23, 1916, there 
 was practically no movement in either cord. There was sufficient 
 space, however, to allow the tube to be cleaned. The voice sounds 
 were fairly good. 
 
 April 11, 1922, he reported that he had been wearing the tube 
 plugged and breathing with a fair degree of comfort through the 
 mouth until a month before the visit, when he had an attack of 
 grippe. Since that time the breathing had been gradually becoming 
 more difficult. Laryngoscopic examination showed both cords 
 fixed in adduction. The left cord showed a polypoid mass apparently 
 growing from the margin and inferior surface of the cord. This 
 flapped up and down with respiration. He was recommended for 
 admission to the Eye and Ear Infirmary for study and removal of 
 the growth. No record of his having visited the Infirmary could be 
 found February 27, 1925. 
 
 Case CIX 
 (Copyright, 1918, by Oscar Richardson, M.D., and William H. Smith, M.D.) * 
 
 A Swedish carpenter of forty-four entered October 15 for relief of 
 shortness of breath. He had always been well and strong. He had 
 possible scarlet fever at ten. He had urinated once at night all his 
 life. A year before admission he vomited every morning and was 
 constipated. Since that time he had taken Russian oil every morn- 
 ing. He was having no more stomach symptoms. He was last 
 employed by a large ship-building company, and worked nine to ten 
 hours a day. The work was noisy, damp, and too hard for him. 
 
 * This and the following case and discussion are used by permission of Dr. Richard- 
 son and Dr. Smith. 
 
ILLUSTRATIVE CASES 305 
 
 During the past year he had worried about his health. At twenty- 
 one he weighed 176 pounds, his best weight. His usual weight was 
 175, his present weight 154 pounds. He denied venereal disease and 
 the use of alcohol and tobacco. 
 
 Two months before admission he noticed that after undue exer- 
 tion he became breathless and dizzy and had a sense of pressure over 
 the precordia. A physician gave him medicine which slowed his 
 pulse. He was able to work somewhat better for a week. A week 
 before admission he became weak and breathless and was told by a 
 doctor to stay in bed. 
 
 Examination showed a well-nourished man, his head nodding with 
 each heart beat. There was marked pulsation of the arteries in 
 the neck and a systolic thrill over both carotids. There were 
 bean-sized inguinal glands. The apex impulse of the heart was seen 
 and felt only in the left lateral position in the sixth space 14 cm. to 
 the left of midsternum, 5.5 cm. outside the midclavicular line. The 
 left border of dullness was 13 cm. from midsternum, the right border 
 of dullness 4 cm. to the right, the supracardiac dullness 6.5 cm. 
 The action was regular, slightly rapid. The aortic second sound was 
 replaced by a murmur. At the apex was a blowing systolic murmur 
 transmitted to the axilla. At the base was a systolic somewhat 
 rougher in character, transmitted to the carotid. There was a 
 blowing diastolic over the precordia replacing the aortic second 
 sound, best heard at the aortic area and along the left sternal border. 
 The pulses were Corrigan. Pistol-shot and Durosiez’s sign were 
 heard over the peripheral vessels. The artery walls were just 
 felt. Theblood pressure was 135/25 to115/15. Thelungs, abdomen, 
 genitals, pupils and reflexes were normal, as were the extremities, 
 except for slight roughness of the left shin. 
 
 The temperature was 100.8° to 96.7°, the pulse 88 to 64, the 
 respiration 32 to 13. The amount of urine was 17 to 28 ounces. 
 The urine was cloudy at two of four examinations. The specific 
 gravity was 1.022 to 1.026, The sediment showed rare leucocytes 
 at two of four examinations, hyaline casts at one. The renal func- 
 tion was 40%. ‘The hemoglobin was 80%. There were 7200 to 
 10,000 leucocytes, 71% polynuclears. The urea nitrogen was 
 22 mgm. per 100 c.c. of blood. Two Wassermanns were strongly 
 positive. The stools were negative. 
 
 There was nothing to account for the elevated temperature at 
 entrance. October 16, after the report on the Wassermann, he was 
 put on potassium iodid. By October 19 the temperature was lower. 
 
366 FACTS ON THE HEART 
 
 There were no signs of decompensation, and he felt better. He 
 continued to gain, and October 31 was discharged relieved. 
 
 Necropsy 164 
 
 A Negro Pullman porter of thirty entered October 15. His past 
 history was unimportant. He used alcohol in moderation, chewed a 
 twenty-cent plug of tobacco a week and constantly had a cigar in his 
 mouth. Seven years before admission he had chancre with double 
 buboes; no secondary manifestations 
 
 Four weeks before admission he was suddenly seized with shortness 
 of breath upon exertion ‘and cough with whitish sputum. The 
 dyspnea had increased, coming in spasms during which he perspired 
 freely. For three weeks he had been unable to lie down. There 
 had been much palpitation and throbbing of the heart. He had had 
 no sleep for a week or more. He passed half a pint of urine at night, 
 about the usual amount by day. 
 
 Examination showed a fairly well nourished negro. The mucosae 
 were pale. The lips were at times somewhat cyanosed. During the 
 paroxysms of dyspnea the veins stood out prominently in the head and 
 forehead. The apex impulse of the heart was in the fifth space. 
 There was no enlargement to percussion. A roughened heart sound 
 was heard through into the back near the vertebral column. There 
 was dullness over the sternum up to within an inch of the supra- 
 sternal notch. Pulsation was felt on palpation. in the notch. 
 Throughout the cardiac area a vibratory systolic thrill was felt and 
 a harsh systolic murmur was heard, loudest at the third cartilage, 
 transmitted into the aortic region downward. ‘The second sound 
 was very indistinct. In the region below this, loudest at the fourth 
 space, was heard a diastolic murmur, blowing in character. At the 
 apex the first sound was somewhat churning in character. The 
 lungs were normal. The liver was just below the costal border. 
 Pressure on it filled the veins of the neck. The pupils reacted. The 
 knee-jerks were present. The extremities showed no edema. On 
 the under surface of the penis was a cicatrix, said to be from a sinus. 
 A crust was seen uponit in oneplace. In both groins were cicatrices, 
 said to be from buboes. : 
 
 The temperature was 95° to 98°, the pulse 95 to 120, the respira- 
 tion 25 to 48 The amount of urine is not recorded. The specific 
 gravity was 1.020. There was the slightest possible trace of albumin. 
 The sediment showed abnormal blood cells and leucocytes at both of 
 two examinations, hyalin and granular casts at both, with a few cells 
 
ILLUSTRATIVE CASES 367 
 
 adherent at one. The hemoglobin was 54%. ‘There were 8g00 
 leucocytes. 
 
 During the afternoon the patient had several attacks of dyspnea, 
 relieved by nitroglycerin. There was no change in the way the air 
 entered the lungs during the attacks. Two doses of morphia gr. 14 
 and 1@ gave relief. He slept most of the night and had fewer parox- 
 ysms next day. He complained of pain in the cardiac region, relieved 
 by an ice bag. A few medium moist rales were heard in the right 
 back. After another fairly comfortable night there were more rales at 
 the right base and some altered blood in the sputum. A few rales 
 were heard over the apex. An increasing number of fine rales 
 
 . ee s, ele 
 oe cor nini Mie 
 by 
 ee 
 fs 
 Be 
 é 
 g 
 i 
 i 
 & 
 ke 
 i 
 / 
 t 
 f 
 i 
 { 
 : 
 f 
 te 
 
 Fic. 65.—Syphilitic aortitis. From a woodcut made about a hundred years ago. A- 
 area of aortitis. C-coronary. D-aortic cusps. 
 
 appeared in the backs, especially on the right, and there was bright 
 blood in some quantity in the sputum. The murmur was somewhat 
 softer. The legs became increasingly edematous. Bright red, 
 frothy blood was raised in considerable amounts. The sclerotics 
 became much ecchymosed. A hemorrhagic area appeared on the 
 tip of the nose, though there was no history of trauma. The dullness 
 in the upper part of the sternum became more marked, extending 
 more to the left. Respiration became more and more difficult. 
 October 23 he began to have difficulty in swallowing. Next day 
 there were some transient pains in the upper sternal region. The 
 lungs began to fill up with coarser rales. These could be felt through 
 
368 FACTS ON THE HEART 
 
 the chest wall. At ten o’clock he was fairly comfortable, with no 
 marked dyspnea. ‘Three-quarters of an hour later he died. 
 Discussion* by Dr. Oscar Richardson.—DR. RICHARDSON: Definite 
 syphilitic lesions in a case follow infection through definite portals of 
 entry, but there are also cases in which there is no such definite portal 
 of entry and the patient knows nothing whatever of having had any 
 
 oreeneereeneesnnnermuummamacmnmneszamnans 
 
 Fic. 66.—A-area of aortitis. C-coronary. D-aortic cusps. 
 
 infection at any time in his life. This statement of the patient can 
 be regarded as truthful in many instances, for the simple reason that 
 he wishes to know himself and is anxious to give as truthful a history 
 as he can for his own benefit. He does not know he has had syphilis, 
 and yet he will die of luetic aortitis. 
 
 Fig. 65 is from a photograph by Mr. Brown of a woodcut of a 
 portion of the heart and aorta made about a hundred years ago. It 
 
 * Copyright, 1918, by Oscar Richardson, M.D., and William H. Smith, M.D. 
 
ILLUSTRATIVE CASES 369 
 
 might be regarded as the fossil remains of an observation made in a 
 previous age of a condition which we now know to be syphilitic 
 aortitis. The picture is irresistibly convincing. Note the broad 
 band-like area (A) extending around the aorta just above the aortic 
 cusps, how sharply it it differentiated from the natural-appearing 
 aorta above, and how it extends down about the coronary artery (C) 
 and involves the aortic cusps below (D). Again, the intimal surface 
 of the band-like area shows the discrete and confluent, irregularly 
 
 Fic. 67.—L. C.-left coronary. R. C.-right coronary. 
 
 shaped, more or less elevated, plaque-like masses with intermingling 
 smaller and larger irregular areas of depression which give the gristly, 
 scar-like aspect to the surface so characteristic of syphilitic aortitis. 
 The aortic cusps show the usual fibrous wrinkling and deformity with 
 narrowing of the width of the cusps and pinning back of their con- 
 tiguous margins. This region of the aorta is the favorite seat of 
 syphilitic aortitis. 
 
 The following pictures are photographs made by Mr. Brown in 
 
 this laboratory and are taken from our own cases. 
 24 
 
370 FACTS ON THE HEART 
 
 Fig. 66 shows the syphilitic lesion in the same situation as it was in 
 Fig. 65. The lesion in this case is a duplicate of the other, and as 
 an added fact the basin-like dilatation of the left ventricle is to be 
 noted. 
 
 In Fig. 67 we see again a case with the lesion in the same region as 
 in the others. The small gaps in the aortic wall are where pieces were 
 removed for microscopical examination. This was the very remark- 
 
 Fic. 68.—A-area of aortitis. D-aortic cusps. (Dr. J. H. Wright and Dr. Oscar 
 Richardson.) 
 
 able case of a young man twenty-one years of age who died suddenly 
 and was thought to have been poisoned. ‘There was nothing unusual 
 in the previous history, and so far as his family knew he had always 
 been perfectly healthy. His death had been associated with distress 
 and pain in the epigastric region and vomiting. I found at the 
 necropsy, however, that his death was due to occlusion of the orifices 
 of the coronary arteries associated with luetic aortitis. 
 
ILLUSTRATIVE CASES 371 
 
 Fig. 68. This case dates back to 1909 and is the one in which the 
 spirochetes were found for the first time in the wall of the aorta. 
 The lesion is in the first portion of the aorta, as in the other cases. 
 The basin-shaped dilatation of the left ventricle is well shown. 
 
 Fig. 69. This picture shows very well indeed the marked involve- 
 ment of the aortic cusps in syphilitic aortitis. This fibrous wrinkling 
 and deformity of the cusps (C, C), and the pinning down of their 
 contiguous margins, which shortens their width and decreases their 
 
 Fic. 69.—C, C-deformed cusps. D-aneurismal dilatation. 
 
 excursions, are the important factors in the production of the aortic 
 regurgitation so characteristic of luetic aortitis. Aneurismal dilata- 
 tion (D) of the first portion of the aorta is also well shown. 
 
 When we open an aorta which is the seat of syphilitic aortitis, 
 the first thing which strikes our attention is the gristly, scar-like 
 aspect of the surface’ of the intima. Closer inspection shows this to 
 be due to smaller and larger discrete and confluent, irregularly shaped 
 
372 FACTS ON THE HEART 
 
 areas and streaks of depression and longitudinal furrows, extending 
 about and between smaller and larger, more or less elevated plaque- 
 like masses. Many of the plaques show rounded, rather smooth, 
 somewhat translucent surfaces. If the process is a long-standing one 
 or if there is accompanying arteriosclerosis there may be areas of 
 calcareous change, but commonly this is absent. On cross section of 
 the wall of the aorta you will find varying degrees of thinning in the 
 
 Fic. 70.—Section of the wall of the aorta in Fig. 69. JI-intima. M-media. A- 
 adventitia. Enclosed in dotted lines are areas of cellular infiltration. The largest, 
 G, G, is a gummatous focus; great cellular infiltration, with three giant cells, H, H, H. 
 V, V, V, some of the vasa vasorum, with partial occlusion, and in instances with sur- 
 rounding cellular infiltration, consisting of cells of the lymphocyte series, plasma cells, 
 and a few polynuclears. ; 
 
 regions of the areas of depression and of thickening in the regions of 
 the plaques. In instances the wall may be thickened up to 7 or 
 8mm. This great thickening is one of the typical characteristics. 
 All three coats of the aortic wall are thickened with more or less 
 fibrous fusion and scarring. The media is also apt to show in places 
 small yellowish, rather soft, necrosis-like areas, while the adventitia 
 
ILLUSTRATIVE CASES SW) 
 
 is thickened and reddened. It is apparent that the areas of extensive 
 fibrosis with great thinning of the wall are the points where aneu- 
 risms, which occur rather frequently in this disease, may form. 
 Syphilis is a septicemic disease; and the spirochetes gaining 
 entrance through an obvious or an unknown lesion in a certain 
 number of the cases are located in the wall of the aorta and possibly 
 in those minute vascular caverns, the vasa vasorum. ‘They multiply, 
 produce their toxins, and as a reaction to this, inflammatory and 
 
 Fic. 71.—Aortic wall. Showing spirochetes of syphilis. From the same case as Fig. 
 70m x 1500. (Dr: J. HeWreht and Dr> Oscar, Richardson.) 
 
 gummatous processes arise in the aortic wall on which as a basis the 
 gross anatomic conditions found in the aorta rest. 
 
 Fig. 70. We see here a low-power microphotograph of the wall 
 of the aorta in Fig. 69. It shows a section of the thickened syphilitic 
 wall of the aorta with the cellular infiltration in full tide. 
 
 Fig 71 is a high-power microphotograph of the spirochetes in the 
 aortic wall shown in Fig. 70, and is taken from the original section in 
 which they were first found. 
 
374 FACTS ON THE HEART 
 
 Syphilitic aortitis is usually confined to the first portion and the 
 arch of the aorta, fading out in the region of the thoracic portion. It 
 
 is to be noted, however, that it is present in the abdominal portion at 
 
 times, and is seen in cases of abdominal aneurisms. 
 
 In all probability the smaller arteries of the body may at times be 
 
 the seat of syphilitic arteritis. We have one case in which sections 
 from the vessels of Willis show this condition. 
 
 A Puysictan: Then death from syphilitic aortitis is purely 
 mechanical? 
 
 Dr. RicHarpson: Death in syphilitic aortitis is commonly due to 
 the following conditions: 
 
 Fic. 72.—Pulmonary artery in Case 4122. G-gummatous focus. Areas of cellular 
 infiltration are well shown at C, C. Cellular infiltration about a blood vessel at V. 
 
 (1) The luetic process extends down and around the openings of 
 the coronary arteries and finally occludes them. 
 
 (2) Aneurism with rupture and hemorrhage. 
 
 (3) Aortic regurgitation, hypertrophy and dilatation of se heart, 
 myocardial insufficiency. 
 
 In (x) and (2) death is usually sudden in character. Of course all 
 of this excepts any intercurrent cause of death. It is worthy of note 
 that patients with well-established cases of syphilitic aortitis usually 
 die before fifty years of age Thirty-five to forty-five 1 is probably the 
 decade in which death is most common. 
 
 A PuysictAn: In what percentage of cases do you find spirochetes? 
 
ti 
 
 ILLUSTRATIVE CASES . 375 
 
 Dr. RICHARDSON: Only in a small percentage of the cases, but it 
 is probably true that if we made serial sections of the lesions the 
 percentage would be larger. 
 
 A PuysicrAn: Is there any particular location in which you find 
 the spirochetes? 
 
 Dr. RICHARDSON: Usually in the region of or nearby the areas of 
 necrosis and cellular infiltration. 
 
 Fig. 72 shows a low-power microphotograph of a section of the 
 first portion of the pulmonary artery. The areas of cellular infiltra- 
 tion and the gummatous focus are well indicated. 
 
 Fig. 73. Here we see an almost perfect picture of the gumma in 
 the heart muscle. 
 
 Fic. 73.—Heart muscle in Case 4122. G-gumma. 
 
 Long before the discovery of the spirochete of syphilis the asso- 
 ciation of peculiar lesions in the circulatory apparatus in cases of 
 syphilis had been noted. The discovery of the spirochete, however, 
 and the finding of spirochetes in the lesions settled the question, just 
 as the discovery of the tubercle bacillus and the finding of tubercle 
 bacilli in tuberculous tissue gave an etiological basis for tuberculosis. 
 So although the necropsy in this case was made in 1897, some time 
 before the spirochetes were found in the lesions, yet from the charac- 
 ter of the lesions and the clinical history the anatomic diagnosis was 
 written as given. 
 
 The pathologic work herein set forth is due to my association with 
 Dr. James Homer Wright, the Director of the Pathological Labora- 
 tory at the Massachusetts General Hospital. 
 
376 FACTS ON THE HEART 
 
 Clinical Diagnosis (from Hospital Records).—Syphilitic aortitis. 
 Decompensated heart. 
 
 Aortic stenosis. Insufficiency. 
 
 Aneurism of the aortic arch. 
 
 Anatomical Diagnosis. 
 
 Syphilitic endoaortitis. 
 
 Gummata of the heart and pulmonary artery. 
 Obliteration of the opening of one coronary artery. 
 Heart thrombi. d 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Syphilitic scars on the penis and groin. 
 
 Case CV 
 
 An army man thirty-three years of age came to Boston, went to 
 a. hotel, and for a week went about his affairs, was well liked, and 
 made no complaints. 
 
 At the end of a week he came in about 5:45 p.m., spoke to the 
 hotel clerk as usual and went upstairs to his room. He had been 
 there only about five or ten minutes when the chambermaid came 
 down and said that he had called for a glass of water, said that he 
 was ‘‘feeling pretty bad,” and asked her to call a doctor. They tried 
 to get the doctor, but he was not in. Then they called in a police 
 officer, who went with the clerk up to the guest’s room. They found 
 him dead on the bed. The whole thing happened within fifteen 
 minutes. 
 
 The dead body lay on its back, completely clothed except for the 
 jacket. It showed full rigor mortis, but otherwise was negative. 
 He was a well set-up man weighing about 135 pounds. 
 
 The landlord said the only unusual things that he had noticed 
 about the man were that when he hired the room he said he wanted 
 one where there was plenty of air, and that he seemed to be what is 
 called a ‘‘hard breather.” 
 
 This man from time to time had been subjected to physical 
 examinations by physicians. 
 
 Dr. William H. Snuth’s Diagnosis ——FProbably syphilitic aortitis, 
 with coronary sclerosis and occlusion. 
 
 Anatomical Diagnosis.—Luetic aortitis. 
 
 Aneurism of the aorta with rupture into the pericardium. 
 
 Hemorrhage into the pericardial cavity. 
 
ILLUSTRATIVE CASES AT] 
 
 Dr. RicHarDsoN: There was some hypertrophy and dilatation 
 of the heart, not very marked however. The valves were negative. 
 The coronary arteries were negative. The aorta itself was the seat of 
 an extensive aneurism which extended up into the region of the arch, 
 involving it to a certain extent. At s (see Fig. 74) you will note 
 that the aneurism gave off a little pocket-like sac and that this sac 
 pressed on the wall of the trachea. The man was a “hard breather.” 
 
 5 
 } 
 
 Fic. 74.—Aneurism showing sac at s. Photograph by L. S. Brown. (Dr. Oscar 
 Richardson. ) 
 A seemingly insignificant point like that in a history may be of great 
 aid in diagnosis. The capacity of his trachea had been reduced one- 
 half from the pressure of this aneurism upon it. (See s, Fig. 75). 
 The sac was wadded around with thrombus. Of course that made 
 a good buttress, and it would have taken a long time before the 
 aneurism would break into the trachea. What it did do was to 
 
378 FACTS ON THE HEART 
 
 break through a thinned-out area in its wall and to rupture into the 
 pericardium, which was found full of fluid blood with a thick layer 
 of blood clot enveloping the heart. ‘There was about 500 c.c. of fluid 
 blood. The lesion itself, judging from its situation and from its 
 character, is due to syphilis. Itis syphilitic aortitis with an aneurism 
 in the situation of the first portion of the aorta and the arch with 
 rupture of the wall and hemorrhage into the pericardium. 
 
 bes | Pe 
 Fic. 75.—Trachea partially occluded by pressure of aneurismal sac at s. Photograph 
 by L. S. Brown. (Dr. Oscar Richardson.) 
 
 These aortitis cases present a variety of pictures. The classical 
 one is where the aortitis attacks the first portion of the aorta for 
 varying distances above the aortic valve, and from that position 
 extends down along the posterior walls of the sinuses of Valsalva 
 and about the orifices of the coronary arteries, and involves the aortic 
 
 ar : 
 ai 
 
 iy 
 
ILLUSTRATIVE CASES 379 
 
 valve. The process may be extensive enough to close either one or 
 the other of the arteries, and may cause sudden death. Less com- 
 monly, as in this case, an aneurism is produced and there may be 
 rupture of the aneurism with sudden death due to hemorrhage. We 
 have had cases of small and large aneurisms, but I have never seen a 
 case with the development of an aneurism at this age and of this 
 character with pressure on the trachea. We know syphilis is a 
 septicemia, because Dr. Hartwell in this laboratory has taken rabbits, 
 inoculated the testes with the blood of syphilitic patients, and later 
 has found syphilis of the testes and still later syphilis of the eyes, 
 keratitis, with recovery of the spirochetes from these lesions. That 
 establishes the septicemia beyond all question. The portal of 
 entrance of the infection isin some cases not known. For some reason 
 in cases like this one the infection is located in the first portion of the 
 aorta. Whether the spirochetes lurk in those minute vascular 
 caverns, the vasa vasorum, or whether the attack is begun on the 
 intimal side is uncertain. I am inclined to think that they locate in 
 the vasa vasorum and that the tissue reaction begins there. This 
 reaction is practically a gumma-like process ending in fibrosis. 
 This accounts for the presence in the aortic wall of the variations 
 between areas of great thickening of the coats and areas of excessive 
 thinning. That makes in the wall points of weak resistance, all of 
 which would favor the production of an aneurism. ‘This is what 
 
 _happened in this case. These areas of thickening and fibrous thin- 
 
 ning and longitudinal striation give to the aorta on its intimal aspect 
 a gristly and scar-like aspect which is peculiar to syphilitic aortitis, 
 and which no other form of sclerosis of the arteries seems to present. 
 
 Of the sudden deaths we have had in aortitis cases I think this is 
 the first one at this age associated with an aneurism. We had one 
 sudden death last year in a young man twenty-one years of age, 
 who was supposed to have been poisoned; but that was a case of 
 occlusion of the orifices of the coronary arteries. The only thing in 
 the history of that case which was important as a single factor was 
 chest pain. In this case the important thing was airhunger. You 
 may, of course, have an aortitis with hypertrophy and dilatation 
 of the heart, marked aortic regurgitation, with death probably 
 due to heart exhaustion, but those cases do not present this picture 
 of everything happening in a few minutes. 
 
 The production of the aortic regurgitation is interesting. ‘The 
 fibrosis extends down usually into the region of the contiguous 
 margins of the cusps and forms a thick band, with more or less 
 
380 FACTS ON THE HEART 
 
 extension on to the cusps themselves. This causes a narrowing of 
 the width of the cusps and a pinning back of the margins so that you 
 have more or less marked regurgitative conditions in the aortic 
 valve without any great increase in its circumference. The cusps 
 cannot come together and so form a base for the column of blood. 
 In this way you get a drop of the column of blood equal to the size 
 of the space due to the lack of closure. 
 
 I found great numbers of spirochetes in the sections of the aorta 
 in the case last year, but so far few, if any, in the sections from this 
 case. They have always interested us here, and it was in this 
 laboratory that they were first found in the wall of the aorta. In 
 some cases they are more or less numerous, but in others none 
 are found. The older the process the less likely you are to 
 find them. 
 
 A PuysictAn: Is it common for people suffering wits angina to 
 have attacks while lying perfectly still in bed? 
 
 Dr. SmitH: Such attacks are uncommon. They do occur, 
 however. Clinically one of the earliest manifestations of a beginning 
 myocardial weakness may be angina pectoris. If you examine the 
 patient you may be able to demonstrate no cardiac enlargement, 
 you may have a pulse rate of go, a soft systolic murmur, but you will 
 always find a slight tendency to dyspnea on exertion which has come 
 on in the last six months or year. Let us say you have a patient fifty 
 years of age who begins to feel dyspneic on exertion. Now you must 
 realize that that man’s heart is becoming senile, in other words, there 
 is arteriosclerosis and not sufficient blood supply to the muscle. 
 That heart has got to hypertrophy in order to enable the man to go 
 through the same exercises that he has gone through for years without 
 discomfort. Take that patient and prohibit all exercise. Put him 
 on digitalis in the appropriate amounts, not large doses but moderate 
 ones, limit his exercise and watch his heart over a period of six months, 
 and you will find increase in the left ventricle with disappearance of 
 symptoms. If you do not do that, and do not put him on digitalis, 
 but give him nitroglycerin, the next step will be that he will have more 
 frequency of dyspnea on exertion and will get into the anginoid state. 
 He will have attacks constantly. You can oftentimes relieve angina 
 by establishing hypertrophy through rest and digitalis. After 
 establishing hypertrophy I have known patients to go for years 
 never having recurrent attacks of angina and with a perfectly 
 competent heart unless forced by unusual exertion. They can do 
 it because their heart has been made a 400-500 gram heart. 
 
—~ 
 
 ILLUSTRATIVE CASES 381 
 Case LIV 
 
 A colored waiter of forty-two entered November 4, 1913, for 
 the relief of pain in the left back and chest. He had had no illnesses 
 except ‘‘grippe”’ at twenty-one. He smoked ten cigars a day and 
 drank three glasses of whiskey until two years before admission. 
 He had used practically none in two years. He had chancre five 
 years before admission. His best and usual weight was 175, his 
 present weight 15114. ‘The loss had occurred during the past year. 
 
 Two years and a half before admission he began to have inter- 
 mittent pains in the left back and flank, usually between one and 
 seven in the morning. For the past two years the pain had become 
 continuous in the left back, side and chest, never on the right. The 
 pain was not sharp, but dull, like hard pressure, and “throbbing.” 
 His throat felt obstructed. Since September 20, when he caught 
 ‘““a cold’’ which had persisted, he had been having dyspnea accom- 
 panied by wheezing on inspiration and expiration. He had no 
 palpitation. He coughed a great deal and raised considerable 
 sputum, at first green and thick, during the past week streaked with 
 blood three or four times, usually at night. 
 
 The Out-Patient Department record, November 19, 1912, notes: 
 “Tmpulse 5th space, 119 cm. outside the nipple line; right border 
 4 cm. outside the midline. Right pulse stronger than left. Lungs 
 negative except that tactile and vocal fremitus were slightly greater 
 on the right.” January 7, 1913, he had been in a hospital two weeks. 
 ‘Pain worse at discharge. Examination as above.” 
 
 Examination showed a well-nourished negro breathing with slight 
 distress and with an occasional coarse tracheal cough. The skin 
 showed dark macules over the upper back and upper legs. The 
 mucosae were slightly cyanotic. A definite pulsation was seen and 
 felt in the left second and third spaces near the sternum. By very 
 light percussion there was dullness over this area. The apex impulse 
 
 _ 9%? __Ist. space 
 3 | 7¥2_ 2nd space 
 534 1244 
 Fic. 76. 
 
 was faintly felt in the fifth space. The percussion measurements 
 are shown in Fig. 76. ‘The sounds were regular, of only fair quality. 
 A very soft systolic murmur, loudest at the apex, was faintly heard 
 
382 FACTS ON THE HEART 
 
 over the precordia, but not in the axilla or neck. No diastolic was 
 heard. The pulmonic second sound was slightly increased. The 
 pulses were unequal, otherwise normal. ‘The artery walls were plainly 
 palpable, but not tortuous. The blood pressure was, right, 150/70- 
 120/45; left, 130/80-110/50. There was tracheal tug. The chest 
 was somewhat barrel-shaped. Air did not enter the left lung as well 
 as the right. The breathing was obscured throughout by coarse 
 guttural sounds, probably from the trachea. Both inspiration and 
 expiration were prolonged, but seemed of fairly normal quality. A 
 few fine rales were heard at both bases. In the left back was an 
 area of doubtful dullness near the midscapula. The abdomen was 
 
 Fic. 77.—Aneurism of aortic arch. 
 
 held rigid. The liver dullness extended from the fifth rib to 3-cm. 
 below the costal margin, where the edge was indefinitely felt. There 
 was a Slightly thickened scar on the penis shaft. The extremities 
 and reflexes were normal. The pupils were slightly irregular, equal. 
 Their reactions were questionable. 
 
 The temperature was 98° to g9.5°, rising to 100.4° November 24. 
 The pulse was 65 to 93, the respiration normal. The urine was nor- 
 mal. The hemoglobin was 76%. There were 10,000 leucocytes, 
 84% polynuclears. The reds were normal. One Wassermann was 
 negative, two later suspicious after provocative salvarsan. X-ray 
 
ILLUSTRATIVE CASES 383 
 
 (Fig. 77) showed a large mass in the upper mediastinum continuous 
 with the aorta, more prominent posteriorly than anteriorly. No 
 definite pulsation was made out. 
 
 The patient had at times a very deep, ringing cough, raising 
 a little yellow-green sputum. When the head was tipped back the 
 trachea ‘could be seen to move to the right with each pulsation. 
 0.15 grams of neosalvarsan was given intravenously November tro. 
 November 16 the breathing over the left lung was found to be 
 distinctly less loud than over the right, but vesicular; air was 
 thought possibly to enter slowly. Hehadlesscough. November 17 
 0.3 grams of neosalvarsan was given intravenously. The next day 
 the diminished breathing all over the left lung was more marked than 
 before and a few scattered moist rales were to be heard over this side 
 of the chest. He complained of a feeling of constriction in the throat, 
 but had no pain during his entire stay. November 23 a visitor, 
 Dr. Wilder Tileston, pointed out a fine, slight pulsation in the back 
 near the spine of the scapula. The next day 0.45 grams of neosal- 
 varsan was given, and a third Wassermann was _ suspicious. 
 November 27 and 28 the cough was more troublesom2. November 29 
 the heart measurements were as shown in Fig. 78. 0.6 grams of 
 neosalvarsan was given. November 30 the patient was discharged 
 slightly relieved. 
 
 534 1114 
 r4 
 FIG 78) 
 
 Clinical Diagnosis —Aneurism of descending aorta. 
 
 Laier Notes from the Out-Patient Record.—April 9, 1914.—Systolic 
 blood pressure, right 160, left 150. Wassermann negative. 
 
 April 11.—Wheezing and shortness of breath on exertion, and 
 cramping but not agonizing pain under the left clavicle over an 
 area about 7 cm. in diameter. Is often troubled at night by similar 
 pain in left shoulder and arm, extending even to fingers. This pain 
 comes on gradually, and may last several hours. Thinks he is 
 improving. Examination: Right clavicle more prominent than left. 
 Visible bilateral subclavian pulsation, and strong epigastric pulsa- 
 tion over wide area. No pulsation or bulging in the back. Apex 
 impulse not visible but barely palpable in 6th space 11.7 cm. to left 
 
384 FACTS ON THE HEART 
 
 of mid-sternal line. Fairly loud, rough systolic murmur at apex, 
 faintly transmitted to axilla. No basal murmurs heard. Ag is 
 greater than Py. Lungs:—Back, dullness between and over scapulae 
 seems more than normal. 
 
 April 13.—X-ray. Greatest transverse diameter of arch 9.5 cm.; 
 oblique diameter of arch 9.5 cm. 
 
 July 14.—Has been working full time right along. Had a little 
 trouble at first; now has no dyspnea. Has had no pain atall! Has 
 taken no medicine. Comes for a “‘cold in the head”’ taken a week 
 ago. Causes a wheezing cough. Present weight 174. Examination: 
 Nose and throat clear, not injected: tonsils not enlarged. Vocal 
 cords seem normal. Heart as in previous record. Lungs:—Tactile 
 fremitus and voice decreased over the left back at angle of scapula. 
 
 Aug. 25.—Cough bothers. Stopped work a few days ago on 
 account of it. No pain, edema or weakness. No diastolic murmur. 
 Squeaking rales scattered in lungs, more on left. 
 
 Outcome.—Feb. 25, 1915, the patient writes, “I am glad to inform 
 you that I have been working since May 15 up to the present time. 
 The pains in chest and back are gone, and with the exception of a 
 slight weakness in the left shoulder I am feeling better than I have 
 for years.” 
 
 March 2. 1916, he writes, “‘I am glad to say I am enjoying good 
 health and have had no symptoms of past trouble, which seems to 
 have left me altogether.” 
 
 A friend adds the information that the patient says he never felt 
 better in his life, and has gained sixty pounds since he was in the 
 hospital. 
 
 Necropsy 3908 
 
 A Canadian-American housewife of twenty-five entered August 
 29, 1891. She had always been delicate, with much weakness and 
 stomach trouble. For nine months she had had debility and cough 
 with sputum; of late increasing pain and tenderness in the stomach. 
 
 Examination was negative except for pregnancy of nine months. 
 She weighed 90 pounds. The temperature was 98.6° to 1o1°, the 
 urine and sputum negative. September 11 she was discharged much 
 improved. 
 
 November 4, 1910, she returned complaining of substernal tight- 
 ness and cough following a severe “‘cold”’ of three weeks’ duration, 
 with general malaise. In a few months her weight had fallen from 
 165 to 110. 
 
 — 
 
ILLUSTRATIVE CASES 385 
 
 Examination was negative except for pyorrhea and redness of 
 the throat. | 
 
 The temperature was 96.4° to 99.3°, the pulse 113 to 73, the 
 respiration normal, the leucocyte count 10,000. No Wassermann 
 was done. ‘The urine, sputum and stools were negative. November 
 12 she was discharged. 
 
 December 7, 1918, she returned for relief of shortness of breath. 
 She now gave a history of scarlet fever and measles in childhood. 
 In 1906 she had a plastic operation on the uterus. She had had many 
 sore throats for years, but none since a second attack of diphtheria in 
 1909. For many years she had been troubled by cough with at times 
 a little tenacious sputum. She had palpitation on excitement and 
 frequent dyspnea on exertion, sometimes at night. For a year she 
 had urinated sixteen times by day and four at night, with marked 
 polyuria. Her best weight was 165, her usual and present weight 
 TIO. i 
 
 For six years she had been treated for asthmatic bronchitis 
 manifested by dry cough with dyspnea. In March, 1918, she began 
 to have attacks of acute dyspnea and ‘‘choking spasms.”” From that 
 time her breathing became more difficult. She had continual unpro- 
 ductive cough, difficulty in swallowing, and several attacks of dysp- 
 nea daily, particularly likely to occur just after eating, and lasting 
 five to twenty minutes. The ‘choking spasms” left her practically 
 unconscious from asphyxia. ‘They never occurred more than once 
 daily until the night before admission, when she had two attacks of 
 great severity. She lived in such continual dread of sudden death 
 that her nights were practically sleepless. 
 
 Examination showed a poorly developed and nourished woman. 
 The sclerae and throat were slightly injected. The thyroid was 
 enlarged. The chest was poorly developed. The superficial veins 
 were rather marked over the left chest in front. The breathing was 
 nearly all diaphragmatic, with very little chest expansion. The 
 throat and tracheal sounds were transmitted down both lungs. 
 There was stridor of maximum intensity over the substernal part of 
 the trachea. The apex impulse of the heart is not recorded. The left 
 border of dullness was 10.5 cm. to the left of midsternum, 0.5 cm. 
 outside the nipple line. The right border was 4.5 cm. to the right, 
 the substernal dullness 7 cm. and slightly increased in degree. There 
 was a soft diastolic murmur, loudest in the third left interspace next 
 to the sternum. The pulses and artery walls were normal. The 
 
 blood pressure was 120/80; right and left the same. The pupils 
 25 
 
386 FACTS ON THE HEART 
 
 were regular. They reacted very sluggishly. The right was greater 
 than the left. The abdomen, extremities and reflexes were normal. 
 The uterus and ovaries had apparently been removed. 
 
 The temperature was 97.4° to 101.6°, the pulse 89 to 155, the 
 respiration 14 to 36. The urine was normal except for a trace of 
 albumin at the second of two examinations. ‘The renal function was 
 50%. The hemoglobin was 80%. ‘There were 10,800 leucocytes, 
 
 Fic. 79.—The diaphragm is low on both sides; the respiratory movements some=- 
 what limited. General thickening of the markings throughout both chests and many 
 calcified glands at the roots, also thickening of the larger bronchi. ‘There is moderate 
 scoliosis. The heart shadow appears considerably to the left of the spine. The 
 aortic arch is prominent. There is also a dense round shadow lying in the region of or 
 behind the upper segment of the sternum, possibly a mass of mediastinal glands. The 
 heart is within normal limits. (Apparently the radiologist did not consider this 
 aneurism.) 
 
 59% polynuclears. The platelets were increased. The reds showed 
 slight variation in size, some achromia, and a rare stippled cell. A 
 Wassermann was strongly positive. The sputum showed Gram- 
 positive diplococci and long and short Gram-negative bacilli. X-ray 
 showed the shadows pictured in Fig. 79. 
 
 A throat consultant reported, ‘Paralysis of the left cord. 
 Obstruction to respiration is intrathoracic.”’ 
 
 The patient had marked respiratory distress and a typical 
 mediastinal cough. ‘There was steady falling off in the character of 
 
ILLUSTRATIVE CASES 387 
 
 the pulse. December 11 she had a period of apnea in which for a few 
 seconds she appeared to be dead. After this she coughed more and 
 became completely aphonic. The periods of cyanosis became more 
 frequent and severe. Oxygen had been used with benefit, but the 
 patient was afraid to breathe it and lost the psychological advantage 
 of it. Caffein seemed to relax the spasm. The distress was well 
 controlled by morphia. An intubation set was kept at hand, but 
 there seemed to be no one acute respiratory spasm. It was thought 
 that the pressure was too low down for intubing to do any good. It 
 was also thought any manipulation within the trachea would be 
 dangerous. December 13 the patient died. | 
 
 Clinical Diagnosis (from Hospital Record)—Cardiac weakness. 
 
 Aneurism of the aortic arch. 
 
 Dr. Richard C. Cabot’s Diagnosis —Syphilitic aortitis. 
 
 Aneurism of the arch of the aorta. 
 
 Anatomical Diagnosis.—Syphilitic aortitis. 
 
 Aneurism of the arch of the aorta with pressure on the trachea, the 
 primary bronchi and the great vessels. 
 
 Purulent bronchitis. 
 
 Bronchopneumonia, lower lobe, left lung. : 
 
 Fibrinopurulent pleuritis, left. 
 
 Congestion of the liver and kidneys. 
 
 Slight chronic pleuritis, right. 
 
 Slight chronic perisplenitis. 
 
 Dr. RicHArDsON: This case, from an anatomical standpoint, is a 
 very important one in regard to differential diagnosis. Practically 
 all the questions I think can be answered. 
 
 The heart weighed 220 grams (normally 200-300) and there was 
 nothing the matter with the valves. The coronary arteries were 
 negative. 
 
 Beginning a short distance above the cusps there was a frank 
 luetic process extending up the first portion of the aorta to the region 
 of the arch. In the region of the arch there was a definite aneurism 
 containing a thrombotic mass. ‘This sac pressed upon the trachea 
 and the left bronchus. ‘That decreased their circumferences, their 
 capacity, and in time bronchitis and bronchopneumonia developed. 
 The bronchopneumonia and the bronchitis in the main were on the 
 left side, where the greatest amount of pressure was. 
 
 In addition, and in line with the question, What did she die of? 
 On the wall of the bronchus was’a very thin area which had not quite 
 
388 FACTS ON THE HEART 
 
 broken through. If she had lived a little longer it would have been 
 broken through. 
 
 The lungs were out of the picture except for what we have said. 
 The bronchial glands were negative. 
 
 A PuysictiaAn: What were the shadows the X-ray man told about? 
 
 Dr. RicHARpDsoNn: I think they were shadows. 
 
 The circulatory apparatus elsewhere was negative. The 
 diagnosis of luetic aortitis was confirmed by microscopical examina- 
 tion, and the case is a typical one, showing irregularities of the sur- 
 face of the intima presenting as fibrous plaques varying in size, with 
 intermingling areas of depression, so that the intima of the aorta 
 looked gristly and scarred. With such a condition scattered along 
 the wall of a vessel which is under constant tension it is easy enough 
 to understand how an aneurism would arise. [ think the pressure 
 on the great vessels by the aneurismal mass was the cause for the 
 congestion of the liver and kidneys that was noted. 
 
 This brings out the point that when the luetic aortitis does not 
 extend to the aortic valve the anatomical basis for an aortic regurgi- 
 tation is not present, and regurgitation ought not to be found 
 clinically. 
 
 The kidneys were negative. 
 
 In a word, this case anatomically was a distinct and clear-cut case 
 of luetic aortitis with aneurism of the arch, pressure on the great 
 * vessels and the trachea and bronchi, no involvement of the heart at 
 all, and with freedom of the coronary arteries. From the pressure 
 resulted the bronchitis and bronchopneumonia. 
 
 A Puysictan: Why was there no pain? 
 
 Dr. RICHARDSON: That isaquestion. It may be from the peculiar 
 situation of the aneurism. It came off postero-laterally to the left 
 of the arch, and it might not in that particular place and for a time 
 have involved the nerves. The laryngeal trouble came late. 
 
 A PuysictaAn: How large was the aneurism? 
 
 Dr. RIicHARDSON: It was about 7 X 6 X 4 cm. 
 
 A PuysiciAn: Why do you think she had no chest pain when she 
 was first admitted ? 
 
 Dr. Caport: That was in 1891—a very long time ago. 
 
 A PuysictAn: Why the diastolic murmur? 
 
 Dr. Casot: I cannot explain it. Ido not believe we should have 
 heard it. 
 
 Dr. RicHARDSON: The last thing was the infection, that is, the 
 immediate cause of death was the terminal bronchitis and pneumonia. 
 
ILLUSTRATIVE CASES 389 
 
 This case is not so very unusual. I think at the same time we 
 had two other cases just like it. When the process begins out of 
 reach of the valve then the picture is entirely non-cardiac. It 
 lacks all the things that give aortic regurgitation. 
 
 Dr. CasorT: It should be noticed that although we can say that 
 this all came down to one thing—the spirocheta pallida got into that 
 person’s blood and was deposited in the arch—still when we come to 
 read the necropsy protocol what a number of things there are in it, 
 what a number of things a person dies of! That is the experience of 
 to the average post-mortem diagnosis. A complete diagnosis should 
 contain many items, and I think one should aim at getting in all 
 there is in a case. 
 
 For instance, the pneumonia was not recognized in this case, 
 perhaps could not have been. They could not have treated it, but 
 the length of life and the prognosis might have been affected by the 
 pneumonia and their knowledge of it. — 
 
 The arch of the aorta saddles the left primary bronchus. It is in 
 very much closer relation to the left primary bronchus than to the 
 right. It is for that reason that when we get pressure symptoms on 
 the lung in aneurism they are almost always on the left lung, as it was 
 here. By pressing on the bronchus the aneurism prevents the secre- 
 tions from coming out, and so we have retention of the secretions and 
 sO pneumonia. 
 
 Dr. RicHARDSON: The cutaneous vessels were notably enlarged 
 on the left and not on the right. 
 
 A PuysictAn: If this patient had had pain where would it have 
 been? 
 
 Dr. CaBor: Usually pain comes when the aneurism is pressing 
 outward toward the front with pressure upon the sternum. In the 
 rarer cases where it goes backward toward the lungs it causes pain 
 in the back radiating around the chest. 
 
 Dr. Hotmes: In the X-ray examination a more careful localiza- 
 tion of the tumor in the antero-posterior plane and an observation 
 as to whether or not the tumor pulsated would have helped consider- 
 ably in interpretation. The presence of the lateral scoliosis in the 
 upper spine produced a shadow which was confusing. 
 
 Necropsy 3656 
 
 An American police officer of forty-five entered October 8, 1915, 
 for relief of pain in the chest and dyspnea. His mother died of 
 “shock” at seventy-nine. His wife had had two miscarriages. 
 
390 FACTS ON THE HEART 
 
 One child died of “‘indigestion’’ at seven months. The patient had 
 scarlet fever at eight, typhoid fever at fourteen, gonorrhea and chancre 
 at eighteen. For years he had had belching of gas after meals and 
 constipated bowels, moving only every other day with laxatives. 
 For years he had urinated once at night. Eight months 
 before admission he had external hemorrhoids for three days. In 
 1912 he weighed 205 pounds, his best weight. His usual weight was 
 180, his present weight 172. He drank two or three glasses of whiskey 
 and smoked four or five cigarettes a day. 
 
 Four years before admission he noticed a swelling at the right 
 sterno-calvicular articulation. This gradually increased in size, 
 but gave no other symptoms for two years. Then he began to have 
 dyspnea and slight difficulty in swallowing, so that if he lay on his 
 back he became choked up. At the same time he began to have dull 
 burning pain in the region of the tumor and several daily attacks of 
 sharp boring pain lasting a few seconds, like a “red hot poker being 
 thrust through to his back,’ also radiating as a dull ache down the 
 right arm as far as the elbow. ‘The pain was worse when he lay on 
 the right side, relieved by lying on the left side and by belching gas. 
 It had been constant since the onset, but had not noticeably increased 
 
 19 
 Fic. 80. 
 in severity. The tumor had increased in size since the onset, though 
 at times he thought it got smaller. He often felt a beating over it. 
 He was told by a physician he had pleurisy. Seven months ago he 
 caught “‘grippe”’ and became “‘all choked up” and dyspneic. The 
 chest pain was worse. His doctor now said that he had rheumatism. 
 Examination showed a well-nourished man with tracheal tug. 
 There were dilated venules over the lower margin of the thorax in 
 front. The apex impulse of the heart was in the sixth space 13 cm. 
 to the left of midsternum, 1 cm. outside the nipple line. In the left 
 lateral position the apex shifted 6 cm. The right border of dull- 
 ness was 6 cm. to the right. The substernal dullness was 17 cm. at | 
 the second rib, rr cm. to the right, 6 cm. to the left. (See Fig. 80.) 
 X-ray showed the measurements as in Fig. 81. The sounds were of 
 fair quality. There was an occasional premature beat. The aortic 
 second sound was accentuated and palpable. At the apex in the 
 
ILLUSTRATIVE CASES 301 
 
 left lateral position was heard a blowing systolic and a long, harsh 
 high-pitched diastolic. There was a systolic at the aortic area, not 
 loud, transmitted upward, with a short diastolic blow. There was a 
 rough low-pitched systolic over the pulsating tumor. The blood 
 pressure was 140/80 left, 120/80 right. The tumor and lung signs 
 
 Fic. 81.—Seven-foot plate showing heart shadow below and aneurismal sac above. 
 Syphilitic aortitis with aneurism filling the mediastinum, compressing esophagus, 
 trachea, and bronchi. 
 
 were as Shown in Fig. 82. There were many dilated venules over the 
 shins. The abdomen, pupils and reflexes were normal. 
 
 The temperature was 96.4° to 99.3°, the pulse 66 to 102, the 
 respiration normal. The output of urine was 32 to 70 ounces, the 
 specific gravity 1.012 to 1.020. There was a slight trace of albumin 
 
 Pulsation visible andi 
 palpable 
 
 Tumor, elevated 223 a 
 
 Za ksi a aN 
 DISS T 
 ON \ 
 
 li ow EW 
 
 ened respiratory sounds 
 
 Slightly dull, with sharp- 
 and increased fremitus 
 
 MiGaas2e 
 
 at one of three examinations. The hemoglobin was 80%. There 
 were 12,800 to 7600 leucocytes, 79% polynuclears. A Wassermann 
 was strongly positive. A throat consultant reported, “Slight chronic 
 laryngitis. The vocal cords have normal excursion in phonation and 
 respiration.”” A syphilis consultant reported, “Salvarsan is a dan- 
 
392 FACTS ON THE HEART 
 
 gerous drug for this man. I should use potassium iodid in preference 
 at first. If that does no good I think it proper to give salvarsan in 
 repeated very small doses, not over o.1 gram.”’ 
 
 The patient was given antisyphilitic treatment. His condition 
 was explained to him. He was discharged unrelieved October 19 
 with the understanding that he would get very light occupation. 
 
 The South Medical (Syphilis) Out-Patient Department record 
 notes November 15 that the patient was doing desk work and was 
 very much better. December 21 he reported that he had entered 
 strenuous duty again and was having pain in the nght chest. Febru- 
 ary 15 he was again at desk work, but was having dyspnea and increas- 
 ing pain of greater frequency and longer duration. 
 
 A year later, November 13, 1916, he reported that he felt almost 
 well, gained weight, and was able to do his work until July, when his 
 wife was in the hospital ten days with her third miscarriage. During 
 her absence he worked strenuously to keep up both home and office 
 duties. As a result he had a “breakdown” and had not felt well 
 since. One night in August he fell asleep in a chair near an open 
 window and awoke a few hours later covered with “cold perspira- 
 tion.’ Since that time he had had cough with a little sputum, a 
 choking sensation due to the mucus which he could not raise, hoarse- 
 ness, wheeziness, and increasing dyspnea, orthopnea, edema, palpita- 
 tion and insomnia. Since August he had had frequency with 
 incontinence every two hours day and night. 
 
 Examination showed him only fairly well nourished. He spoke 
 only in a hoarse whisper. ‘The mucous membranes and hands were 
 cyanotic, especially the left hand, which was colder than the right. 
 No tracheal tug was felt. The heart measurements by percussion 
 were practically as before except that the right border was 7 cm. to 
 the right. At the apex the sounds were regular, somewhat rapid, not 
 forceful, and there was a low systolic murmur. In the aortic area 
 was a faint systolic roll followed by an impure second sound. The 
 pulmonic second sound was not heard. A faint systolic was heard 
 along the right sternal border. The pulses were of poor volume and 
 tension, not Corrigan or pistol-shot. The radials were not felt. The 
 blood pressure was 115/80. The lung signs were as shown in Fig. 83. 
 There was dullness at the right isthmus in front. 
 
 The temperature was 97.2° to 98.8°, the pulse 81 to 100, the res- 
 piration 31 to 17. The amount of urine was normal when recorded. 
 The urine was cloudy at one of two examinations. The. specific 
 gravity was 1.000 to 1.o1c. There was a very slight trace of albumin 
 
™ 
 
 ILLUSTRATIVE CASES 393 
 
 at one of two examinations. The hemoglobin was 80%. There. 
 were 10,400 to 10,600 leucocytes, 71% polynuclears. A Wassermann 
 was moderately positive. X-ray showed a large area of diminished 
 radiance in the region of the great vessels, more to the right than to 
 the left. The heart shadow was enlarged and lay horizontally in 
 the chest. 
 
 The night of November 14 the patient was very restless and com- 
 plained of difficulty in getting his breath. Next morning he was 
 more cyanotic. During the ward rounds he suddenly became very 
 cyanotic, with labored breathing, and soon afterward became 
 unconscious. He remained in this condition until his death at 
 midnight. 
 
 Inspiration loud, rough} 
 accompanied by squeaks 
 and groans. Expiration 
 quiet and prolonged. 
 
 Clinical Diagnosis (from Hospital Record).—Tertiary lues. 
 
 Aneurism of the aortic arch. 
 
 Cardiac failure. 
 
 Dr. William H. Smith’s Diagnosis.—Syphilitic aortitis. 
 
 Aneurism. - 
 
 Anatomical Diagnosis.—Syphilitic aortitis. 
 
 Aneurism of the arch of the aorta with pressure on the neighboring 
 structures. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the liver, spleen, stomach, kidneys, 
 and intestines. 
 
 Focal necrosis of the pancreas with hemorrhage. 
 
 Emphysema of the lungs. 
 
 Chronic pleuritis. 
 
 Slight chronic perihepatitis, and splenitis. 
 
 Dr. RicHARDSON: There was a large aneurism given off at the 
 arch of the aorta filling the mediastinum, pressing slightly on the 
 esophagus and markedly on the trachea, the bronchi, and the great 
 vessels running to and from the heart. The chronic passive conges- 
 tion mentioned in the anatomical diagnosis was largely due to the 
 pressure inside the chest from the aneurismal sac. The coronary 
 arteries were out of the picture, the aneurism springing from the 
 
394 FACTS ON THE HEART 
 
 arch, although the first portion of the arch showed lesions many of 
 which were syphilitic in appearance. 
 
 The kidneys showed some acute degeneration of the tubular 
 epithelium, but were otherwise negative. 
 
 The microscopic appearances of the aortic wall and the region of 
 the aneurism were those of syphilitic aortitis. The case anatomically 
 was clear and formed a basis for the clinical picture. 
 
 Dr. SmiTH: There was not much regurgitation through the aortic 
 valve, was there? 
 
 Dr. RicHARDSON: None. The heart was moderately hyper- 
 trophied; the dilatation was the predominant characteristic. It is 
 very common, of course, in syphilitic aortitis to have the orifices 
 of the coronary arteries encroached upon. In this particular case, 
 however, although the syphilitic lesions in the aorta extended along 
 the first portion, they did not extend around the coronary orifices 
 so as to produce any effect on the arteries. They were free, fairly 
 capacious, and showed a moderate amount of fibrous sclerosis. The 
 whole picture was due to marked pressure of the aneurismal sac on 
 the great structures in the chest, trachea, bronchi, and the great 
 vessels to and from the heart. 
 
 Dr. Situ: Dr. Richardson’s discussion brings out the point I 
 mentioned, that angina pectoris may be due to a stretching of the 
 aortic plexus, in view of the fact that here the coronary arteries 
 were not involved. 
 
 Necropsy 4388 
 
 An Irish laborer of fifty-three entered August 11, 1922, complain- 
 ing of cough and pain in the back and chest. He had measles, 
 chickenpox, whooping cough in childhood, and malaria for two winters 
 in Georgia. He once had ‘‘rheumatism” for a year and a half— 
 swelling, lameness and redness of the knees and hands, with no fever. 
 Six years before admission he had a violent cough like the present 
 one lasting two months. In the Philippines he had dhobie itch— 
 white blisters around the genitals and armpits. His wife had one 
 miscarriage after the birth of two healthy children. For four years 
 his left eye had been more prominent than the right and the pupil 
 larger. His bowels required physic often. He took two or three 
 glasses of whiskey on Saturday nights. 
 
 Six months before admission he began to have spasms of violent 
 dry cough for five to twenty-four hours, each attack leaving him feel- 
 ing short of breath and stifled. For five months he had had dyspnea. 
 
ILLUSTRATIVE CASES 395 
 
 He was more comfortable lying on the left side, but if he lay on it too 
 long he had pain from his left shoulder to his ear. He thought he 
 had had a swelling off and on in the left side of the neck for four 
 months, and thought it was associated with the pain. Four months 
 ago he lost consciousness in church for about five minutes. Three 
 months ago the attacks of cough became more frequent, and he began 
 to raise a good deal of watery frothy sputum. For three months he 
 had had pain under thesternum and in the back between the shoulders. 
 Sometimes, for instance when he moved quickly, it was like a knife 
 stabbing from front to back. If he lay still fifteen or twenty minutes 
 he had dull pain under the sternum and in the back. When he kept 
 moving he did not notice this. ‘Twomonthsago he began to be hoarse, 
 and the cough became wheezing. Twice he lost his voice altogether 
 for half an hour, and at the same time lost power in his right hand, 
 with complete recovery. A week ago he coughed up half a teaspoon- 
 ful of bright blood. He now slept very little. At admission he could 
 climb a flight of stairs only with difficulty. His best weight was 180 
 pounds, ten years ago. For five months he had been losing weight, 
 in all thirty-five pounds. His present weight was 140. 
 
 Examination showed a well nourished man with suffused cyanotic 
 face and neck. The external jugulars were distended. The teeth 
 were very carious, several missing. ‘There was marked pyorrhea. 
 The apex impulse of the heart was not seen or felt. The sounds 
 were not heard. ‘The supracardiac dullness was g.5 cm., the right 
 border 6 cm., the left border 1014 cm., the midclavicular line 11 cm. 
 The left pulse was not felt. The blood pressure in the right arm was 
 128/60, in the left arm 65/55. There was questionable tracheal tug, 
 palpable episternal pulsation. The lungs were clear except for 
 questionable dullness at the right isthmus. Palpation of the abdo- 
 men was rendered unsatisfactory by what appeared to be voluntary 
 spasm. The left pupil was greater than the mght. Both were 
 regular. ‘Their reactions and the other reflexes were normal. 
 
 The temperature was 98.8° to 101.5°, the pulse 112 to 88, the 
 respirations not remarkable. The output of urine was 38 ounces 
 when recorded, the specific gravity 1.018. The urine was cloudy and 
 alkaline at the single examination. ‘There were three to four leuco- 
 cytes to a high power field. The hemoglobin was 70%, the leuco- 
 cytes 39,300 to 12,300, the polynuclears 80 to 64%, the reds 5,220,000; 
 slight achromia August 11, reds normal August 12. No Wassermann 
 ‘was done. The stools were strongly positive to guaiac August 12. 
 X-ray August 14 showed a large fusiform shadow in the upper and 
 
306 FACTS ON THE HEART 
 
 medial portions of the chest obliterating the posterior mediastinal 
 space. (See Fig. 84.) No pulsation was visible in the shadow. 
 
 The day after admission the right apex was dull, possibly the left 
 apex also. The breath sounds at the apices were almost amphoric, 
 more so on the right. 
 
 At five o’clock the evening of August 13 the patient suddenly 
 fainted, became very pale and pulseless, and broke into a profuse cold 
 sweat. He regained consciousness in a few minutes, although he 
 remained pulseless, pale and very weak. He coughed up about an 
 
 Fic. 84.—Necropsy 4388. Aneurism of the aorta. Syphilitic aortitis. A large 
 fusiform shadow occupies the medial and upper portions of the chest, its borders curved 
 and sharply defined. It is about the size of the heart shadow and extends from above 
 the sternal notch down over the upper portion of the aortic arch. The shadow T, 
 T on the right may very well be a much displaced trachea. The left lung is held up by 
 adhesions. Its diminished radiability is no doubt due to limitation of the diaphragm 
 excursion. (Roentgenological Department, Massachusetts General Hospital.) 
 
 ounce of bright frothy blood, and a few minutes later had a stool 
 that was mostly fecal material mixed with bright blood. He remained 
 conscious for about an hour, then went into coma which continued 
 to his death at four o’clock the next morning. 
 
 Clinical Diagnosis.—Aneurism of the aorta. 
 
 Dr. Richard C. Cabot’s Diagnosis —Aneurism of the aorta, with 
 rupture. . , 
 
 Anatomical Diagnosis ——Aneurism of the aorta with rupture into. 
 the esophagus. 
 
ILLUSTRATIVE CASES 3907 
 
 Luetic aortitis. 
 
 Hemorrhage into the gastrointestinal tract. 
 
 Anemia. 
 
 Soft spleen. 
 
 Chronic pleuritis, left. 
 
 Chronic perisplenitis. 
 
 Slightly defective closure of the foramen ovale. 
 
 Dr. Oscar RICHARDSON: We were not permitted to examine the 
 head. The skin and mucous membranes were very pale. The peri- 
 toneal cavity and appendix were out of the picture. The glands were 
 negative. There was no fluid in the pleural cavities, and no adhe- 
 sions on the right, but many on the left. There was a little blood and 
 blood clot in the trachea and bronchi; they were otherwise out of the 
 picture except for a point to be mentioned later. 
 
 The pericardium was negative. The heart weighed 333 grams. 
 It was a good looking heart, with good valves, a little dilatation on 
 the right, but otherwise out of the picture. , 
 
 The liver, gall-bladder, bile ducts, pancreas, duct of Wirsung, 
 and the spleen, the adrenals, kidneys and genito-urinary apparatus 
 were out of the picture, except that the spleen was a little soft. 
 
 The esophagus contained a small amount of bloody fluid and 
 presented an opening in its wall which we shall speak about in a 
 moment. The stomach contained a blood clot weighing 1260 grams 
 —that is nearly as large as a liver—and besides that 200 c.c. of bloody 
 fluid. The mucosa and the pylorus were frankly negative. The 
 intestines contained a large amount of fluid blood and many blood 
 clots, but their walls were negative. 
 
 The only thing left is the aorta. The aorta showed an aneurism 
 and this aneurism was luetic in its nature. The luetic process began 
 above the aortic valve and the coronary orifices were free, so the 
 heart was out of the picture anatomically. But from that point up 
 there was syphilitic aortitis, and in the situation of the arch there 
 was a large sac, nine cm. in diameter,—a frank aneurism. This of 
 course contained the usual concentric layers of thrombotic material, 
 and on the posterior wall where it was against the anterior surface 
 of the vertebra the wall was very thin and there was erosion of the 
 surfaces of the vertebrae. On the left lateral aspect the wall of the 
 aneurism was adherent to the apex of the lung on its mesial aspect. 
 We note however that there was nothing the matter with the lungs; 
 the apices were negative. This aneurism had pushed the trachea 
 away over to the right but had perforated, not the trachea, but the 
 
398 FACTS ON THE HEART 
 
 esophagus. So the death was due to hemorrhage from rupture of the 
 aneurism through the wall of the esophagus, and the man bled to 
 death into his stomach. 
 
 Dr. Casot: Isn’t that in your experience an unusual way? 
 
 Dr. RicHarpson: Yes, it is very unusual. Somewhere recently I 
 saw an article reporting such a case because the writer thought per- 
 foration of the esophagus was so rare. 
 
 Dr. Casor: Looking at the X-ray in connection with your report 
 of the adhesions, would those match up with the appearances at the 
 left base? 
 
 Dr. RicHARDSON: It might be. The left lung was bound down 
 by adhesions of years, on the right none. 
 
 Dr. Casot: When we know a fact like these adhesions on the left 
 it is always good to go back to the X-ray to see if there is any more 
 density of the left lung, any less radiance on the left than in the 
 right. Dr. Richardson has just told us there are adhesions all 
 through the left chest. 
 
 Dr. MEAns: I do not think I should be willing to say that the 
 plate is abnormal. 
 
 Dr. Capsot: No; but there is a question whether the chest does 
 not look on the whole a little less radiant on the left and is not on the 
 whole a little smaller. 
 
 Dr. MEAns: The diaphragm is higher. 
 
 Dr. Casot: It seems as if the rays went through more easily on 
 the right. Of course, I am not pretending that I made the diagnosis 
 before I knew the adhesions were there. 
 
 Dr. RICHARDSON: This aneurism instead of going laterally in its 
 main trend went directly back against the vertebra; the picture shows 
 that. 
 
 Dr. Cazot: Yes, it is right in the middle. 
 
 Dr. Means: We have another man in the wards who has a 
 trachea pushed to one side, who has amphoric breathing, breathing 
 that would make one think of a cavity. But there was no cavity. 
 { think that where there is tracheal stenosis we get extraordinary 
 breathing of all kinds. 
 
 A PuysicIAn: How big was the opening? 
 
 Dr. RicHARDSON: The area of perforation was three cm. above 
 the bifurcation of the trachea and measured three by two cm. 
 
 Dr. Caspot: With even a large eroded area outside, a bulge on 
 the chest as large as one’s fist, the probability is that it will erode 
 through some internal structure before it does through the skin. 
 
ILLUSTRATIVE CASES 399 
 
 I think that is a very important fact. If we can say to the friends 
 especially, and perhaps to the patient himself if he is the right type, 
 “You won’t have this terrible tragedy of an external rupture,” I 
 think that is of some reassurance. I cannot remember ever having 
 seen an aneurism which ruptured externally, and I have seen cases 
 where the skin looked like paper, where one was afraid to touch it. 
 
 A PuysiciAn: I had an instructor once who said he had seen one 
 rupture on the outside. That is the only one I ever heard of. 
 
 A PuysiciAn: I cannot understand why he lived so long if he had 
 that opening into the gullet. 
 
 Dr. RicHARDsoN: The pressure around the opening did not allow 
 the blood to run out very fast. 
 
 Dr. Casot: Also, the bleeding lowered his blood pressure so 
 much that the heart did not pump out more blood. 
 
 Note by Dr. A. S. Merrill.—In Fig. 84 the left diaphragm is held 
 up, evidently by the adhesions. The left lung is a little less radiable 
 than the right, no doubt because of diminished expansion due to the 
 limitation of the diaphragm excursion, not because of the condition 
 of the lung itself. 
 
 The shadow T, T on the right may very well be a much displaced 
 trachea. 
 
 Necropsy 1280 
 
 An Insh iron worker of forty-three entered November 25, 1904. 
 His past history was negative except for measles in childhood and 
 erysipelas at twenty-one. He drank one to two dozen bottles of ale 
 a week and an occasional glass of whiskey. 
 
 Two months and a half before admission he began to have sharp 
 pain in the right breast, constant, worse at times, and increased by 
 exertion. .Once it was so severe that he almost fainted. It extended 
 
 . across the breast and sometimes down the left arm. He had a good 
 
 deal of dyspnea and some palpitation. For four weeks he had had 
 some cough, especially in the morning, and considerable yellow spu- 
 tum. He had occasional headache and rare nosebleed. His appetite 
 was poor. He had distress and gas after meals. Sometimes his 
 bowels were constipated. He sometimes urinated three or four times 
 at night, but usually after drinking the evening before. Except for 
 advice he would have gone to work instead of coming to the hospital. 
 
 Examination showed a well nourished man. The mucous mem- 
 branes were cyanotic, the conjunctivae slightly injected, the throat 
 reddened. The apex impulse of the heart was in the sixth space 
 
400 FACTS ON THE HEART 
 
 seven inches to the left of the median line. The borders of dullness 
 were 814 inches to the left, 114 inches to the right of the median line. 
 The action was regular, the sounds of fair quality, the pulmonic 
 second sound accentuated. Systolic and presystolic murmurs were 
 heard at the apex, the systolic transmitted into the left axilla, nearly 
 replacing the first sound. A harsh systolic murmur, loudest in the 
 pulmonic area, was transmitted into the neck. There was a dias- 
 tolic murmur, loudest at the fourth left interspace, heard over the 
 precordia. (See Fig. 85.) There was marked tenderness in the 
 fourth left interspace near the sternum. The pulse was Corrigan. 
 The artery walls were palpable. There was a suggestion of capillary 
 pulse in the lips. The lungs showed dullness, diminished breath 
 sounds and numerous fine moist rales below the angle of the 
 scapula in the right back and two inches below the angle of the 
 : scapula on the left. The fremitus was slightly 
 diminished on the right. The expiration was 
 somewhat prolonged throughout both backs. 
 The liver dullness extended from the sixth 
 rib to the costal margin. The edge was felt. 
 ee Eee eee There were a few medium sized glands in the 
 ee aT ee groins and axillae. There was very slight 
 edema of theankles. The pupilsand plantars 
 
 were normal, the knee-jerks slight. 
 
 The temperature at entrance was 99.6°, afterwards normal, the 
 pulse 105 to 92, the respirations 28 to 21. The output of urine was 
 22 to 111 ounces, neutral, specific gravity, 1.025, the slightest possible 
 trace of albumin, no sugar, rare hyalin and finely granular casts, 
 occasional blood corpuscles. The hemoglobin was 95%, the leuco- 
 cyte count 16,200. 
 
 The patient was very comfortable except for a dry harsh cough 
 which distressed him a good deal, especially at night. He also had 
 thoracic pain. The heart’s action was good. Fluoroscopic examina- 
 tion of the chest failed to disclose any enlargement of the aorta. A 
 throat consultant found no paralysis of the cords or signs of obstruc- 
 tion in the trachea, but the bifurcation was not seen. November 30 
 another X-ray examination showed increase of the shadow in the posi- 
 tion of the thoracic aorta with a pulsating shadow just above and to 
 the left of the heart. 
 
 The morning of December 1 while he was dressing the patient 
 fell to the floor in a slight convulsion, became very pale, and m a few 
 moments died. ‘There was no marked cyanosis. 
 
ILLUSTRATIVE CASES 401 
 
 Clinical Diagnosis (from Hospital Record).—Acute cardiac dila- 
 tation. 
 
 Coronary obstruction. 
 
 Thoracic aneurism with relative aortic and mitral regurgitation. 
 
 Dr Richard C. Cabot’s Diagnosis.—Syphilitic aortitis with aortic 
 regurgitation, and blocking of the coronary arteries. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis.—Aneurism of the ascending portion of the 
 aorta with rupture into the pericardium. 
 
 Syphilitic aortitis. 
 
 Arteriosclerosis of the aorta. 
 
 Anthracosis of the lungs. 
 
 Dr. RicHarpson: This case occurred before the man who made 
 the post-mortem knew definitely that he was presented with syphi- 
 litic aortitis. In going back over it years afterwards I find that the 
 case was syphilitic aortitis. The death was due to a ruptured aneu- 
 rism of the aorta. 
 
 The peritoneal cavity, including the liver, spleen, kidneys, etc., 
 was out of the picture. There was some congestion of the kidneys. 
 
 The heart was not especially hypertrophied. The reason is 
 apparent when we see that the main lesion was an aneurism. The 
 amount of sclerosis in the aorta was slight, not sufficient to produce 
 much hypertrophy and dilatation. There was slight fibrosis of the 
 aortic cusps. Just above the aortic cusps was a frank aneurism which 
 had ruptured into the pericardium. The aneurism, as stated in my 
 record, was somewhere between the size of a hen’s egg and a goose 
 egg. 
 
 We made the diagnosis here in after years from the description 
 written at the time, which shows good work on the part of the man 
 who did it. It is perfectly apparent from the gross description, 
 whether we have the microscopic or not, that we are dealing with an 
 aneurism of the aorta in that particular spot where syphilitic aortitis 
 is usually located. Aneurism itself produces no definite hypertrophy 
 and dilatation of the heart, but syphilitic aortitis may extend down and 
 involve the aortic cusps and produce aortic regurgitation. The cusps 
 were slightly affected in this case. 
 
 Another point of interest in this case is arteriosclerosis. At 
 forty-three there is usually some arteriosclerosis, and we cannot 
 always dissociate aortitis and arteriosclerosis even after death. 
 
 But the aortitis was well marked, and farther down in the aorta 
 26 
 
402 FACTS ON THE HEART 
 
 there was some typical arteriosclerosis, but not in any great 
 amount. 
 
 This man was an iron worker, and he had what is anatomically 
 called anthracosis of the lungs. There was increase of interstitial 
 tissue, and there was no tuberculosis. The other day we had a very 
 marked case of pneumoconiosis in which again we were unable to 
 find any evidence of tuberculosis. All of which goes to show that there 
 is some argument for the group of men who feel that excessive irri- 
 tation from dusts of various sorts can produce chronic pneumonitis 
 without the aid of tuberculosis. 
 
 Dr. Casot: This was all coal dust, no iron or stone in it? 
 
 Dr. RicHARDSON: There would probably be a mixture. The 
 lungs generally were blackish in color. The posterior and inferior 
 lobes showed sulcus-like furrows more or less outlining the lobules 
 at the pleural surface. This was most marked in the inferior lobe of 
 the right lung. These portions of the lung were tough and leathery 
 to the touch. What better description do we want of chronic pneu- 
 monitis? On section the lung tissue generally showed an excessive 
 amount of blackish pigmentation. In the posterior portions of the 
 inferior lobes the lung tissue on section was tough and showed ill 
 defined streaks and areas of a homogeneous smooth somewhat 
 shining opaque black appearance, the typical picture of anthra- 
 cosis, and extensive enough so that it was perfectly apparent 
 macroscopically. 
 
 Dr. Casot: We got the main points in this case right, and I think 
 if I had not switched off we should have put in the aneurism. [I for- 
 got about the question of aneurism. Butit seems to me that second 
 X-ray report, if we made the diagnosis of syphilis, as we did, should 
 naturally be taken as aneurism. In the present series we find that 
 every aneurismal tumor is syphilitic. There is only one cause. So 
 if we can made a diagnosis of aneurism we have to make a diagnosis 
 of syphilis. We do not confuse that with the compensatory harmless 
 aortic enlargement which comes on in arteriosclerosis. But aneu- 
 rism as such, a definite pocket-like dilatation, means syphilis and 
 nothing else. We have had no cases of any other type, and I have 
 seen no competent account of any other type. 
 
 The other point is the one that Dr. Richardson brought out in 
 the condition of the lungs. In Barre, Vermont, where there is a 
 great deal of granite cutting, careful study has been made in recent 
 years of this question of stone dust in the lungs,—not coal dust. I 
 think, on the basis of what they have done there, and what we have 
 
 ie. 
 
bs) 
 
 i. 
 
 ILLUSTRATIVE CASES 403 
 
 seen here, studying it partly with the stimulus of their interest, that 
 the question is clearly settled now. We can perfectly well have 
 anthracosis without tuberculosis, and pneumoconiosis, the more 
 general word for dust in the lung, without tuberculosis. We had 
 here a very marked case in which the man died from the results of his 
 stone-cutter’s lung disease with no other important trouble. Mr. 
 Frederick L. Hoffman, a statistician formerly with the Metropolitan 
 Life Insurance Company, who studied the disease from a statistical 
 point of view at Barre, gave me the other day a very interesting piece 
 of information which has also been published. He went at the ques- 
 tion of tuberculosis or non-tuberculosis in these stone-cutters who 
 died of lung trouble in a very interesting way. We believe of course 
 that tuberculosis is contagious. If then we had a lot of men dying 
 of tuberculosis, we should have a lot of evidence that their wives and 
 families also caught tuberculosis. He went through at great length 
 the cases of stone-cutters who had died of lung trouble, to find out 
 
 ‘what the wives died of, and he found no evidence that the wives died 
 
 of tuberculosis any more than anybody else’s wives. That was a 
 very important piece of evidence, covering a great number of cases. 
 And he is very definite in his belief that stone-cutters’ lung is not 
 tuberculosis. 
 
 This last case shows the effects, which I did not realize at all, of 
 another dust, coal dust. Coal dust, so far as I know, does not ever 
 bring about death, and Dr. Richardson did not suggest in any way 
 that the injury to this man’s lungs from the coal dust shortened his 
 life. It is a pneumonitis with interstitial increase. But so far as 
 we can see it did the patient no harm. That is the rule. Coal- 
 miners seem to have tuberculosis less than other people. Perhaps 
 they get injury from the dust, but it is not proved. On the other 
 hand people who get steel into their lungs, from scissor grinding and 
 quartz from granite cutting, certainly do often die of the effects of 
 this dust in the lung. Do you remember any other cases in which 
 anthracosis caused a real pneumonitis? 
 
 Dr. RicHarDson: Ido not remember. They are not very many. 
 We had some in which we found what we believed to be tuberculosis. 
 
 Dr. Cabot: This is a debated question. I am on the side of 
 those who believe that pneumoconiosis is not tuberculosis though 
 it may be complicated in the end by tuberculosis. 
 
 A PuysiciaAn: I wonder if the dust is protective in some way. 
 
 Dr. CaBor: That is what has been often claimed about coal-dust, 
 that if there were a few tubercle bacilli in the lung they were sealed 
 
404 FACTS ON THE HEART 
 
 in by this connective tissue reaction to the coal dust, so that they 
 became harmless. | 
 Necropsy 4539 
 
 A Swedish engineer of thirty-nine entered June 11, 1923. No 
 past history was obtained except a positive one of luetic infection. 
 The history of the present illness was given in part by the patient’s 
 physician. A year and a half before admission the patient first 
 complained of precordial pain radiating into his back with very slight 
 dyspnea. He went to the South in the winter for two years. He 
 felt much more comfortable when warm, and even slept in the fur- 
 nace room when working in New Hampshire. He had two stays ina 
 hospital in Boston, one in 1922, another in 1923, about two months 
 each time. A year before admission his left side became suddenly 
 paralyzed. This wore off gradually in three months. About the 
 same time he began to have pain under the upper sternum, slightly 
 
 more on the right, not throbbing but steady, sharp and fairly severe, 
 
 coming in attacks lasting two hours or so, induced by lifting, exertion 
 
 Prolonged high- 
 pitched sonorous 
 inspiration and 
 expiration. 
 
 Ines 6. 
 
 and excitement. The attacks ofthis pain continued until eight or nine 
 months ago, when he began to have thumping pain under the upper 
 sternum. For three months he had not been able to walk across the 
 floor because of dyspnea. He also had severe pain over the precordia, 
 brassy cough, and hoarseness. During the past two months he had 
 had difficulty in breathing and swallowing. 
 
 Examination showed a fairly well developed and nourished man 
 with a very distressed expression, breathing with slow stertorous 
 inspirations and expirations. The face had a reddish cyanotic tinge. 
 The skin was moist; during periods of extreme respiratory difficulty 
 it was dripping with perspiraton. The cervical, epitrochlear, axil- 
 lary and inguinal glands were slightly enlarged. The throat was 
 slightly reddened. There was definite tracheal tug. The chest 
 expansion was slightly greater on the left. The lung signs were as 
 shown in Fig. 86. The apex impulse of the heart was in the fifth 
 space 10 cm. to the left, 1 cm. outside the midclavicular line. The 
 
 > 
 
 , = 
 
' ILLUSTRATIVE CASES 405 
 
 right border of dullness was 4.5 cm., the supraclavicular dullness 13.5 
 cm. The sounds and action were normal. There was a very soft 
 short systolic murmur heard to the right of the sternum in the first 
 interspace. No thrill was felt, although there was a palpable pulsa- 
 tion in the first and second right and left interspaces and above 
 the left clavicle. The pulses were somewhat prolonged in tension. 
 There was slight sclerosis of the radials, temporals and brachials. 
 The blood pressure was 135/85. The liver was palpable, the tip 
 of the spleen barely palpable. Both external inguinal rings 
 admitted the tip of the little finger. There was a small depressed 
 penile scar. The shins were slightly roughened. The pupils and 
 reflexes were normal. 
 
 The temperature was 98.1° to 100°, the pulse 80 to 127, the res- 
 pirations g to 29. The urine was normal in amount, the specific 
 gravity 1.022. There was a slight trace of albumin at the single 
 examination, a very slight trace of bile and leucocytes. The hemo- 
 globin was 70% to 85%, the leucocytes 16,000 to 24,000, the poly- 
 nuclears 80%, the reds and platelets normal. A Wassermann was 
 moderately positive. The non-protein nitrogen was 37.5 mgm. 
 
 The patient complained of very severe pain running through the 
 upper chest and particularly localized in the back in the region of the 
 third and fifth thoracic vertebrae. His respiratory distress was 
 constant and alleviated only by frequent doses of codeia. It was 
 thought that the general problem was to keep him comfortable, there- 
 fore antiluetic therapy was not pushed. Late in the afternoon June 
 13 the character of the heart sounds-was poor. In the early evening 
 he lapsed into unconsciousness. The blood pressure dropped and the 
 heart sounds became more rapid and forcible. That evening he died. 
 
 Clinical Diagnosis (from Hospital Record).—Late syphilis. 
 
 Aortic aneurism. 
 
 Syphilitic heart disease. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Syphilitic aortitis. 
 
 Aneurism of the aortic arch with compression of the trachea and 
 possibly erosion of the vertebrae. 
 
 General arteriosclerosis. 
 
 Anatomical Diagnosis.—Luetic aortitis. 
 
 Aneurisms of the arch of the aorta with pressure on ihe trachea, 
 bronchi, and the great vessels running to and from the heart, with 
 extensive erosion of the thoracic vertebrae. 
 
 Slight hemorrhage into the periesophageal tissues. 
 
 Gumma or old infarct of lung. 
 
406 FACTS ON THE HEART 
 
 Congestion of the liver, spleen and kidneys. 
 
 Chronic pleuritis. 
 
 Dr. RICHARDSON: The examination of the brain was negative. 
 
 _ The pleural cavities showed only a few c.c. of thin pale clear fluid. 
 There were only a few old pleural adhesions on the left. In the region 
 of the lower part of the trachea an aneurism, to be described later, 
 pressed upon the left lateral wall, bulging it inward rather markedly, 
 with considerable decrease of its lumen. The pressure of the aneu- 
 rism shut off to a great extent the left primary bronchus. The right 
 primary bronchus was not definitely pressed upon. There was a 
 small collection of reddish semi-fluid mucous material in the region 
 of the distal end of the left primary bronchus andits branches. The 
 bronchial glands were negative. 
 
 The tissue of the right lung was generally spongy pale red and 
 yielded a small amount of reddish frothy fluid. In the region of the 
 apex of the left lung the aneurism was bound by old adhesions to the 
 upper lobe. The tissue of the upper lobe was dark reddish, a little 
 leathery, and yielded a small amount of dark reddish fluid. The 
 tissue of the lower lobe was pale red, a little leathery, and yielded 
 a small amount of thin reddish frothy fluid. In the region of the 
 upper part of the lower lobe just beneath the pleura there was a 
 rather discrete mass about 3 cm. by 2 cm. On section it showed 
 dirty brownish boggy to resistant tissue, a little disintegrated in its 
 central portions. Along the region of the lower margin of this lobe 
 there was a round firm rim about 9 cm. long and 7 mm. across. Its 
 sections showed tissue like that in the mass just mentioned. The 
 question that arises of course is whether it wasa syphilitic lesion or not. 
 Further examination of the tissue under the microscope showed 
 necrotic material in the midst of chronic inflammatory tissue, but 
 there was no good evidence of plasma cells or lymphocytic infiltra- 
 tion. Altogether the process suggested a syphilitic one, but we 
 were not able definitely to state that it was. 
 
 The heart weighed 321 grams. The myocardium, valves and 
 cavities were negative. The coronary arteries were free and negative. 
 The circumference of the aorta in the region of the sinus was 10 cm., 
 in the region of the junction of the ascending thoracic and the arch 
 1114 cm. The ascending thoracic showed only a few slight areas of 
 fibrous sclerosis in its first portion, but beginning at a point about 5 
 cm. above the aortic cusps, the ascending thoracic all along up to the 
 arch showed much fibrous change, consisting of intermingling plaques 
 and areas of depression and thinning, but with little thickening of 
 
 — 
 
ILLUSTRATIVE CASES 407 
 
 the aortic wall in general. In the region of the middle portion of the 
 arch the process ended in a fibrous rounded ridge margining the 
 opening of a sac about 11 cm. in length and 20 cm. in circumference. 
 In the region of the junction of the arch and descending thoracic the 
 sac ended in a fibrous rounded ridge margining the junction. The 
 wall of the aneurism was generally fibrous and from very thin 
 to 244 mm. in thickness. On its inner aspect the wall of the aneu- 
 rism was lined with laminated pinkish gray-brown thrombotic 
 material to which in turn more recent thrombotic material was 
 adherent, and to this in turn blood clot was adherent. The wall of 
 the aneurism rested on the spine from the second to the seventh 
 thoracic vertebrae and eroded their bodies. In places the wall . 
 of the sac was very thin, slightly disintegrated, and through it there 
 was infiltration of blood in moderate amount along and in the peri- 
 esophageal tissues for a distance of 12cm. The esophageal wall was 
 intact. The pulmonary artery, veins and venae cavae were negative 
 except that from its situation the aneurism pressed on the trachea 
 and the great vessels running to and from the heart. The process 
 described in the aorta faded out as the abdominal region was reached. 
 The great branches were negative. The portal vein and radicles were 
 negative. 
 
 You will note that this syphilitic process in the aorta began some 
 distance above the aortic valve, so that there was no anatomical basis 
 for an aortic regurgitation. 
 
 Case 4494 
 
 An unmarried American girl of nineteen entered March 14, 1923, 
 complaining of difficult respiration with loss of weight and appetite. 
 
 She had measles, whooping coughand scarlet fever (?) when young. 
 Since these illnesses she had always been well. During the past 
 winter she had occasional sore throats. Recently she had had 
 occasional sharp pains on the right side in the breast region, and 
 considerable gas. Two months before admission she lost appetite. 
 
 Fourteen months before admission she began to have “neuritic”’ 
 pain in the right scapular region and later in the right arm, coming on 
 especially at night. It was relieved by electrical treatment. At the 
 same time she noticed a gland in the right supraclavicular region. 
 A physician had X-rays taken which showed a mass in the right 
 chest. She was sent to a hospital, where X-rays of the chest Jan- 
 uary I9, 1922, showed a large mass in the region of the right 
 hilus nearly four inches up and three inches out into the lung. It 
 had the appearance of an encapsulated gland. There was some 
 
408 FACTS ON THE HEART 
 
 fibrosis throughout the lung adjacent to this. The gland involved 
 the mediastinum so that the heart was pushed slightly to the left. 
 The diaphragm was high’on this side and the lung not well aerated. 
 (See Fig. 87.) There was a cervical rib on the left side. She was 
 given five radium treatments averaging 3000 millicurie hours each. 
 August 9 the plates still showed the definite mass in the right lung 
 without much change from the previous observation. Since the 
 radium treatment she had coughed, feeling something in her throat. 
 Three sputum examinations were negative. She could no longer 
 raise sputum. November 1 the small nodule had disappeared, but 
 there was no other apparent change. She was given an appointment 
 
 Fic. 87.—Malignant lymphoma involving the right lung, the right pleura, the 
 pericardium, the wall of the right auricle and the superior vena cava. February 20, 
 1922. Shows essentially the same findings described January 19. The mass in the 
 right hilus region has the appearance of an encapsulated gland, and involves the medi- 
 astinum so that the heart is pushed slightly to the left. There is some fibrosis through- 
 out the lung adjacent to this. The diaphragm is high on the right and the lung not 
 well aerated. 
 
 for deep X-ray therapy, but did not keep it. During her stay at the 
 hospital her leucocyte count varied from gooo to 15,000. The differ- 
 ential count averaged polynuclears 70%, small lymphocytes 22%, 
 mononuclears 6%; red cells showed considerable anisocytosis and 
 achromia. The patient entered another hospital, where she was 
 tapped. She had some chills and moderate cough. During nine 
 weeks she was given one X-ray treatment. She was discharged four 
 weeks before she came to the Massachusetts General Hospital. She 
 had been “‘all right”’ until March 4, when she began having difficulty 
 
ILLUSTRATIVE CASES 409 
 
 with breathing beginning by her losing her breath completely and 
 becoming semiconscious. At first she was thought to be dying. 
 After this she continued to have difficulty in breathing, especially 
 at night. She had lost thirty-five or forty pounds. 
 
 Physical examination showed a poorly developed and nourished 
 girl, breathing rapidly. A few small supraclavicular nodes on both 
 sides, more marked on the right. Heart: Apex impulse and meas- 
 urements not recorded. No apparent displacement. No murmurs 
 or thrills. Beats forceful. Soundsloud. Rate rapid. Blood pres- 
 
 xe 
 
 Fic. 88.—The same, March 16, 1923. Right side of the chest completely dull. 
 Outline of the heart and diaphragm obscured and heart shadow considerably displaced 
 in the opposite direction. Findings probably represent a large quantity of fluid in the 
 right pleural cavity, obscuring the condition of the lung. 
 
 sure 124/83. Chest: Left lung expanded a little more than the right, 
 which lagged a little. Entire right lung flat to percussion. Left 
 hyperresonant. ‘Tactile fremitus decreased on the right. Bronchial 
 breathing in right chest anteriorly and above angle of scapula poste- 
 riorly. Breathing exaggerated at right base posteriorly. Egophony 
 over root of right lung posteriorly. A metallic note to percussion in 
 this area. No rales heard anywhere. Vocal fremitus increased over 
 entire right lung. 
 
 Temperature 98.1°—103°. Pulse 84-150. Respiration 21-41. 
 Amount of urine not recorded. Sp. gr. 1.030. A slight trace of 
 
410 FACTS ON THE HEART 
 
 albumin, a few pus cells and occasional red cells. Blood. MHgb. 
 85%, leucocytes 21,g00-26,500, polynuclears 80%. reds 4,056,000. 
 Wassermann negative. Medical consultation March 16. Signs 
 of fluid at the right base with possible cavity or localized pneumo- 
 thorax. Extensive pathology in therght lung . . . Possibly fluid; 
 may be purulent. X-ray March 16. See Fig. 88. 
 
 The patient had a great deal of respiratory difficulty, particularly 
 at night, relieved by morphia and atropin. March 16 she felt worse 
 than at any other time. Lying on the right side seemed to increase 
 the dyspnea and to cause engorgement of vessels in the neck. March 
 19 the attacks were more severe. The next morning there was a 
 very severe attack of dyspnea lasting twenty minutes with consider- 
 able cyanosis and difficulty of expiration. March 21 in a very 
 severe attack of dyspnea the patient became cyanotic and died. 
 
 Clinical Diagnosis —Tumor of right chest. 
 
 Empyema? 
 
 Dr. Richard C. Cabot’s Diagnosis —Tumors of right lung, proba- 
 bly lymphoma. 
 
 Empyema. 
 
 Anatomical Diagnosis ——Malignant lymphoma (scirrhous type) 
 involving at the right lung, right pleura, pericardium, wall of right 
 auricle, superior vena cava, and tracheal lymph glands. 
 
 Occlusion of superior vena cava. 
 
 Compression of trachea, bronchi and great eect 
 
 Bronchiectasis, right. 
 
 Empyema, right. 
 
 Congestion of liver, spleen and kidneys. 
 
 Dr. RicHarpson: There was a large mass involving the upper 
 two-thirds of the right lung, also a mass between the upper portion 
 of the lung and the trachea and bronchi. Of course the whole thing 
 pressed on the trachea and bronchi and on the great vessels running 
 to and from the heart. The mass pushed the heart over so that the 
 bulk of the heart rested in the left pleural cavity. The pericardium 
 was distended with fluid, 250 c.c. or more. Whether that had 
 anything to do with the X-ray picture or not I do not know. 
 
 Dr. A.S. MERRILL: An observation of pulsation in the mass would 
 have been of some value. : 
 
 Dr. Ricuarpson: The left lung was normal, and there was only 
 a little fluid in the left pleural cavity. On the right side however 
 there was much fibrinopurulent material. There was pus here, 
 empyema. 
 
ILLUSTRATIVE CASES ALS 
 
 The greater curvature of the stomach was within 5 cm. of the 
 pubes. The cecum rested over in the region of the left lower quad- 
 rant, bringing the appendix there. The congestion of the liver, 
 spleen and kidneys was probably due to the pressure on the great 
 vessels to and from the heart. 
 
 We were not permitted to examine the head. 
 
APPENDIX 
 
 1. DISSECTING ANEURISM 
 
 Utterly different from syphilitic aneurism both in etiology and in > 
 clinical development is the so-called dissecting aneurism, a complica- 
 tion of arteriosclerosis in the aorta, whereby a split occurs in the 
 wall of the aorta allowing the blood to seep in and gradually to dissect 
 off or peel off an inner layer, until finally the aorta may be trans- 
 formed into a double tube. 
 
 This is to be regarded as a rare, and from a clinical point of view 
 quite unimportant complication of arteriosclerosis in the aorta. In 
 our series there were five cases of this lesion, which I have not included 
 in the 1846 cases studied in detail for this book. 
 
 Clinically the lesion produces few recognizable symptoms or 
 physical signs, though in case 3681, which follows hereafter, the X-ray 
 picture shows a widening of the aortic shadow presumably due to the 
 dissecting aneurism which was found at necropsy in this case. 
 
 2. SEPTIC OR MYCOTIC ANEURISM 
 
 I have not studied in detail and have not included in this series 
 of cases, the three examples of septic or mycotic aneurism complicat- 
 ing an acute or subacute endocarditis on the aortic valves. This 
 also has little or no clinical importance as it cannot be recognized in 
 life. Itis of course entirely separate from syphilitic aneurism both in 
 etiology and course. None of our cases went so far as to rupture the 
 aorta. 
 
 Necropsy 3681. Dissecting Aneurism - 
 
 A Cape Breton cook of sixty-two entered in 1911 for a fracture 
 of the right external malleolus. With firm bandaging she made an 
 uneventful recovery. The heart at this time was normal. 
 
 October 4, 1916, she returned, very ill, complaining of sharp 
 pains in the back coming through to the chest. Because of her 
 condition and a very poor memory the history is unreliable. One 
 brother died of cancer of the stomach, one sister of tuberculosis. 
 She had measles at twelve years, pneumonia at an unknown age. 
 At thirty-two she had a child stillborn. At this time she had an 
 operation, and developed a ‘‘milk leg” on the right. The leg had 
 
 412 
 
SEPTIC OR MYCOTIC ANEURISM 413 
 
 remained swollen. She had had no other children. For forty years 
 she had had attacks of bronchitis with cough every winter lasting 
 from a week toa month. With these she had sore throat of three to 
 four days’ duration. She passed the menopause at fifty-five. In 
 1906 her memory began to be poor, and in rogrtr it “left her entirely.”’ 
 At that time she had dull precordial pain localized over the heart, 
 with palpitation, dyspnea on exertion, and orthopnea. For four 
 years she had urinated at night. In 1911 she weighed 200 pounds, 
 her best weight. Her usual weight was 130-170. 
 
 The evening before admission she was seized with sharp stabbing 
 pains in the midscapular region radiating straight through to the 
 lower part of the sternum, not to the arm, and lasting for five minutes 
 atintervals of anhour. Dull constant aching followed these attacks. 
 During the night the attacks became more frequent and severe, forcing 
 her to sit up to get her breath and leaving her very dyspneic. They 
 kept her awake all night. The morning of admission she vomited all 
 the food eaten the day before. 
 
 Examination showed an obese woman. The apex impulse of the 
 heart was not found. The dimensions by percussion and by X-ray 
 are shown in Figs. 89 and go. The action was slow and irregular. 
 The sounds were of fair quality. The aortic second sound was 
 accentuated. There was a presystolic roll at the apex. The 
 
 8 cm. 
 
 5 cm. 11 cm. 
 
 16 cm. 
 Fic. 89.—Measurements by percussion. 
 
 arterial walls were palpable. The blood pressure was 260/140 to 
 150/100. There was a few coarse moist rales at the base of the left 
 lung posteriorly, and a possible pleural rub. The abdomen was 
 negative. There was slight edema over the shins. The pupils were 
 irregular and did not react to light. The other reflexes were normal. 
 
 The temperature was 97.1° to 100.8°, the pulse 50 to 120, the 
 respirations 20 to 40. There was a normal amount of urine. The 
 specific gravity was 1.016 to 1.006 There were slight traces of albu- 
 min at five of nine examinations, leucocytes at eight, granular — 
 or hyalin casts at four. Catheter specimens October 23: left ureter, 
 sediment and culture negative; right ureter, sediment shows a rare 
 polynuclear; no organisms; culture negative. Renal function tests 
 
AIA FACTS ON THE HEART 
 
 October 4 and 9 gave no specimens. October 5 in one hour a single 
 specimen showed 20%. October 13 one specimen at the end of two 
 hours showed 10%. <A urine culture October 20 was negative. 
 The hemoglobin was 80%. There were 15,400 to g600 leucocytes, 
 85% polynuclears. A Wassermann was negative. The blood 
 nitrogen was 62 mgm. per 100 gm. blood. The stools were negative 
 to guaiac and the microscope at two tests. The fundi were normal. 
 A genito-urinary consultant reported after cystoscopy, “‘ The bladder 
 is essentially normal; slight redness near the base may be the evidence 
 of a slight cystitis which would cause a mild pyuria. The ureters 
 look normal and have no obstruction. Both kidneys are active. 
 Kidney X-ray might help; if negative there is certainly nothing to 
 justify treatment.”’ 
 
 Fic. 90.—Arteriosclerosis with dissecting aneurism. 
 
 The pulse was slowed by the digitalis and the heart sounds were 
 louder. The patient had no more severe attacks of precordial pain, 
 but the cardiac condition improved very slowly. There was almost 
 constant precordial ache, with radiation down the left arm. Follow- 
 ing the cystoscopy there was slight cystitis. November g, 1916 she 
 was discharged relieved. 
 
 January 13, 1917, she began to vomit after meals and to have 
 increased distress on movement. January 17 she was suddenly 
 seized with agonizing pain over the sternum and through to the back 
 at the scapular level. This persisted without relief. She reentered 
 the hospital five hours after its onset, too ill for examination. The 
 temperature was 98°, the pulse 80, the respiration 48, the hemoglobin 
 80%. There were 12,000 leucocytes, 88% polynuclears. The 
 
SEPTIC OR MYCOTIC ANEURISM 415 
 
 evening of admission she had a sudden very sharp pain in the region 
 of the heart, and died in about ten minutes. 
 
 Inter pretation of X-ray.—Aneurism of the descending aorta. 
 
 Clinical Diagnosis (from Hos pital Record).—Arteriosclerosis. 
 
 Cardiac decompensation. 
 
 Angina pectoris. 
 
 Anatomical Diagnosis—Arteriosclerosis. 
 
 Dissecting aneurism of the aorta with great hemorrhage into the 
 peri-aortic and retropleural tissues. 
 
 Subacute pericarditis. 
 
 Arteriosclerotic nephritis with amyloid infiltration. 
 
 Hypertrophy and dilatation of the heart. 
 
 Organized fibro-calcareous thrombosis of the right external iliac 
 vein. 
 
 Slight hemothorax. 
 
 Slight hemopericardium. 
 
 Chronic pleuritis. 
 
 Defective closure of the foramen ovale. 
 
 Emphysema of the lungs. 
 
 Dr. RICHARDSON: The heart weighed 606 grams (normally 200— 
 300), and the kidneys 107 (normally 200-400). There was some 
 arteriosclerosis of the coronary arteries. The miscroscopical exam- 
 ination showed the condition to be one of arteriosclerosis and not of 
 syphilis. 
 
‘CHAPTER IV 
 HYPERTENSIVE HEART DISEASE 
 I. DEFINITION 
 
 A group of cases believed to be characterized during life by a 
 more or less permanent hypertension and showing a hypertro- 
 phied and dilated heart, without valvular disease or chronic peri- 
 carditis. Nephritis and arteriosclerosis may be present or absent. 
 
 This definition brings together all the hearts in this series which 
 are enlarged but which show no mechanically obstructing lesions in 
 valves or pericardium.* | 
 
 The Relation of Nephritis to Cardiac Hypertrophy.—The 
 nephritic and the non-nephritic hypertrophies are here lumped 
 together: (1) because it is in some cases impossible to distinguish 
 them in life, and (2) because at necropsy the state of things in every 
 part of the body, except the kidney, may be identical in the nephritic 
 and in the non-nephritic cases. There may be the same degree and 
 type of cardiac enlargement, the same dropsy (or lack of it), the same 
 hypertension as in life. ‘‘Uremic”’ or infectious phenomena may be 
 present or absent in both groups; in age and sex they are not con- 
 spicuously different. 
 
 This is not to assert that the presence of nephritis makes no 
 difference, but merely to acknowledge ignorance of what difference it 
 makes. On the average, as will be shown presently, the hearts are 
 larger in the nephritic than in the non-nephritic group, but to this 
 rule there are many exceptions. For example, 18 of our 267 cases 
 of chronic nephritis showed no cardiac hypertrophy at all. In 23 
 others the heart weighed under 450 grams, and in 17 of these 23, 
 under 400 grams. On the other hand, in the non-nephritic group 
 there were hearts weighing 870, 793, 775, 750 grams, and many others 
 of large size. 
 
 What Has Arteriosclerosis to Do with It?—The place of arte- 
 riosclerosis, like that of nephritis, in relation to hypertensive heart 
 disease, is one that I make no attempt to settle on the basis of this 
 series of observations. But though I think that few of us can doubt 
 
 * In this definition other rare causes of hypertrophy and dilatation, such as pernicious 
 anemia and hypoplastic aorta are also assumed to be absent. 
 416 
 
DEFINITION ALT. 
 
 that nephritis (with hypertension) is closely linked with the develop- 
 ment of cardiac hypertrophy, one cannot say the same of arterio- 
 sclerosis. ‘Taking first the simple facts of association or correlation: 
 in 207 cases of nephritis there was hypertrophy and dilatation in 
 249, or 93%. No other so-called “cause” for hypertrophy and dila- 
 tation has so high a correlation. Valvular disease, though not caus- 
 ing hypertension, shows 184 cases or 83% with hypertrophy and 
 dilatation, and 36 without it. Chronic pericarditis shows 89 with 
 hypertrophy and dilatation and 25 without it, a 78% correlation. 
 
 Arteriosclerosis, on the other hand, occurred 668 times with 
 hypertrophy and dilatation, and 283 times without hypertrophy and 
 dilatation, a correlation of only 64%. 
 
 TABLE 81.—CORRELATION OF CARDIAC HYPERTROPHY AND DILATATION WITH 1552 
 CASES OF VARIOUS DISEASES 
 
 SNPS Met se five aires ha a te oe 93% correlation in 267 cases. 
 UR MMISCRICIISUMEE A... oN yaa vets Sie ett aclacea sate 83% correlation in 220 cases. 
 MeMPO ANG DELICATGIUIS. 9.0. rss het sl Sd 78% correlation in 114 cases. 
 MTETIOSCIETOSISs. .. sis... sheer oss ss+.-- 04% Correlation in, o51 cases. 
 
 This is in close accord with Ophuls’ figures.* He found 35% of 
 cases with marked arteriosclerosis but without cardiac enlargement. 
 Our own percentage is 36. Our figures, however, refer to varying 
 grades of generalized arteriosclerosis, including a few cases of slight 
 degree. In 132 cases of especially marked and extensive arterio- 
 sclerosis (with this word mentioned first in the anatomical diagnosis) 
 106 or 80% showed cardiac hypertrophy and dilatation, and 20% did 
 not. 
 
 Arteriosclerosis by itself, uncomplicated by nephritis, by valve 
 lesions or pericarditis, occurred 248 times with hypertrophy and 
 dilatation, a correlation of only 39%, and 383 times without it. 
 Whereas nephritis alone occurred 67 times with hypertrophy and 
 dilatation and only 18 times without it, a correlation of nearly 
 79%, or double that of arteriosclerosis. (See also pages 424 and 
 
 436.) 
 
 In this chapter I have merged all types of nephritis: first because 
 many of those whose nephritis was called “‘acute”’ or “subacute” at 
 necropsy gave every clinical evidence of having had the nephritis for 
 months or years; and secondly, because the terms acute and subacute 
 
 * Archives of Internal Medicine, Vol. 9, page 156 (1912). 
 27 
 
418 FACTS ON THE HEART 
 
 are used in our pathological records to denote certain histological 
 pictures and not with any definite tzme limits in mind. In the 66 
 cases of subacute nephritis occurring in 4000 necropsies, 2I were 
 associated with cardiac enlargement, and 45 were not associated with 
 cardiac enlargement. In 113 cases of acute nephritis 53 had hyper- 
 trophy and 60 none. 
 
 The only type of nephritis that seems to belong in a class by itself, 
 so far as the connection with cardiac enlargement is concerned, is the 
 amyloid variety, long recognized to be connected loosely, if at all, 
 with heart changes. There are but 21 cases designated as amyloid 
 nephritis in our necropsy records. Three of these had also cardiac. 
 hypertrophy, 18 did not. It is well known that this type of nephritis 
 is not ordinarily associated with hypertension. 
 
 The best working hypothesis then seems to be that whatever 
 influence produces a chronic hypertension will produce as a result 
 cardiac enlargement. We have then, beside the local mechanical 
 obstacles—valvular disease and adherent pericardium—only one 
 other common cause for cardiac enlargement, namely, hypertension, 
 however produced. Nephritic hypertension seems a clearly 
 established subtype. Whether arteriosclerotic hypertension is a 
 reality or not seems quite open to question, on the basis of these 
 figures and in accordance with the observations of others. Certainly 
 there are many cases of hypertension without arteriosclerosis or any 
 other supposed “‘cause”’ (Allbutt’s “‘Hyperpiesia”’). All of these, so 
 far as I know, are associated with cardiac hypertrophy. Perhaps 
 whatever causes this hypertension may also result, if long continued, 
 in arteriosclerosis, in nephritis, or both. The term “hypertensive 
 heart disease”’ then, expresses the belief that almost all the enlarged 
 hearts not due to valvular disease or pericardial adhesions, develop 
 as an organic response to vascular hypertension, however produced. 
 I have never known a case of long-standing hypertension* without 
 enlarged heart. If such cases can be proved to exist, the hypothesis 
 and the terms here used must be modified. Until then they seem 
 to express best the present state of our knowledge. 
 
 Discussion of certain rarer causes of cardiac enlargement follows 
 in the next section. 
 
 * Temporary hypertension due to muscular work, to emotion or to intracranial 
 disease (e.g. cerebral hemorrhage) certainly does not enlarge the heart. H. Batty 
 Shaw (Hyper piesia and Hyper piesis, Oxford Press, 1922) finds enlargement of the heart 
 in all cases of hypertension lasting more than four days. 
 
HYPERTENSIVE CARDIOVASCULAR DISEASE 419 
 
 Il. HYPERTENSIVE CARDIOVASCULAR DISEASE 
 
 Hypertrophy and Dilatation of the Heart is the Commonest of All 
 Diseases of the Heart. 
 
 Although the boundaries of the group here described are not 
 accurately determined, it is reasonable, I think, to include in it all 
 the necropsied cases showing a hypertrophied and dilated heart 
 associated with nephritis, with arteriosclerosis, with both, or with 
 neither, but without valvular disease, chronic pericarditis, and any 
 other recognized cause of cardiac enlargement. Thus limited the group 
 includes 599 cases. ‘There are about 50 other cases, possibly of this 
 type but here excluded, because other more prominent lesions carry 
 them into other groups. For instance, among the 80 cases of uwncom- 
 plicated acute pericarditis* there were 11 with enlarged hearts. Sim- 
 ilarly there are 19 cases of uncomplicated acute endocarditis with car- 
 diac hypertrophy and dilatation not accounted for; 17 of chronic non- 
 deforming endocarditis, 4 of myocarditis. All these may have been 
 in fact cases of chronic hypertension with a harmless local thickening 
 of a valve, a trifling myocardial scar, or with terminal infection of 
 endocardium or pericardium. If they were all added, the number of 
 cases here analyzed would be 649. Roughly, then, we deal in this 
 chapter with from 600 fo 650 cases as compared with 220 cases with 
 valve lesions, 114 with chronic pericarditis, 94 of syphilitic aortitis, 
 gi of myocarditis. 
 
 This overwhelming excess of hypertensive cases is entirely in 
 accord with clinical experience. 
 
 TABLE 82.—HEART DISEASE MANIFEST OR LATENT 
 
 Hypertensive heart disC@SC ttt EEE ems (OO 
 Rheumatic valve lesions 
 
 SERRA TS Ee 220 
 Adhesive Pericarditis (enna RE II4 
 Syphilitic Aortitis eA ATT Q2 
 Myocarditis pero | gl 
 
 MANIFEST HEART DISEASE 
 
 Hypertensive COREA ABATE I 230 
 Valve Lesions Nea TR! 127 
 Chronic Pericarditis wae 34 
 Syphilitic Aortitis res 247 
 
 * 185 cases of acute pericarditis in all, but tos of these are complicated by other 
 lesions, some of which are often linked with hypertrophy, and so are not considered 
 here. 
 
420 FACTS ON THE HEART 
 
 Ill. LATENT VS. MANIFEST CASES OF HYPERTENSIVE HEART DISEASE 
 
 About 230% of these 600 cases were of the manifest type, 1.e., 
 associated with dropsy and chronic passive congestion at necropsy 
 and without any obstruction, such as mediastinal or peritoneal neo- 
 plasm, to account for the dropsy. The remaining 369 were symptom- 
 less and represent the cases of enlarged heart discovered at necropsy 
 after a death due chiefly to neoplasm, infection, violence, toxemia, 
 or angina pectoris. 
 
 Compare now these 230 manifest or dropsical cases with the 
 figures in other types of heart disease known to produce dropsy.T 
 
 Among the 220 cases with valve lesions............. 127 were dropsical 
 
 Among the 114 cases with chronic pericarditis....... 34 were dropsical 
 
 Among the 92 cases with syphilitic aortitis......... 27 were dropsical 
 Totaliis sacs sl inde aie et chad aen Sane nee nae en 188 
 
 It appears then that among 418 cases (188 plus the 230 mentioned 
 above ) of manifest dropsical heart disease, 230, or 55%, are of the 
 hypertensive type, while only 188, or 45%, are of any other type. 
 
 These figures justify our calling cardiac hypertrophy and dilata- 
 tion a disease rather than, like fibrous myocarditis, a mere post-mor- 
 tem finding. 
 
 Cardiac hypertrophy and dilatation is often latent, but so are all 
 the other types of heart disease, as the following table shows. 
 
 TABLE 83.—LATENCY OF HEART DISEASE 
 
 Hypertrophy and dilatation latent in 61% Congestive death in 39% 
 Valvular disease latent in 38% Congestive death in 62% 
 Syphilitic Aortitis latent in 730% Congestive death in 27% 
 Chronic Pericarditis latent in 70% Congestive death in 30% 
 
 AGE INCIDENCE 
 
 In the 230 manifest cases of hypertensive heart disease the aver- 
 age age was forty-nine years; Batty Shaw’s average is fifty years; in 
 our inactive or latent cases, fifty-three years. 
 
 SEX 
 
 Males predominate in the active cases in the proportion of twelve 
 to five. Among the latent cases the ratio is fourteen to five. 
 
 * There are probably twenty or thirty more cases belonging with these, but so much 
 entangled in other groups that I cannot definitely distinguish them. 
 
 + Myocarditis is not here included since I am not convinced that by itself it is a cause 
 of dropsy. 
 
 oy #8) 
 
THE ETIOLOGY OF CARDIAC ENLARGEMENT 421 
 HEART WEIGHT 
 
 The average heart weight in active cases is 474 grams, in the latent 
 cases 433 grams. 
 
 IV. THE ETIOLOGY OF CARDIAC ENLARGEMENT 
 
 (a) Work-hypertrophy.—The data of this study are consistent with 
 the belief that all cardiac enlargement is a work-hypertrophy, if we 
 mean by this the heart’s response to the need to do more work so as 
 to maintain the circulation despite the burden of valvular lesions 
 tight pericardial adhesions or vascular hypertension. To keep up the 
 circulation in the face of such obstacles demands more work, more 
 muscle, i.e. a hypertrophy of the heart. In this sense the causes of 
 cardiac hypertrophy are, so far as we know, the causes which throw 
 continuous extra work upon the heart over a period of months or 
 years. 
 
 But the term ‘“‘ work-hypertrophy”’ has been used also to mean an 
 enlargement supposedly caused by the individual’s intermittent 
 muscular exertions in work or sport. Of such a cause this series gives 
 no evidence although some evidence has been adduced forit by others. 
 The hearts of “Marathon runners” repeatedly examined, year by 
 year, after the annual 25 miles run ending at Boston, Mass., have 
 never shown evidence of hypertrophy or of dilatation. Indeed the 
 X-ray measurements have shown apparently a slight diminution in 
 the size of the heart shadow alter the race. But C. Ward Crampton 
 in his book on Physical Exercise for Daily Use refers to cardiac hyper- 
 trophy in six-day bicycle racers. Possibly the more conlinuous 
 nature of this exercise gives it a special effect on the heart. 
 
 In the Massachusetts General Hospital series there was no evi- 
 dence that the hearts of athletes or of men who had done very heavy 
 work during life were any larger than the hearts of sedentary 
 people. Men of large frame have large hearts and men of small 
 frame have small hearts but without any discernible relation to 
 their daily occupations. 
 
 (b) Alcohol also played no discernible part in the cardiac hyper- 
 trophies of this series. Heavy drinkers, whether of beer or whiskey, 
 showed no larger hearts than temperate people. 
 
 (c) Emphysema and chronic pneumonitis have often been supposed 
 to produce a predominantly right-sided cardiac hypertrophy and 
 dilatation. But we could find evidence of this in only one case 
 (3191) in which a right-sided hypertrophy and dilatation was 
 
422 FACTS ON THE HEART 
 
 associated with emphysema. Even then the heart weighed only 294 
 grams and there was no chronic passive congestion. 
 
 (d) Syphilis has, so far as our observations go, no effect on the 
 size of the heart unless syphilitic aortitis with an incompetent aortic 
 valve is present. 
 
 There remain the long-familiar causes or associates of cardiac 
 hypertrophy, such as valvular disease, chronic nephritis and peri- 
 cardial adhesions. ‘The frequency of these associations has been 
 carefully studied in this series of cases, with the following results: 
 
 * 
 
 TABLE 84.—CARDIAC ENLARGEMENT AND THE ASSOCIATED (PossIBLy CAUSAL) LESIONS 
 
 Total No. showing | Percent 
 Sufferers | Cardiac Hy- | showing 
 with this pertrophy Hyper- 
 
 Lesion at Necropsy trophy 
 
 Lesions 
 
 Rheumatic? Valvular: Disease, 2 ee oe 83 
 
 Chronic Pénicatditisr: 9-2 serene 78 
 
 Nephritis* 73 
 
 Syphilitic Aortitis 68 
 
 95 
 
 Arteriosclerosis, with arteriosclerotic degen- 
 eration of kidneys 
 
 Chronic non-deforming Endocarditis..... . 
 
 ACutesEndocarditis: ce inte inser eee 
 
 Acute Pericarditis 
 
 ArteriesClerokise. 2: te oe ee a Se 
 
 * 108 chronic, 66 subacute, 113 acute. | 
 t Of these, 6 were exophthalmic, 3 toxic adenoma, I doubtful. 
 t Including myocardial abscess (15 cases) and myocardial infarct (20 cases). 
 
THE ETIOLOGY OF CARDIAC ENLARGEMENT 423 
 
 tr. Among the 1846 individuals harboring the 4037 cardiovascular 
 lesions which this book studies, 1209 were recognized by the pathol- 
 ogist as having some enlargement of the heart.* 
 
 But there is so much overlapping among some of these items that 
 without explanation they are quite misleading. For instance, out of 
 the 668 cases of arteriosclerosis, only 248 were uncomplicated by 
 other lesions very possibly capable of producing hypertrophy and 
 dilatation. Out of 83 cases of myocarditis only 4 were uncomplicated! 
 
 Let us therefore separate out the uncomplicated cases of each 
 lesion, i.e., those in which hypertrophy and dilatation is associated 
 with only one other recognized cardiovascular lesion. We then find 
 in 508 cases the following figures: 
 
 TABLE 85.—CARDiAC HYPERTROPHY IN UNCOMPLICATED (“‘SINGLE”’?) CARDIOVAS- 
 CULAR LESIONS 
 
 With Hypertension Hypertrophy in 12 out of 12 | or 100%. 
 
 With Leucaemia Hypertrophy in VeOUtEOL Mn Tan Ors LOO Gy. 
 With Pernicious Anemia Hypertrophy in I2 out of I3 |or 92% 
 With(a)R heumatic Valvular Disease Hypertrophy in 609 o0ut of 86 | or 80% 
 Group I. 
 With (b) Syphilitic Valvular Disease Hypertrophy in T7 Out Of °20 *llor™ 85% 
 With Nephritis Hypertrophy in 67 outof 78 Jor 85% 
 With Goitre Hypertrophy in Avout of | 36) 1 or, 66% 
 With Chronic Pericarditis Hypertrophy in 16 out of 28 |or 57%. 
 With Arteriosclerosis* Hypertrophy in 248 out of 513 | or 46% 
 With Myocarditis Hypertrophy in 4, 0ut of 10 | or “40%, 
 With Acute Endocarditis Hypertrophy in TOlOWGL Of 954. | Or. 35% 
 Group II. j i ] : 
 With Chronic non-deforming Endo- Hypertrophy in I7 out of 56 |or 30% 
 carditis 
 With Hypoplastic Aorta Hypertrophy in SrOtUt Olan se Ore 33°05 
 ‘With Acute Pericarditis Hypertrophy in TL OU OL SOu.| OF © 13 % 
 508 
 Add the cases in which Hypertrophy and dilatation is pre- 
 sent alone and without any of these “‘causes”........ oe Ue. 
 662 
 
 *In 46 the arteriosclerosis was very marked and was written first in the anatomical diagnosis, 
 40 of these 46 cases, or 8%, 9 had hypertrophy and dilatation. (See below.) 
 
 * Of these 1088 are recorded as showing hypertrophy and dilatation and 121 as 
 showing hypertrophy alone. This distinction, however, is of very little importance 
 here, since the single word “hypertrophy” has often been used in our records to cover 
 the same facts as the longer phrase “hypertrophy and dilatation.” 
 
424 FACTS ON THE HEART 
 
 Among 662 cases of hypertrophy and dilatation, then, there were 
 (1) 154 with no anatomical “‘cause’”’ discovered and (2) 248 with no 
 ‘“‘cause’”’ except arteriosclerosis, which (if it is a ‘‘cause”’ at all) is 
 active in only 46% of cases. 
 
 Cardiac Hypertrophy and Arteriosclerosis.—No one, I take it, 
 
 would suppose that uncomplicated acute pericarditis, though asso- 
 ciated in 13% of cases with hypertrophy and dilatation, is a real 
 ‘cause”’ for hypertrophy and dilatation, except possibly in a few of 
 the prolonged, (i.e., nearly or quite subacute,) cases, in which a tough, 
 though plastic exudate might conceivably bring increased work upon 
 the heart. Similar speculations are justified regarding all the 
 members of group II in Table 85. In a few cases of ‘‘acute”’ endo- 
 carditis, the lesions may have lasted long enough and interfered with 
 valve-function sufficiently to increase the heart’s work and so to 
 bring about hypertrophy. A few cases of chronic endocarditis 
 believed by the pathologist to involve xo valvular deformity, may in 
 fact have produced some deformity and so have acted as valve lesions 
 to burden the heart. Most myocardial fibrous scars are so small 
 that (as the figures show) they do not embarrass the heart’s action 
 enough to produce hypertrophy and dilatation. But sometimes 
 the damage might conceivably be so extensive (e.g. near the apex) . 
 as to call out hypertrophy in the rest of the organ. 
 
 We know that hypertension can by itself cause cardiac hypertro- 
 phy, even in the absence of nephritis and arteriosclerosis. It is 
 therefore entirely possible that in most of the cases of group II (or in 
 many of them) the hypertrophy and dilatation may be due to a 
 chronic hypertension, and that therefore the association with arterio- 
 sclerosis or with any other of the lesions set down in this group is one 
 of coincidence and not of cause and effect. 
 
 What Degree of Arteriosclerosis Is Concerned Here?— But if we 
 confine ourselves to arteriosclerosis of the extremest grade, that 
 actually was associated with hypertrophy and dilatation in 40 out of 
 the 46 uncomplicated cases. These 46 cases are selected from the 
 whole group of 1202 arteriosclerotics by two marks (a) because they 
 show so marked and widespread a type of the disease that the words 
 ‘arteriosclerosis’? was written first in the pathologist’s summary of 
 his anatomical diagnosis and (b) because no other known cause for 
 hypertrophy and dilatation (such as nephritis, valvular disease and 
 pericarditis) was present. They present, therefore, a type of pure 
 yet extreme generalized arteriosclerosis and, as has been said, 
 almost 90% of them showed hypertrophy and dilatation. The 
 
THE ETIOLOGY OF CARDIAC ENLARGEMENT 425 
 
 average age of these individuals was 58 years and three-fourths of 
 them were males. The degree of hypertrophy, however, was not 
 marked, the average cardiac weight being 480 grams, which for 
 men of 58 is not an extreme grade of enlargement. Moreover there 
 remain 467 cases of general though not extreme arteriosclerosis in only 
 208 of which, or 44%, was there any hypertrophy atall. Exactly 
 where these cases of arteriosclerosis belong between the ‘‘slight”’ and 
 the “‘extreme,’’ we have no way to determine. They are not con- 
 fined to a few spots, such as the aortic arch; thev all represent a 
 generalized process. But precisely ow generalized they were could 
 not be ascertained without a minute dissection of many peripheral 
 arteries, which was not undertaken. 
 
 In the 208 cases of arteriosclerosis with hypertrophy and dilata- 
 tion, (the 44% above referred to) the average heart weight was 429 grams. 
 In contrast with this, take the 154 cases of “‘pure” hypertrophy and 
 dilatation without arteriosclerosis or any other known ‘‘cause.” 
 The average weight is 384 grams, 1.e., 45 grams difference. Thisisa 
 considerable difference in the average, although there were in this 
 group hearts weighing 694, 618, 564, 559, 534, 518. But the 
 contrast is here greater than it would be but for leaving out the cases 
 dying with hypertrophy and dilatation and various terminal lesions, 
 such as acute pericarditis, essentially the same condition with a 
 different end. In these (9 cases) the heart averaged 471 grams in 
 weight. 
 
 In a further attempt to estimate how much effect, if any, is pro- 
 duced upon the heart by arteriosclerosis alone, I have separated out 
 the cases of hypertrophy and dilatation plus nephritis alone, and 
 compared them with cases of hypertrophy and dilatation plus 
 arteriosclerosis plus nephritis. In 53 cases of hypertrophy and dila- 
 tation with nephritis alone, the heart weight averaged 453 grams. 
 In 65 cases of hypertrophy and dilatation with nephritis and arterio- 
 sclerosis, the average heart weight was 487 grams, a difference of 34 
 grams. 
 
 Further graphic representation of the nephritic group of cases 
 is as follows: 
 
426 FACTS ON THE HEART 
 
 TABLE 86.—HyYPERTROPHY AND DILATATION PLus NEPHRITIS ALONE 
 
 Heart weights Number and type of cases 
 250-300 grams| = 1 (subacute) 
 = acute, 6 chronic) 
 
 301-350 grams] = 9g (3 
 
 351-400 grams | = 12 (1 = acute) 
 (2 = subacute) 
 (9 = chronic) 
 
 401-450 grams | = 7 (chronic) 
 A51I—-500 grams| = 6 (1 = subacute, 5 chronic) 
 501-550 grams | = 8 (1 = subacute, 7 chronic) 
 551-600 grams | = 4 (1 = subacute, 3 chronic) 
 601-650 grams get 2 (chronic) 
 651-700 grams | = 1 (chronic) 
 
 740 grams | = 1 (chronic) 
 
 750 grams| = 2 (1 = subacute 1 chronic) 
 
 53 
 
 faa eae ce ads De i 
 4 = acute nephritis 
 7 = subacute 
 42 = chronic 
 
 “2 
 SG 
 
 TaBLE 87.—HEART WEIGHTS IN UNCOMPLICATED NEPHRITIS 
 
 ol 
 ce 
 350 
 
THE ETIOLOGY OF CARDIAC ENLARGEMENT 427 
 
 TABLE 88.—HYPERTROPHY AND DILATATION PLUS NEPHRITIS PLUS ARTERIOSCLEROSIS 
 
 Heart weights eye Den Bad ty Be 
 
 of cases 
 250-300 grams | = 1 chronic 
 301-350 grams | = 6 chronic 
 351-400 grams | = 11 (1 = subacute) 
 
 (x = acute) 
 
 401-450 grams| = 9g (zr = acute) 
 (1 = amyloid) 
 
 451-500 grams | = 8 chronic 
 
 501-550 grams | = 11 chronic 
 
 551-600 grams | = 10 chronic 
 
 601-650 grams| = 3 (zr = acute) 
 
 651-700 grams| = 2 chronic 
 
 701-750 grams} = 3 chronic 
 
 751-800 grams} = 1 chronic 
 
 65 
 
 Eg A dal pee eR AO ey Ere OS A a en ee a 
 PEPERPSERI DENT OnE e P,  AUNT IE St Sattl, wah GRICE BS os WA Mein Pabeala es whe I 
 TGQ ANTE Soa Nain pyar the Arce RiGa EE te te a aa ah 60 
 OER US CLUE eee ete att extant hig MUN ea came RL AR se ote ae, 6 dhe the I 
 
 re 
 
 3S] 4a (| 451] S001 551] Gol} 651] 701 
 2801505! fo | fo | tw | fo | | w | te | ie 
 3 ov |3 Bo} 400 | 450] 500 | 5501600] G50} 700] 750 
 
 TS 
 $o0 
 TABLE 89.—HEART WEIGHTS IN NEPHRITIS PLUS ARTERIOSCLEROSIS 
 
428 FACTS ON THE HEART 
 
 It appears then on the evidence of pure association that arterio- 
 sclerosis is only a 34 gram factor in the total sum of the factors, linked 
 with cardiac hypertrophy. Of course it 1s possible to read the whole 
 matter in the opposite direction, and to suppose that arteriosclerosis 
 is not a cause of cardiac hypertrophy at all. We may say that it is 
 one result of hypertension and that cardiac hypertrophy is another 
 result. And we can suppose that hypertension, arteriosclerosis, 
 and enlarged heart are all three the results of some unknown (perhaps 
 toxic) cause. 
 
 ‘‘Arteriosclerotic Degeneration of the Kidney”’ in Its Relation to 
 Hypertrophy and Dilatation of the Heart.—By this term is meant 
 foci of arteriosclerosis in the kidney, perhaps sufficient to diminish 
 its function to some degree but not sufficient to constitute a nephritis. 
 The kidney has its share of the general arteriosclerosis of the body, 
 but no more. 
 
 Among 142 cases so diagnosed at necropsy, in our series 93 (or 
 about two-thirds) were associated with enlargement of the heart. 
 In these 93 there were other ‘“‘causes”’ for hypertrophy in 34, leaving 
 59 (or 41%) in which there was no obvious cause for the enlargement 
 except the general arteriosclerosis, of which the renal lesion formed 
 part. But general arteriosclerosis alone (without renal degeneration) 
 occurred in 248 cases (or 48%) with hypertrophy and dilatation, 
 and in 265 cases without it, in a total of 513 cases, so that there is no 
 evidence that the renal degeneration alone added anything to the 
 cardiac hypertrophy. 
 
 V. HYPERTROPHIED AND DILATED HEARTS OCCURRING WITHOUT 
 NEPHRITIS OR ARTERIOSCLEROSIS, IN YOUNG PERSONS 
 
 We are apt to think that hypertension, without nephritis, is 
 confined to persons at or past middle life. Certainly we do not often 
 see it clinically in young people. Hence if hypertension is (as I 
 believe) the cause of most of the cases of cardiac hypertrophy without 
 obvious anatomical cause, we should expect the cases of hyperten- 
 sive heart disease to be mostly in persons past the fortieth year. 
 This turns out to be true. 
 
 A study of our 402 cases of hypertrophy and dilatation without 
 nephritis, valve lesions or chronic pericarditis, reveals but ten indi- 
 viduals under 40 with any considerable degree of hypertrophy. 
 The details of these 10 cases are shown in Table go. 
 
 One of these cases, however, (No. 2086) is enough to prove (if the 
 observations are accurate, as I believe they are) that even at 30 
 
 i 
 
ale 
 
 THE LARGEST HEARTS 429 
 TABLE 9o 
 Heart’s 
 ‘as i Blood Cz f 
 Case | Necropsy | Age & weight Bo ep te Remarks 
 No. | number sex aaah pressure death 
 I 606 37-M Chee od Soe Ot ates Pneumonia | No arteriosclerosis or nephritis 
 2 2890 30-M 564 120 systolic Chronic No arteriosclerosis or nephritis 
 two days passive 
 before death | congestion 
 3 650 36-M SE ba dD Me Reed ton Sepsis No arteriosclerosis or nephritis 
 4 2086 30-M 520 200 systolic Chronic No arteriosclerosis or nephritis 
 two mos. passive 
 before death | congestion 
 5 3000 39-M 518 105/80 Sepsis Chronic pneumonitis 
 one day 
 before death 
 6 2201 34-M ‘SO Tans eee ie Crushed 
 7 1972 36-M ASO Me |\trceo erree Poisoning 
 8 3940 32-M 480 138/78 
 three days 
 before death 
 from pneu- 
 monia 
 9 506 35-M AT Oe Neth Bees a ke Cirrhosis No. artsclerosis or nephritis 
 10 1924 35-M AOS eae Ne mete Snares Pneumonia 
 
 a man may have a hypertension of 200 mmHg. of systolic blood 
 pressure without nephritis, arteriosclerosis or any other known cause. 
 The other cases may have been of the same type, for although three 
 of.them showed no hypertension, these measurements were taken so 
 near the time of death as to be without great significance. 
 
 VI. THE LARGEST HEARTS 
 
 1. In Table or are shown the measurements of fifteen of 
 the largest hearts in this whole series of 1906 cases. As we study this 
 table, certain facts become evident. The first of these is that chronic 
 pericarditis with mediastinitis produces the largest hearts that are to 
 be found. In the largest of all the hearts of this series, and in four 
 others very close to it in size, chronic pericarditis was the only recog- 
 nized causative factor. In one other case, (No. 2 in this table) 
 valvular disease and subacute glomerulonephritis were also present 
 and may well have contributed to enlarge the heart. But the out- 
 standing fact remains that zm the five largest hearts of this entire series 
 
430 FACTS ON THE HEART 
 
 chronic pericarditis was the sole cause in four and one of the causes in 
 the fifth. Ina sixth case chronic pericarditis was a factor along with 
 valvular disease. Although this heart is set down as the sixth in our 
 series it should by right belong much higher up, since it occurred in a 
 boy of eleven, while all the others in this group of fifteen occurred in 
 persons who had reached the limit of their growth. For a boy of 
 eleven a heart weighing 799 grams represents probably as great an 
 enlargement as those at the top of this table. 
 
 Besides the cases thus far mentioned there was one more, No. 7 
 in this series, in which chronic pericarditis was also an important fac- 
 tor. Hence chronic pericarditis apparently played a part in enlarg- 
 ing seven out of fifteen of the largest hearts in this total series and was 
 the only known factor in four out of the five largest. 
 
 2. In old times one used to say that the cor bovinum, standing for 
 the largest type of heart known, was due primarily to pure aortic 
 regurgitation. ‘This cause appeared as the second in our list. If we 
 take the average weight of the hearts with syphilitic aortitis and aortic 
 regurgitation, this cause for cardiac hypertrophy stands first and 
 rheumatic stenosis second as compared with the average weight of the 
 hearts enlarged by other causes. But here we deal with individuals 
 not averages (see Table 92). The roth, 11th and 12th hearts among 
 the 15 largest of our series were due to syphilitic aortitis with aortic 
 regurgitation and aneurism, but without aortic stenosis. 
 
 3. Two very large hearts—the 13th and 14th of this series— 
 showed no anatomical ‘‘cause’”’ for this enlargement unless general 
 arteriosclerosis is such a cause. But according to the interpretation 
 which seems to me most plausible this heart represents the result of 
 ‘primary’ hypertension, the arteriosclerosis being an associated but 
 not in all probability a causative factor. Arteriosclerosis was also 
 present in association with two other of the cases of very great cardiac 
 enlargement already mentioned (Nos. 8 and 9). 
 
 4. Mitral stenosis uncomplicated by a lesion at any other valve 
 does not appear in this series of very large hearts. For comparison 
 I add at the bottom of it, the largest heart of this type; weight 750 
 grams. The multiple valvular lesions of rheumatic origin in this 
 series produced 6 hearts weighing over 750. But in general one may 
 say that in rheumatic heart disease the heart does not reach an 
 extreme degree of enlargement unless the aortic valve is involved. 
 
 It has repeatedly been suggested by writers on cardiac disease 
 that youth is an important adjuvant to disease in producing cardiac 
 
+ 
 
 THE LARGEST HEARTS 431 
 
 hypertrophy. From our table this observation seems to have only a, 
 very limited amount of truth. Thus among the possessors of the 15 
 largest hearts that I have studied, only six were under the fortieth 
 year at the time of death, four were between forty and fifty, three 
 were between fifty and sixty, while one was 78. Youth does not 
 appear to be much of a factor. If we examine the ages of those at, 
 the very top of the list it appears that five out of the first six were 
 below the age of thirty-two. But all these patients were suffering 
 from chronic pericarditis. It appears therefore to be true that when 
 chronic pericarditis (the most powerful of all the hypertrophy-producing 
 causes that are known) is in evidence, it acts most strongly in young 
 people. But this may merely mean that the severe cases die young. 
 Case 4 is obviously an exception to this remark. The average age 
 in the series of fifteen patients with huge hearts is forty years. 
 
 TABLE 91.—THE LARGEST HEARTS 
 
 Chronic Pericarditis 
 
 Necropsy Heart’s Age and 
 No. number weight sex Remarks 
 
 I 266 1328 31-M Chronic pericarditis with mediastinitis. Rheumatism 4, 
 6 and 8 years ago. Double murmur over precordia. 
 Aortic valve 7 cm. Chronic passive congestion. 
 
 2 2550 273 30-M Chronic pericarditis with mediastinitis. Rheumatism 
 at 7 and 15. Frequent tonsillitis. Aortic orifices 
 enlarged. Acute endocarditis (aortic). Subacute glom- 
 erulonephritis. Chronic deforming aortic and mitral. 
 Blood pressure 205/almost zero. Double murmur 
 everywhere. Chronic passive congestion. 
 
 3 3345 1158 19-M Chronic pericarditis with mediastinitis. Rheumatism 
 with peri- 2x. Valve orifices enlarged. Chronic non-deforming 
 cardium endocarditis aortic. Double murmur. Corrigan and 
 
 pistol shot. 
 
 4 1975 1150 52-M Chronic pericarditis. Rheumatism 2x. Valve orifices 
 enlarged. Systolicat apex (loud). Acute endocarditis, 
 aortic, mitral and tricuspid. Chronic passive con- 
 gestion. 
 
 5 32090 II4o0 31-M 'Chronio pericarditis with mediastinitis. Chronic passive 
 
 (1205 with congestion. Valve orifices enlarged. Chronic non- 
 
 pericar- deforming endocarditis. Double murmur, Aortic second 
 
 dium loud and ringing. Blood pressure 180/120. Diagnosis 
 made in life. 
 
 6 1063 799 r1-M Pick’s syndrome. Rheumatism at 5. Double murmur. 
 Chronic non-deforming endocarditis, mitral, aortic and 
 tricuspid. 
 
 Chronic Pericarditis with Aortic Stenosis 
 
 7 3345 1000 19-M Dyspnoea 4 years. Chronic pericarditis, mediastinitis 
 
 and pleuritis. Valoular disease. 
 Aortic Stenosis Alone 
 
 8 2603 900 49-M Rheumatism 4x. Angina pectoris; sudden death without 
 stasis. 
 
 9 3610 872 55-F Orifice admits only scissor blades. Slight arterio- 
 
 sclerosis. Blood pressure 152/115. 
 
32 FACTS ON THE HEART 
 
 AN 
 
 TABLE 91.—TnHeE LARGEST HEARTS.—(Continued) 
 
 Aortic Regurgitation with Syphilitic Aortitis 
 
 10 2936 1000 50-M Aneurism also. 
 II 3930 950 49-M Aneurism also. 
 12 2734 940 47-M Aneurism also. 
 
 General Arteriosclerosis 
 
 ui! 1468 910 45-M 
 14 1833 870 78-F 
 15 706 844 390-M Valves M A T 12, 7, 13, cm. Presystolic thrill at apex. 
 
 Three murmurs, Angina pectoris. Az2 very faint. 
 Heart and lung clots. Arteriosclerosis of aorta only. 
 
 Rheumatic Heart Disease 
 
 | 341 | 750 | 39-M | Mitral stenosis. Acute glomerulo nephritis. 
 
 VII. DEGREES OF CARDIAC HYPERTROPHY IN DIFFERENT LESIONS 
 
 TABLE 92.—AVERAGE CARDIAC WEIGHTS 
 
 12 Syphilitic aortic'regureitationw..7.. 9-2 toe eee eee 613 grams 
 2. Aortic stenosis (rheumatic) 580 grams 
 3. Chronic pericarditis—uncomplicated cases*........... 567 grams 
 4. All valve lesion except those given above............. 512 grams 
 is. Chromic pericarditis (all cases): ay netic, ee eee 500 grams 
 6... Mitral stenosis alone: 22.4.. 223. 2. ose re eee 426 grams 
 T aATLETIOSCIETOSIS ANG MCD NTACIS. 6 eee ee eee 487 grams 
 8. Nephritis:alone x 2 Ae Wen ee ays tee 453 grams 
 g. Arteriosclerosis alone... set net ae ot eee ee 429 grams 
 10. Hypertrophy and dilatation without any “‘cause”’...... 384 grams 
 With these may be compared 
 Li: Chronic endocarditis alone) cee ee ee eee 423 grams 
 42: Acute endocarditis (alone) t? 724 <5. semsnn ee eee 420 grams 
 13. Acute pericarditis (alone) (8 cases)... 2.5... /...45. ss a yoreraans 
 *See Table 91. + See Table 85. 
 
 These figures show (1) that the cor bovinum, the classical extreme 
 of enlargement, is most often a result of aortic regurgitation, as has 
 been so frequently observed before. 
 
 (2) That although chronic pericarditis with mediastinitis produces 
 the largest of all hearts met with in this series, the average case of 
 chronic pericarditis (without mediastinitis) has less effect on the 
 heart than aortic disease. 
 
 (3) That when several valves are involved in a rheumatic lesion 
 it comes next to pure aortic disease and to uncompticated chronic 
 pericarditis as a stimulant to cardiac overgrowth, while 
 
 (4) Pure mitral stenosis produces on the average but slight enlarge- 
 ment and 
 
— 
 
 DEGREES OF CARDIAC HYPERTROPHY IN DIFFERENT LESIONS 433 
 
 (5) Is exceeded by nephritis (with or without arteriosclerosis) 
 in the effect on the heart muscle. 
 
 (6) That the ‘‘uncaused”’ and uncomplicated cases of hypertrophy 
 and dilatation are mostly of slight degree—slighter indeed than any 
 group except those associated with uncomplicated arteriosclerosis. 
 
 TABLE 93.—ELEVEN CASES OF CARDIAC HyPERTROPHY ASSOCIATED WITH CHRONIC 
 PERICARDITIS ALONE 
 
 Case | Necropsy | Heart | Age and 
 
 R k 
 No. No. weight sex ata ae 
 I 266 1328 31. M_ | Chronic non-deforming mitral and aortic endo- 
 carditis. Mediastinitis. Rheumatism 4, 6 
 and 8, years ago. 
 2 1535 337 | 31. F 
 3 1673 528 53. M |“Orthopnea_ since 16.” No _ rheumatism. 
 Chronic passive congestion. Tb. of a rib. 
 Diagnosis ‘‘Myocarditis and mitral regurgi- 
 tation.” Mitral valve = to cm. 
 4 1700 625 69. M | Died of appendicitis and general peritonitis. 
 5 2314 297 36. M | Hemiplegia and epilepsy. Pericarditis very 
 slight. 
 6 2504 400 56. M | Calcified pericarditis. Died of pneumonia. 
 7 2737 305 40. M | Tuberculosis of lungs and peritonitis. 
 8 | 3009 448 20. F_ | Pick’s syndrome. Diagnosis correct in life. 
 9 3290 TI40 31. M | Rheumatism 4 times. Diagnosis correct in life. 
 Valve orifices enlarged. Mediastinitis. 
 Double murmur. 
 IO 3520 425 40. M | Valve orifices enlarged. Mediastinitis. Pneu- 
 monia. 
 II 3714 308 22. F -| Cancer of stomach with metastases. 
 (slight 
 hyper- 
 trophy) | 
 
 (7) Arteriosclerosis alone is associated witha slight though definite 
 cardiac hypertrophy, but may, as already said, be itself a concomi- 
 
 tant result of a common cause (hypertension) producing the hyper- 
 28 
 
FACTS ON THE HEART 
 
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436 FACTS ON THE HEART 
 
 trophy of the heart and the arterial changes as parallel compensatory 
 lesions. 
 
 It is noteworthy that in twenty cases of arteriosclerosis (see Table 
 94) confined to the aorta* and slight even there in four cases, the 
 average heart weight was 463 grams, or greater than in the “ gener- 
 alized”’ cases with sclerosis extending beyond the aorta. Among these 
 twenty cases were hearts weighing 844, 711, 556, and 500 grams, 
 and another called ‘‘very large” but not weighed. How can 
 anyone suppose that the arteriosclerosis was an important cause 
 of cardiac enlargement in these cases? But if not in these, then why 
 should we pay attention to it when it is associated with smaller hearts 
 in its generalized form? All these patients may have had hyperten- 
 sion before we saw them in their terminal hospital weeks. The 
 cardiac enlargement may perfectly well have been due to that, 
 the arteriosclerosis being due also to the hypertension or to some 
 unknown cause. | 
 
 It would be natural that slight arteriosclerosis should go with 
 slight cardiac hypertrophy and extensive arteriosclerosis with exten- 
 sive hypertrophy if the possibly causative hypertension had lasted 
 but a short time in the first group and a longer time in the second. 
 
 VIII. CARDIAC FAILURE IN HYPERTROPHY AND DILATATION 
 
 For unknown reasons a hypertrophied and dilated heart of the 
 type that I have been describing is prone sooner or later to fail—more 
 prone, that is, than hearts of normal size. Just why this failure ~ 
 occurs I do not know. It used to be said that the hypertrophied 
 heart was as strong as the normal heart or stronger, but that when 
 dilatation supervened, the stretched, thinned organ naturally became 
 ineficient. Dilatation used to be regarded as a late untoward 
 mechanical complication of the benign process which began with simple 
 hypertrophy. But there is in most cases, so far as I know, no reason 
 to believe this. Hypertrophy and dilatation are ordinarily associated 
 together, and this not merely in the late and incompetent states of 
 the disease, but in the very early and mild cases. Nor has myocar- 
 ditis any demonstrable part in producing the failure of enlarged 
 hearts. Most of them show no myocarditis. 
 
 THE ASSOCIATION OF HYPERTROPHY WITH DILATATION 
 
 In 4000 necropsies hypertrophy and dilatation together occurred 
 1088 times as the records stand. 
 
 * And in a few extending to the cerebral or iliac arteries. 
 
CARDIAC FAILURE IN HYPERTROPHY AND DILATATION 437 
 
 In 4000 necropsies hypertrophy alone occurred 121 times.* 
 
 In 4000 necropsies dilatation alone occurred 118 times. 
 
 As soon as we canrecognize the one we usually find the other. 
 Moreover there is just as much reason for supposing that dilatation 
 is a compensatory and helpful change as there is for such a belief 
 regarding hypertrophy. Probably without dilatation compensation 
 never could be established or maintained. 
 
 All that we know is that very large hearts (without valve lesions 
 or péricarditis) are apt to fail, perhaps from chronic effort against 
 hypertension. Cuzrculatory failure in the absence of considerable 
 cardiac enlargement is not common except in connection with some 
 quite obvious cause such as surgical operation, hemorrhage, infection, 
 or poisoning. But the greatly enlarged heart may become incompetent 
 without any special “cause” and without our having any considerable 
 warning that it ts failing. In many cases it seems clear that infection, 
 intoxication, or operative insult is the exciting cause of circulatory 
 heart failure (see statistics in Table 95). But there seems no doubt 
 that these causes act much more strongly on hearts already hyper- 
 trophied and dilated as a result of some previous agency, known or 
 unknown. It is true that a heart of normal size, wholly free from 
 anatomical defect or disease, may in a few days become seriously or 
 fatally weakened as the result of an infection such as pneumonia or 
 typhoid fever, or of a toxemia such as acidosis. Much less common 
 are the instances of circulatory failure following operation upon a 
 patient whose heart was sound at the beginning of the operation. 
 But although these facts are well established there is no question 
 that these three dangerous influences—infection, inioxication, and 
 operative insult—are more often followed by death when the heart is 
 already hypertrophied and dilated. 
 
 Mode of Death in 230 Cases with Congestive Heart Failure among 
 599 Cases of Cardiac Hypertrophy and Dilation 
 ‘with and without Nephritis 
 
 1. Of these the death seemed due wholly to chronic passive con- 
 gestion in 95 cases. 
 
 2. In the other 135 cases, although there was chronic passive con- 
 gestion post-mortem, it was not obvious in life or of exclusive influence 
 in producing death as judged post-mortem, the picture being over- 
 shadowed by 
 
 *This is the number as it stands in the pathological records. But it is too large 
 for Dr Richardson tells me that the record often says “hypertrophy” when it means 
 “hypertrophy and dilatation.” 
 
438 FACTS ON THE HEART 
 
 TABLE 95 
 CASES 
 
 Uremia SS oat. coe to ao Ga es ee a 24 
 Uremia plus Sepsisn.t co tas. A. ta eine 21 63 
 Sepsis 30.245 So alent ete gh Seah ec hee te ee i 18* 
 Apoplexy,.2 2905 ee tae tense dus een pace ine ee ‘5 ae 7 
 Operative insult. sn Cad tain ee nae 3 
 Cancer? avin pee bo ast RG ote ty ese 4 
 Prewmoma (sg 5 feat eee a en ee 7 
 Périicious Anemia oy. os icre uk Neco on oe ene ea oe 6 
 LéuGemid ts. ees Sec Lente len ee Oe te oa eee 
 Phthisis 2? ee eS. Se ee ee 4 
 Cirkhosis: (53 sean tere Sai ute, sale os, Meee has eee 3 
 Cirrhosis pis ‘Sepsis.;t2 ese a nia ne eee ke a 3 
 efSitlash-Ups'.. vac vise 5. tease cee Geen Teen eee 3 
 Diabetes: and Sepsis was wana. on ese oa 3 
 ANBINaY! 5 Sari ais SH Aig sea Fe oe aie eee 2 
 Eclampsia, Status lymphaticus, Stokes-Adamssyndrome,eachr 3 
 Doubtful seks Saks ho ance a ke oats cS eal eas ne er 17 
 
 Total anc tic tees ine Vs SEE « CR ate a 135 
 
 *Sepsis in all combinations totals 47 cases excluding the consumptives, whose condition may 
 have been essentially sepsis also. 
 
 In many of these latter cases the finding of an enlarged heart 
 and chronic passive congestion at necropsy was a total surprise. The 
 other lesions seemed in life the only ones of importance. Yet the 
 presence of the chronic passive congestion is sufficient, I take it, to 
 show that the cardiac hypertrophy and dilatation played some part in 
 the patient’s death. 
 
 There is little if any evidence for believing that sepsis or any 
 infectious disease can in and of itself produce chronic passive conges- 
 tion in the absence of hypertrophy and dilatation or any other heart 
 lesion. Among the twenty-five cases of extreme general septicemia 
 with secondary acute endocarditis studied in Chapter VII there was 
 not one which showed any chronic passive congestion post-mortem. 
 The same is true of the eighteen cases of chronic nephritis without 
 cardiac hypertrophy. But doubtless the infections (especially strep- 
 tococcus sepsis, pneumonia and tuberculosis), the toxemias (uremic, 
 diabetic, neoplastic, hepatic and eclamptic), and the mechanical inju- 
 ries (operative, traumatic, apoplectic), as well as the anemias and 
 angina pectoris, may join in the attack upon the body’s resources 
 and cooperate with chronic passive congestion to cause death. 
 
 3. The heart weight in the 95 ‘‘pure”’ cases* averaged 548 grams. 
 In 24 cases dying with a chiefly uremic clinical picture (though show- 
 ing chronic passive congestion and hypertrophy and dilatation of 
 
 * T.e. cases dying with enlarged heart and general dropsy but without other known 
 cause for death. 
 
CARDIAC FAILURE IN HYPERTROPHY AND DILATATION 439 
 
 the heart at necropsy) the average heart weight was 501 grams; in 
 the 18 showing chiefly sepsis the average heart weight was 487 grams. 
 Apparently then the hearts of about 550 grams weight have reached 
 the danger point even if no infection or kidney trouble complicates 
 the situation. 
 
 4. The ages in 93* of the ‘‘pure cases averaged fifty-two, and the 
 sex (in 95) 64 men to 31 women, i.e. two to one. 
 
 5. The duration of known symptoms or complaints averages nine 
 months in 87 ‘‘pure” cases in which it could be fairly well estimated. 
 This is calculated from the duration of dyspnea and edema, which 
 were the standard complaints. If, from this 87 cases, 16 long ones 
 are subtracted (averaging two and a half years’ duration) the 71 
 remaining cases averaged five months; so that we can say that in 
 four-fifths of the cases the average duration of complaints is five months. 
 
 6. In a group of 192 cases showing no passive congestion after 
 death, 136 had no circulatory symptoms at any time; 56 had some 
 complaints which might have some relation to the circulation, though 
 in many of these the complicating uremia or pneumonia which finally 
 produced death may well have been the cause of ali the symptoms. 
 There was, however, a small but definite percentage in which the ante- 
 mortem symptoms led us to expect that chronic passive congestion would 
 be found after death, though in fact no such congestion was found. These 
 cases number nineteen. ‘This figure, which is 5% of our cases, may be 
 taken as the error inherent in the principle of division which I have 
 here adopted between active and latent cases of heart disease. In 
 95% of cases of cardiacenlargement, inactive yet with some symptoms 
 apparently of circulatory origin during life, we may consider that ure- 
 mia, pneumonia or some other factor not primarily circulatory caused 
 these symptoms and the patient’s death. These complications, how- 
 ever, in the inactive cases extended over more than a year in half the 
 cases; in the rest they lasted three months or less. 
 
 Hence it appears that about 5% of cases of cardiac enlargement 
 may be associated with chronic circulatory symptoms not demon- 
 strable as chronic passive congestion after death. In this degree the 
 classification here adopted (‘‘Active”’ or ‘‘Inactive’’) is incorrect. 
 
 Age and Sex in Relation to Latency or Congestion.—Allowing 
 however for this error, it appears that while men suffer two or three 
 times as much as women from cardiac disease of the hypertensive type, 
 the disease when it does affect women is oftener of a more serious type 
 _ than when it affects men. For women made up 32% of the serious 
 
 * Age not recorded in two cases. 
 
440 FACTS ON THE HEART 
 
 or active cases and only 21% of the inactive cases. The discrepancy | 
 is not striking but probably has some significance. 
 
 The age difference, as one contrasts the two groups of cardiac cases, 
 latent and manifest, has no interest. The difference between fifty- 
 three years, the average age of the latent cases, and fifty-two, the 
 average for those dying of passive congestion as shown at necropsy, 
 has no significance. | 
 
 7. Arteriosclerosis (post-mortem) was present in 78, absent in 17 
 patients dying of hypertensive heart disease without complications, 
 i.e., arteriosclerosis is the rule. The heart-weight in sixteen of the 
 seventeen cases without arteriosclerosis averaged 455 (in one the weight 
 was not recorded). The general average of the 95 cases was 548 
 grams. But the ages of these sixteen non-sclerotic cases averaged 
 forty-one years as against fifty in the whole group. So that these 
 figures prove nothing so far,as I see. 
 
 8. Blood pressure was recorded in 82 cases. 
 
 TABLE 96 
 
 Systolic blood pressure 120 or less in 15 cases 
 Systolic blood pressure 130-139 in 5 cases 7 30 
 Systolic blood pressure 140-159 in Io cases . { 
 
 Systolic blood pressure 160-180 in 13 cases 
 Systolic blood pressure 181-200 _ in 13 cases 
 Systolic blood pressure 201-220 in 13 Cases | 52 
 Systolic blood pressure 221-240 in 6 cases 
 Systolic blood pressure 241-280 in 6 cases 
 Systolic blood pressure 300 in 1 case 
 
 i.e., hypertension was usually present even at the end of life. In 
 my belief it had always been present earlier in life and was the cause 
 of the cardiac enlargement and weakening. 
 
 g. Diastolic pressure was recorded in 49 cases. 
 
 TABLE 97 
 
 Diastolic blood pressure 48 in 1 case 
 Diastolic blood pressure 60-75 in 6 cases 
 Diastolic blood pressure - 80-95 in II cases 
 
 Diastolic blood pressure 110-125 in 11 cases 
 Diastolic blood pressure 130-f50 in IO cases 
 Diastolic blood pressure 165-188 in 5 cases 
 
 Diastolic blood pressure 100-105 in 4 cases | 
 Diastolic blood pressure 220 in’ I case | 
 
CARDIAC FAILURE IN HYPERTROPHY AND DILATATION 
 
 10. Pulse Pressures in 49 cases. 
 
 TABLE 93 
 
 Pulse pressure 15-25 in 5 cases 
 Pulse pressure 30-40 in 6 cases + 22 
 Pulse pressure 45-55 in 11 Cases | 
 
 Pulse pressure 58-60 in 4 cases 
 Pulse pressure 70-75 in 7 cases 
 Pulse pressure 80-95 in Io cases /[ 27 
 Pulse pressure 100 in 4 cases | 
 Pulse pressure 120 in 2 cases 
 
 441 
 
 11. Nephritis (subacute or chronic), was present in 33 of 95 ‘‘pure”’ 
 
 cases dying a cardiac death with chronic passive congestion. 
 
 In 
 
 the whole 230 cases-with-some-chronic-passive-congestion there 
 were 112 cases of nephritis subacute or chronic, and three of acute, = 
 
 I15 or just one half. 
 
 That this nephritis itself chemically contributed to the chronic 
 passive congestion, aside from any mechanical hypertrophy and dilata- 
 tion with weakening, is of course possible, but of this there is, as I have 
 
 said above, no evidence. 
 
 12. The largest hearts among the 230 cases of manifest or dropsical 
 
 hypertensive heart disease are listed in Table go. 
 
 TABLE 99 
 
 (a) Chronic Nephritis with Arteriosclerosis...............+. 
 
 (b) Chronic Nephritis without Arteriosclerosis. .. 
 
 PM rATLETIOSCICTOBIS ALONG. o.ta.n tthe es Deke cagta es 
 
 eNGe ease wy pitever >. 0 he coed heh. oak mr) na. 
 
 780 grams 
 750 grams 
 740 grams 
 720 grams 
 705 grams 
 700 grams 
 700 grams 
 
 . 750 grams 
 
 870 grams 
 710 grams 
 
 gIo grams 
 793 grams 
 
 775 grams 
 750 grams 
 711 grams 
 
 13. Murmurs.—Systolic murmurs, usually loudest at the apex, 
 were heard in most cases, if carefully looked for.* They were defi- 
 nitely noted as absent in only 20%. Diastolic murmurs were also 
 noted in 24% of the cases despite normal aortic valves. 
 
 * Some of the patients died in surgical wards, where little attention was paid to the 
 
 minutiae of cardiac examination. 
 | 
 
442 FACTS ON THE HEART 
 
 Relation of Systolic Murmurs to the Size of Valve Orifices.—Select- 
 ing five cases characterized by especially loud apical systolic mur- 
 murs widely transmitted (axilla and back) we find the valve 
 measurements post-mortem as follows: 
 
 TABLE I00 
 
 Necropsy No. Mitral valve Tricuspid valve 
 
 Average 
 
 Compare with these a set of six cases in which the absence of 
 murmurs 1s definitely recorded. 
 
 TABLE -5OT 
 
 Necropsy No. Mitral valve Tricuspid valve 
 
 Average 
 
 Obviously one can make no prediction of an enlarged valve orifice 
 (‘‘relative insufficiency’’) on the basis of loud systolic murmurs in 
 life. The orifices are no larger (actually a trifle smaller) in the cases 
 with systolic murmurs than in those free from murmurs. 
 
CARDIAC FAILURE IN HYPERTROPHY AND DILATATION 443 
 
 With diastolic murmurs the case is not so clear. The following 
 table lists seven cases of hypertensive heart disease with diastolic 
 murmur loudest along the left sternal margin but without valve 
 lesions at necropsy. 
 
 TABLE 102 
 
 Necropsy No. Aortic valve 
 
 Average 
 
 This shows a slight increase in the aortic ring circumference, 
 whether enough to be significant I cannot say. 
 
 Cerebral Symptoms.—In contrast with rheumatic and syphilitic 
 types of heart disease the patient of the hypertensive group (mostly 
 elderly) presented as a rule some cerebral disturbances—usually 
 delirium in the last weeks of life. Apoplexy is of course the terminal 
 event in many cases largely similar to the 230 here analyzed. But 
 these apoplectic cases are not here considered as I am isolating the 
 cases with death by congestive heart failure. 
 
 False Pericardial ‘‘Friction.””— Eight of these cases were supposed 
 to have an acute pericarditis because of “friction sounds” heard 
 along the left sternal edge; but no pericarditis was found at necropsy 
 in these cases.* Possibly the dryness of the pericardial surfaces in 
 some dying patients of this type may account for these sounds. 
 
 Diagnosis.— Most of these cases of Hypertensive Heart Disease 
 were called ‘‘Mitral Regurgitation” or ‘‘Myocarditis” in life. 
 
 * Though in 102 other cases acute pericarditis was associated with hypertrophy 
 (see Acute Pericarditis). 
 
444 FACTS ON THE HEART 
 
 ‘Aortic Regurgitaion”’is also a not infrequent diagnosis and ‘‘ Cardio- 
 renal”’ appears occasionally. In some heart disease was not sus- 
 pected at all. The true diagnosis was seldom made. 
 
 IX. PHYSICAL SIGNS 
 
 The only reliable evidences of this type of heart disease during 
 life are, hypertension and demonstrable cardiac enlargement. 
 
 Only in the minority of the cases here analyzed was blood pres- 
 sure measured, as a large number of them date from a period when 
 blood pressure measurements were not a routine of our records. 
 The results of the measurements recorded as shown in Tables 103k, 
 104), and 106. 
 
 In some of these cases doubtless the pressure was low because 
 thé patients of this series were seen only near the close of life. But 
 experience in office practice and out-patient work with patients 
 seemingly of this type leads me to believe that in cases of this type 
 hypertension is almost invariably present for months or years before 
 compensation fails. That is to say, we almost never see enlarged 
 hearts in clinical work without evidence of valve lesions or pericarditis, 
 unless there is a definite chronic hypertension. 
 
 In a minority of cases there is elevation of systolic blood pressure — 
 without any considerable change in the diastolic. But many of these 
 I believe represent the later stages of cases which (if seen earlier) 
 would have shown a higher diastolic pressure as well. When nephri- 
 tis was present the diastolic as well as the systolic was usually ele- 
 vated. When no nephritis could be found elevation of systolic blood 
 pressure alone was not uncommon. 
 
 As regards the evidence of cardiac enlargemeni there is little to 
 be added to what any textbook on physical diagnosis teaches, but 
 a good deal to be subtracted. X-ray is of course the most reliable 
 agent for proving whether the heart is or is not enlarged. This 
 was available in only a small minority of our cases, but often brought 
 to light enlargements which would have escaped us otherwise. 
 Indeed in this group of cases the usual methods of physical diagnosis 
 yield little evidence of value as to size of the heart, because in 
 elderly persons (such as form the great bulk of those in this type) the 
 costal cartilages are often ossified and the whole thorax enlarged into 
 the shape designated as the “barrel chest.’’ With this change in the 
 shape of the chest there comes the general hyperresonance on percus- 
 sion (long falsely supposed to point to pulmonary emphysema) 
 
BLOOD-PRESSURE AND OTHER DATA 445 
 
 which makes it difficult or impossible to outline the cardiac dullness 
 by percussion. The same change in the shape of the chest often 
 makes it impossible for us to identify the position of the cardiac 
 apex by palpation. In many, possibly the majority of these cases no 
 cardiac impulse whatever can be found. 
 
 Hence previous to the introduction of X-ray plates and blood 
 pressure measurements we were helpless in the attempt to diagnose 
 most of these cases, unable to decide whether a cardiac hypertrophy 
 was or was not present. But now the presence of hypertension 
 allows us to conclude with only a negligible percentage of error that 
 the heart is enlarged, even when by percussion and palpation we get 
 no such evidence. As for the degree of enlargement we must rely on 
 the X-ray or guess at it. : 
 
 None of the auscultatory signs of cardiac enlargement proved of 
 much value in patients of this series, probably because they were seen 
 as bed patients, shortly before death rather than in the early stages 
 of their malady. Accentuation of the aortic second sound, for 
 instance, was present in only 14 of the cases. Asarule both second 
 sounds were feeble, the aortic especially so. Change in the quality 
 of the sound (the so-called ‘‘metallic” or “‘ringing”’ second) was occa- 
 sionally noted but was usually absent. 
 
 Arrhythmia, alternation, defects of conduction may be absent 
 until near the close of life in these cases. Murmurs and heart sounds 
 give us no information of value. Hence the discovery of the disease 
 prior to the terminal stage rests wholly on our ability to recognize 
 hypertension and cardiac enlargement. Without X-ray the latter is 
 often impossible to be sure of. Thus the essential diagnostic data 
 are reduced to one,—blood pressure measurement—the most impor- 
 tant fact to know about the majority of all heart cases, since hyper- 
 tensive heart disease is commoner than any other type. 
 
 X. BLOOD-PRESSURE AND OTHER DATA IN THE GROUP OF 179 CASES 
 OF CHRONIC, 15 OF SUBACUTE AND 13 OF ACUTE NEPHRI- 
 TIS ASSOCIATED WITH HYPERTROPHY AND DILATATION 
 
 AND WITHOUT VALVE LESIONS OR PERICARDIAL 
 ADHESIONS 
 
 In chronic nephritis, 179 cases, we have 112 with arteriosclerosis 
 and 67 without it. The statistics of blood pressure and other data 
 are shown in the following tables. 
 
~ oWe te hag 
 * tf py 
 
 FACTS ON THE HEART 
 
 SCLEROSIS—112 CASES 
 
 (a) Age 
 21-30 2 
 31-40 19 
 41-50 oY 
 51-60 30 
 61-70 24 
 71-80 12 
 81-90 
 112 
 (b) Duration 
 QE VCATS xc sean eka Mes Gakic oe, Ae eee Ree a 
 SOMERVERTS S12 os aces aa 8 cy ey eka I 
 POL VETS hy 5 oe ok te Bee: Oe aa eae 2 
 © Veare Sos bore he aie eels ee on ee ee Tie a 
 BW CATS a. sco Ae ita tl Oe eke ce ete er a 4 ms years, 1 a 
 50 VCaTS 4%. Ge ech eye his iN ee ee cee 5 
 B VOATS Ss Mites ite aetna AE eee ep ees 2 
 Bi Stea Es. Pash te un ta oe ea ee 7 ¢I-3 years, 20 cases 
 TB VEATS dhe. Pe th pe ca ae Cr ene II 
 TL. MODS | eee le Fer Ree ae one ee I 
 TO’ Months fa. 2) Wh eae, Pea ea he eee eee 2 
 O months..0 Sant on ere ee ee ee eee I (4-12 mos. IO cases 
 S monthsaa--s a rasehiesce et rath ee ee ee I | 
 4-5 Months 28.25, ota tO eh es ee 4 
 MODUS heath he 7 8 ie ea ae ee 2 
 2 Months Mile wera Ce Ot eile ce een une 4 
 T<3 MONS Mog oo de how eer ce ee ie eae 8 ; 2-12 weeks, 17 cases 
 3 WEEKS eae che siete oe alt te, Meee a I 4 
 DING COKE clei aa MR eee eine ee a.h: ea ere Ie eas 22 
 TWEE Kare tt kites MUR, Fn iy eee Ae, Ene Under a week, 7 
 Tay taut Gay wat race ane ee ee eee en cases 
 Unknown ies. bcp gece eyes are ete 44 
 112 
 (c) Sex 
 Malet ons 5 hte: on sete Marca oe rN er 81 
 Be male ere caring Rey + vediglac ss acing he elie ete ca acne one ese 31 
 (d) Type of Nephritis 
 Chronic (unspetified)+).¢. 4m. ete ote Pe ee 10 
 Chronic diffuse P98 P24 bn. wwe ate ene 5 
 Chronicwlomerular. fils 1% te Aiuleaee ee ee 20 
 Chronic interstitials Ri. oe ee ea ee ee a ae 
 Chronic; arteriosclerotic.1< s.r. 4..gsen west ots ioe oe ae 45 
 Subacute glomerular. v4 .« Sou. Soe acer ete cee ee I 
 112 
 
BLOOD-PRESSURE AND OTHER DATA AA 
 
 (f) ANALYSIS OF 42 NECROPSIES 
 
 WITH WitTHOoUT 
 CHRONIC CHRONIC 
 (e) Heart Weight iy sea tide SRR 
 Bee SOON eas vn is wn I oe aes Nat Ce om I 
 Bp eS hecar god te 8 COR ee eee ee eee 4 
 ue Ge ee eee I5 ;51 
 ~ lop Se Os ie ae 2 att reer 13 LP as ae WA tee hE 5 
 Re ROC gee te egy ha he 14 Bee Sng BN eA, 5 2 
 1.2 fed ot ae 22 | fe eee eh ae 3 
 4 a OOOO Carer eee 12 Ppa ae ae ee I 
 Uy Sona Ras BST ae ee 9 ” i Phris gan et et I 
 EES eo 8 ee res ae 8 Te CNA COUR aE AR eg ° 
 716) Covet eT aeons Ss 6 DEE, ord dg ais: at eR fo) 
 Tah, ise ROL Pee wea I OBS cy Ne Poe a ° 
 Sale telve I re See Daeg I Pipes etree ee fo) 
 SVR OOO ge Wo Ton, ines 2 ——— = 
 — 25 17 
 112 
 
 Average heart weight—508 grams. 
 
 (g) Chronic Passive Congestion 
 
 PEPE ePOGUSIIOLLOL. Satie Been eee tenn. ie uk cee ¢ 48 or 42% 
 
 cise GLNTTS aac Ral RE CORN ae EN end oer oe ee 77 0r 6% 
 
 Reis Ls OME ere OE AAR, Sod, OL Se She as ee ag is eee 14 or 12% 
 
 Ce eA et eri Ly he ane Mik, Ay ee Oe eee har Eh ie Ss 43 or 39% 
 LIZ 
 
 ROR OL CMEC Man rine cuciey Mi phe RO tls Saad Ad shes scary a 
 Eee Ey MENT aR eis, Mr Dat eid aR NR it Bae ete s Yh ah 
 TC CRM Omreer mis Stee Maat ov tReet I es CaM anes hats chs 3 
 
 TEE ie RA ee re ee A ck ge ST ae 83 
 Le Cee Mee Te, Mirek SEAL, Te ning ARR LA MA ke MOT eal es 9 
 Pa tar AC OTea Le Dra Clee etch fh amrud at care an ark Ae Leer Sea! chy ae Whe 13 
 Pty Pearle VesselstOl VLG. og Gol aa) AR tat cme Ren Otay yk ay 2 3 
 ere SCAT OLODATICS him Aa: (teh crue he ett s ign Wr tie cies grote | 6 
 _SURYAUE Sag) J OM BR gree a aan Scotts AE ape. en 2 
 RerROTIAL Yate ic 5.05, de eh esha any cern Meet ORM TEMS coy tg ATID Oia I 
 Sent Except COLOnaries. .. fobs. oan Er, BR eet RO ee I 
 PRUE OTL ere hes tei bs 52% RGR AP Nar can NAS Pai ANDRE MAME 9, aoe Oe 4 I 
 err aTOTS WC IiisWat.r aete oth ies @ . cetiies Wee me dient 2 Rae Ging d I 
 Aorta, Coronaries, vessels of Willis, branches................... I 
 
 112 
 
 * 821 (aortic 8), 2256 (aortic 8), 2270 (aortic 7), 2689 (aortic 7.5), 3364 (aortic 7), 
 
448 FACTS ON THE HEART 
 
 (j) Type of Death 
 
 Uremia. . 2005 Gala} een et i lcg oe 52 
 Sepsis. 22455 yah te win ava S Nee Ue ees aie ae cn ee 18 
 Passive congestion s..6y ool 4).- 28 «4s we ee A ee II 
 Post-operative eet toe eee ey ee 8 
 Cerebral lesions (apoplexy)... 42.02... 25. feck* oe 4 
 Pneumonia, oe er ca sw oat ak he at en oe Pe. 
 Coma. of doubtful ofiginsts4.<, 2a ee ee 2 
 Angina pectovis.< ocak. cy eee eee te Se 9 eee ee ae I 
 Heart: block vireo ett < Saeel e s S ece I 
 Hemorrhage 2.0 oct Abs 00s ste bes eta ee a ae . 
 Cancer, oi says Bis ct ala at mene cge ee Me ne I 
 Eclampsia 4. :a.58 sc0ts roids eee seis bee ai me rein Oath oie I 
 Girrhosis. ss cio.) SRR oh 8 eke byl tlagetg ho nade Canvey eee ee 4 
 Coronary: thrombus? 2.7.02 “le. S26 okies eats ee I 
 Fracture of fémur.4 so0..% fas ies, os San ps ete oe 2 
 ree ee re Oe AAR Se Na Ge 2 
 
 173 
 
 (k) Systolic Blood Pressure 
 
 Recorded in 63 of 112 cases 
 
 2EOM ZOO! Gora ys cea el aa ee ike) 
 TOO=2 4.055 LL sie / cade, Seng nena ie eee ee 33 
 L7ORLOON: e087 ono shee ee eee ee 14 
 TSO7T6G.0 6 Ly ais Mie cl eee nee ee at 
 Under tsi chit eee tee 3 
 63 
 
 t had Blood Pressure 300/220 with heart of 384 grams 
 1 had Blood Pressure 220/160 with heart of 303 grams 
 1 had Blood Pressure 220/188 with heart of 4or grams 
 1 had Blood Pressure 160/155 with heart of 664 grams 
 t had Blood Pressure 115/100 with heart of 780 grams 
 t had Blood Pressure 98/68 with heart of 390 grams 
 
 TABLE 104.—CARDIAC HYPERTROPHY AND DILATATION WITH CHRONIC NEPHRITIS, 
 BUT WITHOUT ARTERIOSCLEROSIS—67 CASES 
 
 Average age 36 years 
 (a) Sex 
 
 Increased 
 
 Oy ale Ei aa ee ake cated ee 3 
 BBO 3 OC os wha Act yn ht ee en ce I 
 POO=OAQs.« ulitis Sooty ait sacec ene a ore mee II ; 
 TSOSTOO Lf vo. € Shain ee Mae oF! 
 EOOATAO TH. 5.0 dks his Sar eues oie Nios couee Onan ae 5 
 Wourecorde sh. SS) ea ieee 2 a 39 
 
 67 
 
 * + had blood pressure 160/130. 
 
BLOOD-PRESSURE AND OTHER DATA 
 
 (c) Heart Sounds 
 
 SUITES OR Ter) 1, har Ge, Aen vet ing tele sm Go tord ate ale Sik Be ahs bce, we | 
 CAEP TICULA CEC ss) ovteew wrt eee in MEM Vd ged RT aay oes 4 ae 8s 31 
 AECL, ee er oh eh one SE Sede MeL le wt Ay oa, 4 
 MTT teats cs tae ie Oy nee te ee deere ch eho /d oe 14 
 PELCCCSS GUAPO te Sts ie er ee Moraes Wea etter i eievk, Palievele 4 II 
 
 67 
 (d) Chronic Passive Congestion 
 ITEM TISteE SCs VILOTLOIN a cicact ae ws 2 ssn aurea PEE oe et oe aie e's" s 39 | 
 Lf Ug ole S00 Ne Mg TE og ae ee AGN 8 ta Mc 6 p45 
 are VAN eh ey Au) SEEN, 4. Sa ie eaten eee se ee: 14 
 aE RULES CTL) Woy ae ad tinh Shek re Ot, eRe Ela al es cia ae Mules 4 
 of Cees aa th ikke ip eR, 9g Ae at Aaa. AC ope, Nira. RAR Mn eee Sh ee aCe 4 
 67 
 (e) Heart Weight 
 SRE at er ee Neo ae ae Aha cet dg of eRe Gea ate ae 470 
 (f) Heart Enlarged in Life 
 OEPMIUL AATEC Chiccey S.ciies. Wet Ghee aes, ae! NN Ls aan BAG bs 23 
 cof gate othe Aen Gin Abas Sener Re Se EA, SER UE eae An Meee MPa Ya 23 
 | SOP TES AETV A A Pa CA ie RA PR a SOR is has a Pe a 13 ¢40 
 TREE RIB be te a oe Sa ey Ar Am gen eae ell Ue aad nt ee 4 
 REE OCA CUM NR oe OMe Ae ete ee are th Re he aint a ces, SRM NEC Ot 4 
 67 
 (g) Type of Nephritis 
 nrc Come UC ETS tit la | on eam a ce aoe amelie Nate Paha veh bi clcls ne i Sag 12 
 SMES ac) Sg ED ag ire ba Ae Ee aay Se alee ea Ie tie 10 
 BIRT ML TLMSESGCLIIOC Sehr rice steaks nem mE AT AS tr hls Leas cya ecee rg Boe 36 
 SUMMMAS LCE CHIC MING [SN I4C1S «Sk feo yh tule Men Pre i naveag es 2 allay Ghee gi 6 3 
 I CeIn ct. ik ict. eg Nat Oat RG peyoh fast eS Ue ous Bebo ae Wee core 4 
 Beeclopepnrosis and pyelonephritis). veces oe sac es ete e ae we lel I 
 OSU Coys Bore da at ig Se ae) oN A ara 2 pa gn nMnene coke! ates) aha AZ 
 07 
 (h) Murmurs 
 ICR fail ts. ade 37 (1 musical and loud.) * 
 Systolic and diastolic.. 6 (2 with friction) 
 mone....... Ene at 
 oC 6 
 Presystolic...... 2 
 67 
 Thrill(Systolic) ...... 3 
 (i) Arrhythmia 
 ROTI LER ree aR: Shir, Ove es hc d ok Pema ree Le Bina hte Tend we Be Late de 7 
 RCE PENEYE le TEE Dlg in, SPs Sy Lyon ath ears cee eR, Be ta tigen SST Ut 44 
 SURREETOAT Ween 35k, a, hie Pa rh Ded bee MRI Thc ars Ae eae! apes a. inkess 3 16 
 67 
 (7) Palpitation 
 US STN "a2 i So RR pg conieite Ul aN AS) iL a RP 6 
 MALT TONMTOCOT Us nih canis se OR ee Benetelc in ee aly & huey & 61 
 67 
 FENG OT Osu bo ek. SeieattlO.ken eos bee 2071056 
 29 
 
450 FACTS ON THE HEART 
 TABLE 105.—HYPERTROPHY AND DILATATION WITH SUBACUTE NEPHRITIS, * 15 Ca ES 
 y 
 
 WITH GEN- 
 
 P WITHOUT ERAL i 
 ARTERIO-  ARTERIO- 
 SCLEROSIS SCLEROSIS — G 
 (a) Age -- 
 20-29 2 ji 
 39-39 5 I 
 40-49 i I 
 50-59 I I 
 60-69 fe) I 
 70-70 ae) I 
 9 6 ‘ 
 (b) Sex 
 Malas’.\ oder: cas, Gna eee 6 3 
 Fomales’) 1.4. cqee eek ee 3 3 
 (c) Duration 
 OMN0S- tary tee eee reer I ° 
 A WOAOS Scan! 3 ea oA ee I 2 
 Bi MNOS ining. Oh, cnc AMM RAR a ed fe) 2 
 DINOS ots tos aes ee ee ° I 
 6 weeks. I ° 
 4 weeks. fo) 
 3 weeks. I ° 
 T—2>WeeeSs, 2. . fe) er 
 T-Webkiss Neos pote aula. on eee toe ° 
 Unknown2..,0 “see ee 3 ° 
 9 6 
 (d) Chronic Passive Congestion 
 Ante and Post-Mortem...... 6 5 
 Post-Mortents sce aerate ee er 2 i 
 INO TECOIG Avee ohne eee eee I fe) 
 9 6 
 (e) Murmurs 
 SyStolichtc nate Ma ee ees a 4 
 Diastolich wt he hee eee I ° 
 Doubler nt 22s eer ee I I 
 INONGS« jor Sate DER hes Ra eee ° ts 
 NOSTECOLd. ais ate eee gee 4 ° 
 9 6 
 (f) Heart Weight 
 700-750 I ° 
 551-600 2 2 
 451-500. 2 ° 
 401-450 I 2 
 351-400 2 a 
 250-300 I I 
 ee a R 
 ais 6 4 
 
 * All subacute glomerulonephritis, (1 capsular, 1 diffuse, I intracapillary. 1 intracapillary 
 and capsular.) a 
 
DIAGNOSIS ACTUALLY MADE IN THESE CASES 451 
 
 TABLE 106.—HYPERTROPHY AND DILATATION WITH ACUTE NEPHRITIS, 13 CASES 
 
 WITHOUT WITH WirHoUT WITH 
 ARTERIO- ARTERIO- ARTERIO- ARTERIO- 
 SCLEROSIS SCLEROSIS SCLEROSIS SCLEROSIS 
 (a) Age | (g) Type of Nephritis 
 o-9 I o * Chronic and acute. . 2 ° 
 10-19 I o Acute glomerular. . 6 3 
 20-29 4 o Acute intersterial. . I ° 
 30-39 2 o Papillary mycotic.. I ° 
 50-59 2 I ae rr 
 60-69 fo) I Io 3 
 72-79 ) I 
 10 3 
 (b) Sex (h) Blood Pressure 
 5 records only. 
 pe er 4 2 180/100, 150/?, 125/70, 
 ee eas es 6 I 100/70, 100/60 
 (c) Duration (Four records only) 
 I yr. 4 weeks 
 17 days 
 4 days 
 No further data. 
 (d) Chronic Passive Congestion 
 Ante and Post-Mortem..... I I 
 (ao a BR Ea ed 2 
 PEECEOPO Ag hk 2 Fi e555 ia 0 2 Oo 
 10 G; 
 (e) Murmurs 
 0k A ee | O° 
 NITE esas id evs) dps chinese fe) I 
 1 8 2S ae er 2 
 EE as cs 82 fo) 
 IO 3 
 (f) Heart Weight 
 551-600 fo) I 
 451-500 vt O 
 351-400 fe) I 
 301-350 a I 
 251-300 4 fe) 
 201-250 7 ° 
 Under 200 I ° 
 IO a 
 
 XI. DIAGNOSIS ACTUALLY MADE IN THESE CASES 
 
 In the first ten or fifteen years of the period covered by the cases 
 of this group the diagnosis standing on the hospital record was usually 
 “myocarditis” or “‘mitral regurgitation.”” Only within the last 
 
452 FACTS ON THE HEART 
 
 ten years has it been recognized at the Massachusetts General Hos- 
 pital that neither of these diagnoses is ever justified before death as a 
 statement of the main cause of death. Facing the same facts as those 
 once called myocarditis or mitral regurgitation, we now call these 
 cases ‘‘hypertrophy and dilatation of the heart” or ‘‘ hypertensive 
 cardiovascular disease,” 77 case we are able to recognize cardiac disease 
 at all. 369 out of 599 had no suggestion of a cardiac diagnosis. The 
 old diagnosis of mitral regurgitation rested on the presence of a 
 systolic murmur, often loudest at the apex but not infrequently 
 loudest at the base of the heart. Even this murmur was not audible 
 in most of the cases of our series, though 62 cases showed it. The 
 mistaken use of the term ‘‘myocarditis”’ in our records rests on the 
 evidence of arrhythmia in an elderly patient without clear signs of 
 valvular disease. 
 
 Of most interest is the occasional occurrence of diastolic or pre- 
 systolic murmurs without any lesions of the aortic or mitral valve. 
 The interpretation of these murmurs is wholly a matter of speculation. 
 Some prefer to believe that they are due to a relative insufficiency of 
 the aortic or of the pulmonary valve due to high blood pressure above 
 the valve, or to dilatation of its ring. Others are inclined to suppose, 
 as an explanation, some disturbed function at the mitral orifice 
 or in the mitral leaflets. All this however is mere uncontrolled specu- 
 lation. The solid fact is that in any markedly enlarged heart, dias- 
 tolic or presystolic murmurs may be heard in the region of the cardiac 
 apex, without there being also any reason to believe that a valvular 
 lesion is present. I have long been accustomed to teach that when 
 the heart is much enlarged, especially in an elderly man, we can rarely 
 draw any conclusions from murmurs heard in the vicinity of the apex. 
 Neither systolic, diastolic nor presystolic murmurs under these condi- 
 tions have any particular significance. 
 
 Out of 599 cases of this group examined we have found only 230, 
 or 39%, to be of the active or manifest type. This may be contrasted 
 with 62% of-the rheumatic type, 27% of the syphilitic, and 30% of 
 chronic pericarditis, which are the figures for the proportion of 
 active or manifest disease in those lesions (see above, Table 2). 
 
 XII. SUMMARY AND CONCLUSIONS 
 
 1. Hypertensive heart disease means an enlarged and often incom- 
 petent heart without valve lesions or pericarditis. The cause, 
 though not established in all the cases of this series, is probably hyper- . 
 tension however produced. 
 
yh 
 
 SUMMARY AND CONCLUSIONS 453 
 
 2. The relation of nephritis and of arteriosclerosis to hypertensive 
 heart disease is not clear. Certain it is however that the disease often 
 exists for years without evidence of either renal or arterial disease. 
 But the longer it exists the more apt are we to find nephritis or arterio- 
 sclerosis at the necropsy, whether as results or complications or 
 concomitant symptoms of some cause underlying both them and the 
 hypertension, we do not know. 
 
 3. The disease is much commoner than any other cardiac malady. 
 In this series it is commoner than all the other types of heart disease 
 put together, whether we consider all cases or only those showing 
 decompensation before and after death. It is often wrongly diag- 
 nosed as myocarditis, mitral regurgitation, “‘cardiorenal disease,”’ 
 ‘senile heart”’ etc. 
 
 4. It is more than twice as common in men and appears usually 
 about the fiftieth year, though cases occur in every decade except the 
 first. 
 
 5. There is little or no evidence that muscular work or alcohol 
 can produce any cardiac hypertrophy. 
 
 6. Hypertensive heart disease is to be per emened from the 
 cardiac enlargement associated with pernicious anemia and with 
 leukemia, in both of which blood pressure is normal or low. 
 
 7. The degree of cardiac hypertrophy in hypertensive heart 
 disease is, in early cases, slight; and even in long-standing and decom- 
 pensated cases is never of the extreme grade caused by chronic peri- 
 carditis (with or without valve lesions). No hearts in this series are 
 enlarged beyond gio grams as a result of hypertensive heart disease. 
 Most of them are much smaller. Comparing averages they are 
 smaller than those associated with syphilitic aortic regurgitation, 
 rheumatic aortic stenosis (with regurgitation), and the multiple valve 
 lesions. But hypertensive heart disease enlarges the heart more on 
 the average than uncomplicated mitral stenosis does. 
 
 8. Hypertensive. heart disease in its earlier and milder stages — 
 lasts for years without producing any considerable discomforts and 
 
 _ limitations of the individual’s activity. The patient is not aware of 
 
 it unless he chances to undergo, while in full health, a physical exami- 
 nation, e.g. for life insurance or as a protective hygienic measure. 
 Increased blood pressure is then found and perhaps a slight cardiac 
 enlargement detected, though without X-ray measurements this is 
 often impossible. 
 
 g. As the disease progresses its effects show themselves in a slight 
 dyspnea on exertion, in a “‘pounding” in the arteries of the neck, 
 
454 FACTS ON THE HEART 
 
 or an awareness of the cardiac impulse. Or it may contribute its 
 influence to prostrate the patient when infection, toxemia, accident, 
 or surgical operation bring an unusual strain upon him. 
 
 to. Less often—in only about one-third of our cases—are cardiac 
 decompensation and stasis the cause of the patient’s death, without 
 cerebral hemorrhage, surgical operation, infection or toxemia. 
 In 46 of the cases the duration of the patient’s complaints is extra- 
 ordinarily brief, averaging 5 months in our series. 
 
 tz. In such cases the physical signs are those of a failing heart— 
 arrhythmia, tachycardia, general passive congestion—usually with 
 hypertension persisting, less often with low or normal blood pressure. 
 Systolic (and occasionally diastolic) murmurs are present but are of 
 no diagnostic value. The same is true of an accented aortic second 
 sound. 
 
 Diagnosis rests on the hypertension, the cardiac enlargement, 
 and the lack of evidence pointing to valvular disease or pericarditis. 
 
 HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 
 Necropsy 4769 
 
 A Finnish grocer of fifty-six came to the Emergency Ward Decem- 
 ber 17 for relief of generalized edema of a week’s duration. A frag- 
 mentary history was obtained from his wife. He had been married 
 over twenty years. Hiswife had had no children and no miscarriages. 
 She knew of no illnesses of his before the present one. Twenty years 
 ago he weighed 160 pounds. He had gradually gained weight until 
 four months ago he weighed 260 pounds and two weeks ago 280 pounds. 
 He became disinclined to work, but maintained an appetite. For 
 three years he had not seemed well, had been dyspneic, had seemed 
 sleepy day and night, and frequently dozed off during a conversa- 
 tion. During the naps he talked to himself a good deal. In the 
 past few years he had developed frequent nosebleeds which grew pro- 
 gressively worse until the past summer, but had decreased in fre- 
 quency and severity during the past few weeks. For four months his 
 feet had been swollen. Four months ago he became noticeably dysp- 
 neic, and during the past. month still more so. For six weeks he had 
 been unable to sleep in a reclining position because of orthopnea and 
 cyanosis; he sat up in a chair or walked about most of the night. 
 On some days during the past week he had raised a tablespoonful of 
 blood. For two weeks he had had generalized edema. He had com- 
 plained but little of pain, and that over the precordium. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 455 
 
 Examination showed an obese, water-logged, cyanotic man with 
 Cheyne-Stokes respiration. The skin showed diffuse erythema over 
 the lower abdomen and legs, many excoriations on the legs, and two 
 ulcers on the right knee. The mucous membranes were cyanotic. 
 There was moderate pyorrhea. The heart did not seem enlarged. 
 The sounds were faint. (The chest wall was very thick.) A soft 
 systolic murmur was heard over the whole precordia. The blood 
 pressure was 170/100. The lungs were clear except for a few coarse 
 bronchial rales in the left upper back and the right upper chest in 
 front. The abdomen was enormously distended, tense, dull to per- 
 cussion except high in the midline. There was fluid wave. Over the 
 lower portion was induration. Palpation of masses was impossible. 
 There was pitting and massive edema of the genitals and legs and 
 moderate edema of the hands, arms; and back. The left pupil was 
 greater than the right and irregular; both reacted normally. The 
 reflexes could not be obtained because of edema. 
 
 The temperature was 98~—100.8°, rectal, the pulse 112-58, the 
 respirations 23-32. The amount of urine is not recorded. The 
 specific gravity was 1.016. ‘There was the slightest possible trace 
 of albumin at one of two examinations. The sediment was loaded 
 with pus and showed five to ten red blood cells at both examinations, 
 two trichomonas were seen in motion at one. The hemoglobin was 
 90%, the leucocytes 8000, the polynuclears 71%, the reds 6,496,000, 
 with moderate stippling and polychromatophilia. The non-protein 
 nitrogen was 46 mgm. A Wassermann was negative. An abdom- 
 inal tap gave 2500 c,c. of opaque yellow fluid, specific gravity 1.012, 
 leucocytes 1700, polynuclears 13%, lymphocytes 79%, large mono- 
 nuclears 8%, 2500 red blood cells, no organisms. Culture was 
 negative. 
 
 The orders were as follows. December 17, salt free low protein 
 diet, magnesium sulphate § iin the morning. December 18, digi- 
 folin ampules vi intramuscularly at once, digitalis gr. vi by mouth 
 at once and gr. iii 4 i.d., morphia gr. 1 s.c. at once and gr. 16 s.c. 
 every three hours p.r.n., limit fluids to 3 50. December 18, caffein 
 sodium salicylate gr. x intramuscularly at once and gr. xv intramuscu- 
 larly p.r.n. for marked cyanosis or collapse; digifolin ampules iv. 
 December 109, caffein sodium salicylate gr. xv. 
 
 December 18 the patient became very cyanotic and the Cheyne- 
 Stokes respiration was marked. Caffein and oxygen were tried. 
 He had in all thirty-three grains of digitalis. At three o’clock the 
 morning of December 19 he died. 
 
456 - FACTS ON THE HEART 
 
 Clinical Diagnosis —Hypertensive heart disease with congestive 
 failure. 
 
 Hypertension. 
 
 Anasarca. 
 
 Obesity. 
 
 Dr. ‘Richard C. Cabot’s Diagnosis——Hypertension, ‘primary.” 
 
 Hypertrophy and dilatation of the heart. 
 
 Arteriosclerosis. 
 
 Chronic passive congestion. 
 
 Terminal infection? 
 
 Anatomical Diagnosis —(Hypertension. ) 
 
 Great hypertrophy and dilatation of the heart. 
 
 (No Arteriosclerosis) 
 
 General chronic passive congestion. 
 
 Hydropericardium. 
 
 Beginning hydrothorax. 
 
 Ascites. 
 
 Anasarca. 
 
 Chronic pleuritis. 
 
 Lymphoma of the mesenteric and retroperitoneal lymph glands. 
 
 Slightly defective closure of the foramen ovale. (Not abnormal). 
 
 Dr. RicHarDsoN: An enormously stout man. We were not per- 
 mitted to examine*the head. There was massive edema of the lower 
 extremities and genitals. The abdomen was distended, but the wall 
 was not rigid. There was also edema of the upper extremities and the 
 dependent portions of the trunk. The face and ears were purplish. 
 I go into this a little more in detail because it is a classical picture of 
 hypertension. 
 
 The muscles were large. The subcutaneous tissues were wet. 
 The peritoneal cavity contained at least 2000 c.c. of thin pale clear 
 fluid. The peritoneum and appendix were negative. The mucosa 
 of the esophagus was pale bluish red, otherwise negative. The 
 stomach and intestines showed a very striking picture of chronic 
 passive congestion,—the purplish red velvety mucosa oozing thin 
 bloody fluid. This was even better marked in certain portions of the 
 small intestine than in the stomach, but was extraordinarily well 
 marked all along the tract. 
 
 The right pleural cavity contained a small amount of fluid, the 
 left 300 c.c.—beginnings of hydrothorax. 
 
 The diaphragm on the right was at the fifth rib, on the left at the 
 seventh. There were no pleural adhesions at the apex, but some 
 
 i 
 
HYPERTENSIVE HEART DISEASE—_ILLUSTRATIVE CASES Ase 
 
 posteriorly to the diaphragm and some to the pericardium on the 
 right. On the left side there were scattered adhesions to the dia- 
 phragm and the pericardium. 
 
 L 
 
 Fic. 91.—Necropsy 4769.—Hypertensive heart disease with great hypertrophy and 
 dilatation of the heart. Heart weighed 960 grams. No nephritis. No arterio- 
 sclerosis. Valves negative. (Photograph by Lewis M. Adams. Dr. Oscar Richardson.) 
 
 The mucosa of the trachea and bronchi was brownish red. They 
 contained much thin bloody frothy fluid. The bronchial glands were 
 plump, brown-red and juicy. The lung tissue was spongy to slightly 
 
458 FACTS ON THE HEART 
 
 leathery, brown-red, and yielded a moderate amount of brownish- 
 red frothy fluid,—chronic passive congestion. 
 
 The pericardium contained 300 c.c. of thin pale fluid,—hydro- 
 pericardium. The heart weighed 960 grams,—greatly enlarged. (See 
 Figure 91.) The myocardium was generally thick, of good consist- 
 ence, pale brown-red. The right ventricle was five to six mm., the 
 left sixteen mm. The columnae carneae were large and _ thick. 
 There was slight dilatation on the left, marked dilatation on the right. 
 The cavities contained much blood and blood clot, in greatest amount 
 on the right. The valve circumferences were: mitral 11.5, aortic 
 7.5, tricuspid 13.5, pulmonary 8.5 cm. The valves were frankly 
 negative. The auricular appendices were free. There was a 
 slightly defective closure of the foramen ovale. The aorta and 
 great branches showed only a very slight amount of fibrous 
 sclerosis. Coronaries, capacious, free, and the circulatory apparatus 
 elsewhere negative. 
 
 The liver weighed 2307 grams, and showed chronic passive con- 
 gestion. The gall-bladder, except for a little edema of the wall, was 
 negative. The spleen weighed 430 grams,—moderately enlarged, 
 the tissue plump, elastic, brown-red, bloody,—chronic passive 
 congestion. 
 
 The kidneys weighed 427 grams; the capsules stripped readily, 
 the surfaces were bluish-brown-red and smooth, the tissue of good 
 consistence, plump, wet. The vessels were engorged, the pelves and 
 ureters negative,—chronic passive congestion. 
 
 There was a slight hydrocele on each side. 
 
 The inguinal rings were large but free and there was no definite 
 pouching of the peritoneum. The mesenteric and retroperitoneal 
 glands generally were markedly enlarged up to 414 cm.,—lymphoma. 
 
 A Puysictan: You did not find any reason why the urine should 
 be loaded with pus? 
 ~ Dr. Ricuarpson: No. 
 
 Dr. Casort: I think syoebodiat here present should remember 
 the looks of this heart and this history, because it fixes certain things 
 once for all: that we can have a huge heart due to hypertension so far 
 as we know, with no nephritis, no arteriosclerosis, no valve lesion,— 
 nothing. Isitrare? No. Isuppose itis the commonest of all types 
 of heart disease. It is the commonest of all heart disease. In my 
 opinion the nephritis or arteriosclerosis which often goes with it is 
 not the important thing, and no one knows what causes the 
 hypertension which, therefore, is called “‘essential.’’ 
 
‘= 
 
 ag 
 
 HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 459 
 
 A PuysiciAn: I think that is a fact that is very little appreciated 
 by the general profession. What details would you require added to 
 the picture to make a. diagnosis of arteriosclerosis? 
 
 Dr. Casot: None. As I said, I expected to find some arterio- 
 sclerosis. If we looked in the retina and saw it, or if we felt it in 
 the brachial, we should say he had arteriosclerosis there but we should 
 not know that it was present elsewhere or in any important degree. 
 We have no diagnostic signs of generalized arteriosclerosis. 
 
 A PuysicraNn: Does that mean that the diagnosis of arteriosclero- 
 sis is apt to be in fact this condition? 
 
 Dr. CaABorT: Yes. 
 
 Necropsy 960 
 
 A railway engineer of forty-eight was brought to the Accident 
 Room uneonscious. A policeman said the patient suddenly dropped 
 while at work in the dynamo room of the railway and was picked up 
 in the same condition as at entrance. Later a friend said that the 
 patient had been working all the time for twenty years and had 
 always been well. He drank a little ale and beer. After dinner the 
 day of admission he had some discomfort. 
 
 Examination showed a very obese man with cyanotic face and 
 noisy, labored, jerky respiration. There was some blood on his 
 lips and mouth. His tongue was bitten in two places. His breath 
 smelt alcoholic. A few coarse rales were heard in the lungs in front. 
 The back was not examined. The apex impulse of the heart was not 
 recorded. The left border of dullness was about at the nipple line. 
 There was no enlargement to the nght. A systolic murmur was 
 heard all over the precordia. The aortic second sound was accentu- 
 ated. The pulses were regular, very full volume, very high tension. 
 The artery walls were sclerosed. The pupils were small, equal, and 
 did not react. The other reflexes were normal. Supraorbital pressure 
 was negative. There was no edema. The temperature, pulse and 
 respirations were not recorded. 
 
 While the examination was being made the breathing stopped. 
 It was soon restored by artificial respiration and oxygen. About fif- 
 teen minutes later it again ceased. The patient vomited several 
 times, brownish material with the odor of beer. He was catheterized, 
 bled about a pint, and infused with normal saline while the bleeding 
 was being done. His condition grew steadily worse, he became very 
 cyanotic, and died in less than two hours after his admission. 
 
460 FACTS ON THE HEART 
 
 Clinical Diagnosis —Chronic diffuse nephritis. 
 
 Uremia. 
 
 Hypertrophied heart. 
 
 Anatomical Diagnosis —Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the lungs. 
 
 Soft spleen. 
 
 Hypernephroma of the right kidney. 
 
 Cholelithiasis. 
 
 Foci of fat necrosis in pancreas. 
 
 The heart weighed 694 grams. The cavities generally were large. 
 The wall of the left ventricle opposite the base of a papillary muscle 
 was about 17 mm. thick, the wall of the right ventricle 6 mm. thick. 
 There was no arteriosclerosis or nephritis. The hypernephroma 
 did not diminish the amount of secreting renal tissue. 
 
 Necropsy 1854 
 
 An American weaver of thirty-nine entered December 31. Two 
 of his brothers died of consumption. He had measles in childhood 
 and frequent sick headaches in his youth. At twenty-five he had 
 gonorrhea and at thirty-one typhoid fever. Since that illness he 
 had never been strong, and his headaches had been more severe. For 
 eight years his eyes had been prominent. At thirty-six he had 
 ‘‘malaria,’’—fever without chills for six weeks. He took a glass of 
 whiskey a week and an occasional glass of beer. 
 
 Three months before admission he began to have severe constant 
 generalized headache with some nausea. He vomited every other 
 day and felt weak and played out. He gave up work and was in bed 
 off and on for a day or two at a time. At the end of a month the 
 headache left him, but the vomiting continued. He lost weight and 
 strength. Four weeks before admission the vomiting became more 
 severe. Since that time he had vomited nearly everything taken. 
 His bowels were constipated,.not moving for four days. He urinated 
 three or four times at night. Two weeks before admission he began 
 to have dyspnea, which had grown steadily worse. Six days before 
 admission he began to have edema of the feet and legs which increased 
 rapidly for three days, then subsided somewhat. For two weeks he 
 had had a considerable nosebleed every two or three days. 
 
 Examination showed a very round shouldered, fairly well nour- 
 ished man looking haggard and sick. His skin was dark, his mucous 
 membranes pale. The teeth were poor, many missing. The throat 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 461 
 
 showed three small ecchymoses on the uvula and the posterior pharyn- 
 geal wall. The apex impulse of the heart was seen and felt in the 
 fifth space 414 inches to the left of the midsternum, half an inch out- 
 side the nipple line, coinciding with the left border of dullness. The 
 right border of dullness was an inch and a quarter to the right of 
 midsternum. The action was regular, the sounds rather loud, the 
 aortic second sound sharp and ringing. A rather hissing early sys- 
 tolic murmur was heard slightly over the whole precordia, best at 
 the apex, and transmitted a short distance into the axilla. The 
 pulses were normal. The systolic blood pressure was 210. The 
 lungs showed a few fine moist rales at both bases behind. The liver 
 dullness extended to the iliac crest. An indistinct edge was felt. 
 There was much tenderness over the liver. There was marked soft 
 edema of the feet. The pupils reacted very slightly. The other 
 reflexes were normal. 
 
 The temperature was 97° to 98.3° with a terminal rise to 102°. 
 The pulse was 97 tor1ro. ‘The respirations were 9 to 31. . The output 
 of urine was normal, the specific gravity 1.007-1.800. There was a 
 slight trace of albumin at both of two examinations. ‘The sediment 
 _ showed pus at one. The hemoglobin was 55%, the leucocytes 8600, 
 the polynuclears 90%, the reds 2,972,000, with no marked achromia, 
 poikilocytosis or polychromatophilia and no stippling. 
 
 The patient was unable to lie down, slept very poorly even with 
 opiates, and grew rapidly worse. He vomited several times. The 
 edema diminished. His respirations slowed down to six or eight 
 a minute with no opiates. Unless roused he lay with his eyes rolled 
 up and lids half closed. When roused, however, the respiration 
 improved and he looked bright. The night of January 3 he became 
 very delirious and sank rapidly. The morning of January 4 he 
 quietly died. 
 
 Clinical Diagnosis.—Chronic nephritis. 
 
 Uremia. 
 
 Myocarditis. 
 
 Arteriosclerosis. 
 
 Dr. Cabot’s Diagnosis —Chronic nephritis. 
 
 Uremia. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Terminal infection. 
 
 Anatomical Diagnosis —Chronic arteriosclerotic nephritis. 
 
 Hypertrophy and dilatation of the heart. 
 
462 FACTS ON THE HEART 
 
 Septicemia, streptococcus. 
 
 Pneumonia. 
 
 Soft hyperplastic spleen. 
 
 Foci of obsolete tuberculosis of the lungs. 
 
 Dr. RicHARDSON: The head was not examined in this case. There 
 was a slight amount of fluid in the peritoneal cavity. The liver at 
 the time of necropsy was only three fingers down in the right mammil- 
 lary line. It makes a difference where the line is that is taken when 
 the liver is measured. The distance between the lower margin 
 of the right lobe of the liver in the anterior axillary line and the crest 
 of the ilium is pretty short. But if taken in the right mammillary 
 line the liver might have been much farther up. 
 
 Dr. Cazot: We have noticed over a long period of time a great 
 many observations in which clinically we got a very big liver and post 
 mortem you got only passive congestion, no enlargement. Are 
 the anatomical conditions such that you can easily imagine a liver 
 greatly engorged in life and collapsing after death? | 
 
 Dr. RicHArRDSON: Yes, to a certain extent, but not so marked as 
 in this case. 
 
 Dr. Casot: Have you ever tried the experiment of injecting 
 the liver to see if it can be made to reach this size? 
 
 Dr. RicHARDSON: No. 
 
 Dr. Casort: It is always in this type of case that these discrepan- 
 cies come. They do not come in leukemia, where we have a tough 
 firm liver. It is always in the circulatory cases that we differ from 
 the post-mortem findings. 
 
 Dr. RicHarpson: The diaphragm on the right was at the fifth 
 rib, on the left at the fifth interspace. That is about right, although 
 with these levels the pleural cavities were full of fluid,—hydrothorax. 
 The pleura was coated with fibrinous exudate in places, and the lungs 
 showed here and there small focal areas of frank pneumonia, other- 
 wise some congestion. 
 
 There was moderate hydropericardium. The heart weighed 740 
 grams. ‘That is a pretty large heart. The myocardium was pale, 
 opaque. Some question was raised at the time about the myocar- 
 dium. We madea histological examination. There was no increase 
 of interstitial tissue, but a note was made that the individual fibers 
 seemed to be enlarged. The cavities were increased in size. The mitral 
 valve measured twelve cm., the aortic eight, the tricuspid thirteen 
 and a half. But there were no lesions of the valves, nothing within 
 the heart to account for its size. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 463 
 
 The aorta was fairly smooth; no definite amount of arteriosclero- 
 sis except that in the renal arteries there was some, not very marked. 
 I mean by that, the artery that runs from the aorta to the kidney and 
 the first branches where it breaks up into kidney substance. As a 
 matter of fact we found later that there was considerable sclerosis 
 of the arteries in the: kidney substance. 
 
 The liver weighed 2190 grams. That is a large liver, but still 
 only three fingers down. The tissue was slightly doughy and cin- 
 namon brown in color. 
 
 The spleen weighed 240 grams, slightly soft, the follicles and 
 trabeculae visible; some congestion and some softness from the infec- 
 tion present, a streptococcus septicemia. 
 
 The combined weight of the kidneys was 200 grams. That is 
 740 grams of heart against 200 grams of kidney. Even with small 
 kidneys that is a markedly hypertrophied heart. The question from 
 the anatomical standpoint is raised whether there may have been an 
 earlier “essential”? hypertension. The capsules came off fairly easily, 
 leaving granular surfaces generally. The tissue was tough, the mark- 
 ings indistinct, the cortex varying from two to four mm., the cut ends 
 of the vessels prominent. On the whole, macroscopically an arterio- 
 sclerotic nephritis, and the histological examination bore that out. 
 There was no evidence of any glomerulonephritis. 
 
 The gastro-intestinal tract showed a velvety mucosa, dull red- 
 dish, juicy,—passive congestion. 
 
 Case 3971 
 
 An Irish stationary engineer of sixty-four entered July 28. Two 
 days before admission he was seized with acute pain in the epigas- 
 trium. He was nauseated, and after a while began to vomit a green 
 watery fluid. He continued to vomit frequently all the next day. 
 The pain became localized in the right lower quadrant. He had no 
 appetite, and no movement of the bowels in spite of five soap-suds 
 enemata. During the day his abdomen became slightly distended 
 and ‘“‘sore all over.”” The morning of admission he awoke feeling 
 nauseated, but did not vomit. He had never had a similar attack. 
 
 Upon examination he was well nourished. The lungs were 
 normal. The heart was moderately enlarged to percussion. The 
 aortic second sound was accentuated. A systolic murmur was heard 
 at the apex, a systolic and a diastolic at the base. The radial arteries 
 were palpable, the brachials tortuous. The systolic blood pressure 
 was 174, the diastolic 122. The abdomen was somewhat distended, 
 
464 FACTS ON THE HEART 
 
 very tympanitic, with questionable shifting dullness; no liver tym- 
 pany. The right side of the abdomen was spastic. There was slight 
 tenderness throughout, decidedly more marked in the right lower 
 quadrant. The genitals and extremities were negative. The rectum 
 was ballooned, the prostate slightly enlarged. The pupillary reac- 
 tions and the other reflexes were normal. 
 
 Before operation the temperature was 99.6°, the pulse 85; the 
 respirations are not recorded. The leucocyte count was 18,000. 
 No specimen of urine could be obtained. 
 
 Operation was done at once. The abdomen was found filled with 
 a large amount of dark, old blood, mostly liquid. The appendix was 
 normal. Stones were felt in the gall-bladder, but the gall-bladder 
 felt normal. The condition of the pancreas could not be definitely 
 determined, but was thought to be the cause of tne trouble. 
 There was no evidence of obstruction, malignant disease, or active 
 hemorrhage. 
 
 The patient returned to the ward apparently little worse for the 
 operation. Considerable staining persisted; also draining of bile. 
 July 30 there was more distension. No peristalsis was heard with the 
 stethoscope. The patient grew rapidly worse and died that day. 
 
 Clinical Diagnosis (from Hospital Record) —Acute pancreatitis. 
 
 Dr. Hugh Cabot’s Diagnosis —Mesenteric thrombosis? 
 
 Acute hemorrhagic pancreatitis? 
 
 Intestinal obstruction? 
 
 Arteriosclerosis. 
 Cholelithiasis. 
 Cholecystitis with necrosis 
 Anatomical Diagnosis.—1. Pri- and perforation of the blad- 
 mary fatal lesions. der wall. 
 
 Hemorrhages into the gall- 
 bladder and the peritoneal 
 cavity. 
 
 Acute peritonitis. 
 
 Arteriosclerosis. 
 
 2. Secondary or terminal lesions. ;Hypertrophy and dilatation 
 
 of the heart. 
 
 Hemorrhagic edema of the 
 lungs. 
 
 [Slight scoliosis. 
 
 Operation wound, explora- 
 tory laparotomy. 
 
 ————_____, 
 
 3. Historical landmarks. 
 
a? 
 
 HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 465 
 
 The heart weighed 520 grams. The myocardium was pale brown- 
 red and of fair consistence. ‘The right ventricle wall was 3 mm. thick, 
 the left ventricle wall 11 mm. 
 
 Here is a case of purely latent or inactive hypertrophy and 
 dilatation of the heart, with hypertension probably chronic. Wehave 
 no evidence that the heart was even a minor contributary factor in 
 his death. 
 
 Autopsy 3034 
 
 An English blacksmith of fifty-four entered March 18. Except 
 for the diseases of childhood the patient had been well until the pres- 
 ent illness. His wife had had one miscarriage and lost one child an 
 hour after birth. For a year he had noticed occasional dyspnea on 
 heavy exertion. The attacks seemed to be related to cold, disagree- 
 able weather. For two months he had had increase of dyspnea on 
 exertion and excitement. Walking up hill or in the face of the wind 
 seemed to affect him more than heavy work. He had some palpita- 
 tion and slight dry cough, occasionally at night raising white phlegm. 
 Within two weeks he had had to increase to two pillows. He stopped 
 work May 8 on account of dyspnea. He had made little or no 
 improvement, had lost appetite, and had epigastric distress relieved 
 by considerable eructations of gas. 
 
 Examination showed a well nourished, strong man. The mucosae 
 were slightly cyanotic. The teeth were decayed. There was 
 marked pyorrhea. The apex impulse of the heart was faintly felt in 
 the fifth space 11 cm. to the left of midsternum and a centimeter and 
 a half outside the nipple line, coinciding with the left border of dull- 
 ness. The right border was 3 cm, to the nght of midsternum. 
 
 - The action was occasionally irregular. There was a strong sugges- 
 
 tion of gallop rhythm, and occasional reduplication of the second 
 
 sounds at the base. The sounds were distant and varied in intensity. 
 
 The pulmonic second sound was accentuated. A soft systolic mur- 
 mur was heard over the lower precordia; transmitted to the axilla. 
 The pulses were of poor volume and fair tension. The vessel walls 
 were slightly thickened. The blood pressure was 115/95; 130(?)/95. 
 There was prominence of the second ribs and upper sternum, with 
 moderate lower sternal retraction. There was dull tympanitic reso- 
 nance throughout, except at the right base posteriorly and in the 
 right axilla, where it shaded off into dullness. Expiration through- 
 out was prolonged and roughened. There were occasional rales 
 
 throughout at the end of inspiration, a few moist sticky rales at the 
 
 30 
 
466 FACTS ON THE HEART 
 
 right base with both inspiration and expiration. The abdomen was 
 held slightly rigid, especially in the epigastrium, where there was 
 some protuberance, with dull tympany. The liver dullness extended 
 from the fifth rib to 1.5 cm. below the costal margin. The edge was 
 not felt. The genitals were normal except for a small right varico- 
 cele. ‘There was moderate edema of both upper and lower legs, very 
 little at the ankles or over the feet. The pupils were irregular, other- 
 wise normal, as were the reflexes. ) 
 
 The temperature was 95.3° to 98° until March 3, then rising 
 rapidly to 105.8°.. The pulse was 88 to 120. The respirations were 
 20 to 48; until March 3 not remarkable. The output of urine was 
 3 to 28 ounces, the specific gravity 1.026-1.030. ‘There was a slight 
 trace of albumin at the last of five examinations, the slightest possi- 
 ble trace of bile, leucocytes and hyalin and granular casts at the last 
 two. The hemoglobin was 75%, the leucocyte count 19,600- 
 8000-27,600, the polynuclears 74%. A Wassermann was negative. 
 The fundi were normal. 
 
 March 21 the edema was gone, but the patient still felt very weak 
 and ill. Digipuratum was not well borne; the heart became more 
 irregular, the stomach upset. After three days the digitalis was 
 omitted. A surgical consultant declined to make a diagnosis, but 
 agreed to operate if the condition warranted it later. March 30 
 the left border of dullness was four centimeters outside the nipple. 
 The patient had occasional attacks of great weakness, precordial 
 distress, belching of gas and labored breathing lasting five to thirty 
 minutes, relieved by morphia or nitroglycerin. By April 3 these 
 attacks were occurring twice to four times during the twenty-four 
 hours, chiefly at night. He became jaundiced, the liver enlarged and 
 very tender. Nothing was found in the lungs. April 9 he died. 
 
 Clinical Diagnosis (from Hospital Record).—Arteriosclerosis. 
 
 Coronary sclerosis. 
 
 Myocarditis. 
 
 Decompensation. 
 
 Terminal pneumonia. 
 
 Dr. Richard C. Cabot’s Diagnosis —Arteriosclerosis. 
 
 Coronary sclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Cholangitis. 
 
 Cholecystitis. 
 
 Anatomical Diagnosis. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 467 
 
 1. Main cause of death.—Streptococcus sepsis. 
 Slight arteriosclerosis. 
 2. Secondary or terminal lesions. | Hypertrophy and dilatation 
 of the heart. 
 Chronic passive congestion, 
 general. 
 
 [Slight icterus. 
 Slight chronic perihepatitis 
 and splenitis. 
 
 3. Historical landmarks. Chronic pleuritis. 
 
 Meckel’s diverticulum. 
 Horseshoe kidney. 
 
 The heart weighed 699 grams. The organ was considerably 
 enlarged and the chambers were distended with blood clot. On 
 section the myocardium generally was rather lax, pale brownish red 
 and slightly cloudy. In the region of the upper part of the posterior 
 wall of the left ventricle Bok were two areas of eh wee one of 
 which measured 314 by 114 cm. and the other 4 by 214 cm., which 
 showed through the een In ue posterior oa ef, the right 
 ventricle there was an area about 214 by 114 cm. similar to the 
 others. These areas showed in their “eas portions a narrow 
 irregular dirty pinkish brownish yellow margin with pale brownish 
 yellow central portions. 
 
 The kidney structure appeared normal. 
 
 Note by Dr. Cabot.—In view of the anatomical findings, his chronic 
 dyspnea probably depends on hypertension and its results. The 
 amount of arteriosclerosis present does not account for so much 
 hypertrophy and weakening of the heart. The icterus is probably 
 to be explained as a manifestation of septicemia. The surgical 
 consultant showed good judgment in refusing to operate. 
 
 Necropsy 3865 
 
 [The following case though not one of hypertensive heart disease 
 is included here because I do not know where else to put it. The 
 enlarged heart certainly seemed a factor in bringing about the 
 patient’s death. It was not enlarged by mechanical obstruction or 
 leak. The blood pressure was low throughout his illness. The case 
 presents a challenging problem.| 
 
 An American teamster of thirty-two entered June 14, 1913, 
 five years before his final] admission, for relief of vomiting, anorexia, 
 weakness and dyspnea. He had had gonorrhea at fourteen. At 
 twenty-eight he was ill two weeks with “typhoid malaria.”’ For 
 
the past two or three years he had had stomach trouble with occa- 
 sional vomiting and diarrhea. He became pale and yellowish. His 
 stools were sometimes black. Six weeks before admission he began 
 to have stomach trouble, vomited nearly every day, and had sore 
 gums, dizziness and palpitation. He grew pale and weak, lost about 
 forty pounds in weight, and at entrance was unable to walk fifty feet. 
 
 Examination showed a very pale man. The heart sounds were 
 irregular and rapid. There was a loud blowing systolic murmur 
 over the pulmonic area, not SENSED Se 
 
 The temperature was 99° to 102.2° for the first four weeks, then 
 normal. The pulse was 80to120. Therespirations are not recorded. 
 The hemoglobin was 10% to 65%, the leucocytes 4500 to 8800, the 
 polynuclears 49% to 60%, the reds 700,000 to 1,700,000. The smear 
 showed great variation in size, shape and staining, much stippling 
 and polychromatophilia. The platelets were rare. 
 
 The patient made marked improvement while taking Fowler’s 
 solution, gained thirty-two pounds in weight, and was discharged 
 relieved August 3. . 
 
 After leaving the hospital he felt much better for four weeks. 
 From September to December and from March to July he had had 
 attacks similar to the previous ones. The following autumn he 
 grew progressively weaker and more dyspneic. 
 
 December 21, 1914, he returned. During his stay in the hospital 
 he grew progressively worse. January 5 he was transfused with 
 600 c.c. of blood. Splenectomy was done, with uneventful recovery. 
 The red count was 2,300,000 at entrance, 1,700,000 at discharge. 
 
 After leaving the hospital he felt well until May; then he was 
 weak and vomited until August, when he began to improve. In 
 December he went to work in a shop, weighing 206 pounds, his best 
 weight. After six weeks he again began to lose weight and strength. 
 May 28 he had fainting attacks, with a burning sensation in his chest, 
 lasting about fifteen minutes. June 1, 1916, hereentered the hospital. 
 
 June 11 he received 600 c.c. of blood by transfusion. For the 
 next three days he suffered from hallucinations, and while demented 
 tried to injure a neighbor and to kill himself. 
 
 The hemoglobin rose from 12% at entrance to 56 % at discharge. 
 The leucocyte count was 4000 to 16,200. The reds were 792,000 to 
 2,128,000. The smear at entrance showed marked achromia, poly- 
 chromatophilia, 3 normoblasts and one megaloblast in too cells. 
 The platelets were much decreased. At discharge, June 18, there 
 was tendency to macrocytosis of reds. No blasts were seen. 
 
 468 FACTS ON THE HEART 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES ‘469 
 
 After leaving the hospital he gained a pound a day for twenty 
 days. He worked out-cf-doors during the summer. Four weeks 
 before readmission he began to grow weaker and had a great deal of 
 gas from the stomach. At readmission, October 16, 1916, he could 
 barely walk. 
 
 During his stay in the ward he continued to fail until October 11, 
 when transfusion was done. October 29 a second transfusion was 
 done. The second seemed to have a little effect, but the bone mar- 
 row did not respond as on previous occasions. The reds rose from 
 1,228,000 to 1,628,000 at discharge, the hemoglobin from 34% to 
 35% at discharge, the leucocytes from 7400 to 6600 at discharge. 
 The smear showed seven blasts per too cells. November 5 he was 
 discharged. 
 
 For two weeks after leaving the hospital he felt well. Then he 
 had severe gas pain for four or five hours every day without much 
 relation to meals. In the late autumn he felt very weak and had 
 increasing numbness of the hands and feet. December 8 he was 
 hysterical. December g he entered the hospital for the fifth time. 
 
 At entrance the hemoglobin was 20%, the leucocytes 3600, the 
 reds 1,200,000. ‘Transfusion of 600 c.c. was done December 21. 
 At discharge December 24 the hemoglobin was 33%, leucocytes 
 8400, reds 1,500,000. The smear at entrance showed marked 
 variation in size and shape, moderate numbers of Jolly bodies, two 
 blasts; at discharge there was more stippling, Jolly bodies increased, , 
 polychromatophilia, five blasts. 
 
 March 6, 1917, he entered a sixth time, having felt fairly well 
 and gained ten pounds since his discharge. Ten days before read- 
 mission he began to fail rapidly, to have much flatulence and dyspnea 
 and to be very weak. 
 
 March 3 transfusion of 600 c.c. of blood was done. He was dis- 
 charged relieved March rt. 
 
 September 11, 1918, he came to the Emergency Ward to be trans- 
 fused, very pale and in a state of collapse. He died before he reached . 
 the ward. 
 
 Discussion by Richard C. Cabot.—The history of the first entry 
 gives undoubtedly a diagnosis of pernicious anemia. It isa clear and 
 typical history. The remarkable thing about it is that the signs 
 of pernicious anemi€appeared about seven years before his death. 
 That is a longer course than most of the cases run. The intermission 
 between the first and second entries is a little more than usual. 
 There is no question, however, about the diagnosis. The post- 
 
470 FACTS ON THE HEART 
 
 mortem examination ought to show fatty degeneration of the organs, 
 a slightly enlarged heart, very possibly fatty degeneration in it, and 
 hyperplastic marrow. 
 
 Clinical Diagnosis (from Hospital Record).—Pernicious anemia. 
 
 Dr. Richard C. Cabot’s Diagnosis —Pernicious anemia. 
 
 Fatty degeneration of the organs. 
 
 Slight hypertrophy and dilatation of the heart. 
 
 Possibly fatty degeneration of the heart. 
 
 Hyperplastic bone marrow. 
 
 Anatomical Diagnosis —1. Pri- 
 
 mary fatal lesion. Pernicious anemia. 
 Hyperplasia of the bone mar- 
 row. 
 Fatty degeneration of the 
 myocardium. 
 
 Hypertrophy and dilatation 
 | of the heart. 
 
 Edema of the lungs. 
 
 Slight hydropericardium. 
 Very slight hydrothorax. 
 ites slight anasarca. 
 
 [Scar of old operation wound, 
 | splenectomy. 
 
 | Slight chronic pleuritis, left. — 
 hrniesians of the liver. 
 
 Dr. RicHARDSON: A point which has been brought out at this - 
 necropsy table for some years is the association of hypertrophy and 
 dilatation of the heart with pernicious anemia. Here we havea very 
 remarkable instance. The heart weighed 710 grams. The aorta, 
 its great branches and the valves were negative, and there was 
 nothing in the kidneys to account for the marked hypertrophy of 
 the heart. ‘The myocardium showed well marked fatty degeneration, © 
 -but no evidence of myocarditis. This was the largest heart I have 
 ever seen associated with pernicious anemia, and with no other 
 basis of hypertrophy. 
 
 The kidneys were large, weighing 532 grams (normally 200-400), 
 with a wide cortex; but microscopically they showed nothing 
 remarkable. 
 
 The hyperplastic marrow was typical of this disease,—meaty, 
 dark raspberry red, and the microscopical examination showed 
 numerous megaloblasts. 
 
 2. Secondary or termina! lesions, 
 
 3. Historical landmarks. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 471 
 
 The hydropericardium, hydrothorax and anasarca indicate that 
 the heart had become a little decompensated. 
 
 The lesions as tabulated in the anatomical diagnosis present a 
 typical anatomical picture of pernicious anemia. 
 
 Dr. CaBot: We had more hope in the combination of splenec- 
 tomy and transfusion four or five years ago than we havenow. After 
 splenectomy the transfusion holds them a little longer than if trans- 
 fusion were done without splenectomy. If there is some one at hand 
 who is accustomed to doing splenectomy, it does not add any consid- 
 erable risk to have it done. My feeling is that if I had pernicious 
 anemia I should have my spleen taken out, although it would not 
 be brilliant therapeutics. I do not believe this man would have 
 lived so long if he had not had splenectomy. | | 
 
 This man’s age is a notable fact. The average age for pernicious 
 anemia is between forty and fifty; rarely anywhere near thirty. 
 
 It is a fact of some interest that we have almost never made a 
 wrong diagnosis of this disease in this hospital. Some years ago I 
 figured up the percentage of failure in diagnosis here,“ from 16 % of 
 right diagnoses in acute nephritis up to practically 100% of right 
 diagnoses in this disease, in typhoid fever (92%) and diabetes (95%). 
 That is of importance. We ought to realize just where we are strong | 
 and where we are weak. | 
 
 A PuysicIAN: How about splenectomy in cases of leukemia? 
 
 Dr. Casort: I do not see the benefit of splenectomy in leukemia; 
 at least up to date I do not know ofany. Iregret that the operation 
 has been popularized by the example of the Mayo clinic. 
 
 Necropsy 3845 
 
 An American tanner of fifty-eight entered May 17 for relief of 
 dyspnea and palpitation. His father died of heart trouble, his 
 mother of kidney trouble. He had all the diseases of childhood, 
 including scarlet fever and diphtheria. He had occasional attacks 
 of sick headache when a boy. He had gonorrhea at twenty-one and 
 again at twenty-two. He denied syphilis. His wife had four or 
 five miscarriages before the birth of two children who were living and 
 well. His general health had been excellent until the present illness. 
 He had been on a good many drinking parties, but never was a steady 
 heavy drinker. He smoked a great deal until the present illness, 
 and chewed one plug a day, He drank more than a gallon of coffee 
 
 *R. C, Cabot, Diagnostic Pitfalls Identified During A Study of 3000 Autopsies. 
 Jour. Am. Med. Assoc., Dec. 28, 1912, Vol. LIX, pp. 2295-2208. 
 
472 FACTS ON THE HEART 
 
 a day until a year before admission. For a year he had taken none. 
 Until the present illness he used a great deal of salt. 
 
 A year and a half before admission he began to feel his heart 
 beating, and was short of breath on any exertion. These symptoms 
 gradually grew worse, and forced him a year ago to give up his work. 
 For a year he had urinated two or three times at night. For the same 
 period he had been taking digitalis in various amounts. Exertion 
 brought on occasional attacks of shortness of breath with some dizzi- 
 ness. With them was some pain in the stomach region, not severe. 
 These attacks became more frequent until they sometimes came on 
 without exertion. In the intervals the dyspnea and palpitation grew 
 gradually worse. At times he noticed some puffiness about the eyes. 
 Six months before admission he suddenly began to have blurring in 
 front of the right eye. Since that time he had been on a low-protein 
 salt-free diet and had taken an occasional purge. His condition how- 
 ever grew gradually worse. His weight two years ago was 240 
 pounds; six months ago, 170 pounds. 
 
 . Examination showed a fairly well nourished man with slight 
 exophthalmos. The skin was dry. There was much pyorrhea with 
 sordes. The apex impulse of the heart was felt in the sixth space 15 
 cm. to the left of midsternum and 6.5 cm. outside the nipple line, coin- 
 ciding with the left border of dullness. The right border was one cm, 
 to the right, the supracardiac dullness 5 cm. ‘There was no shift 
 in the left lateral position. The action was irregular, with occasiona] 
 premature beats. The sounds were of good quality. Both the pul- 
 monic and the aortic second sounds were loud and ringing, the pul- 
 monic accentuated. There was a blowing systolic murmur at the 
 apex and a systolic at the base. The artery walls were markedly 
 palpable, the brachials very tortuous. The lungs, abdomen genitals, 
 extremities, pupils and reflexes were normal. 
 
 The temperature was 96.8° to 99.6° until June 19. The pulse 
 was 100 to 59, the respiration 15 to 26. The systolic blood pressure 
 was 200 to 230, the diastolic 100 to 140. The output of urine was 
 23 to 63 J till June 17, the specific gravity 1.006 to1.o14. The urine 
 was cloudy, alkaline at one of three examinations, with a trace to a 
 slight trace of albumin at all, rare granular casts at one, leucocytes at 
 two. The renal function on May 20 was zero; May 22, it was 5%. 
 The hemoglobin was 75%, the leucocyte count 5200 to 11,000, 
 the polynuclears 88%. The urea nitrogen was 57 to 153 mgm. per 
 too c.c. of blood. A Wassermann test was negative. The fundi 
 showed well marked retinitis of the right eye with a few retinal hemor- 
 
 T 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES ATS 
 
 rhages, and star-shaped arrangement in the macular region. The 
 left eye showed a few hemorrhages. 
 
 The dyspnea became much less. May 25 the patient was up ina 
 chair. After this however he was troubled with nausea and vomiting 
 and a “‘bad taste.” There was considerable improvement after a 
 sweat bath. Then he became weak and tired and had occasional 
 nausea and vomiting. His mentality became cloudy. He was 
 delirious at night. His eyes looked staring. His breath was ammo- 
 niacal. June 19 the temperature dropped to 93.3°, the pulse to 60. 
 He became practically comatose and bled profusely from the nose 
 and mouth and beneath the finger nails. June 21 he died. 
 
 Clinical Diagnosis (from Hospital Record) —Chronic nephritis. 
 
 Arteriosclerosis. 
 
 Uremia. 
 
 Dr. W. H. Smith’s Diagnosis —Chronic nephritis. 
 
 Uremia. 
 
 Anatomical Diagnosis. —Arteriosclerosis of the aorta and its great 
 branches. 
 
 Arteriosclerosis of the vessels of Willis. 
 
 Arteriosclerotic nephritis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Edema piae. 
 
 Slight chronic pleuritis, right. 
 
 Obsolete tuberculosis of a bronchial lymph node. 
 
 Papillary adenoma of the right kidney. 
 
 Dr. Oscar RicHarpson: The background was one of arteriosclero- 
 sis. The heart weighed 625 grams (normally 200-300). The myo- 
 cardium was generally thick, and at the time of necropsy the cavitiés 
 showed considerable dilatation. The valves were negative. .The 
 coronary arteries showed a rather peculiarly arranged sclerosis. At 
 first they seemed to be fairly capacious and free, but rather tortuous. 
 On laying them open fibrous plaques were found scattered along the 
 walls, then a piece which was fairly good, then plaques again. This 
 peculiar arrangement caused tortuosity of the vessel without marked 
 decrease in its lumen. The aorta and the great branches were capa- 
 cious and showed marked fibrous, fibrocalcareous and atheromatous 
 sclerosis. ‘The vessels of Willis and their remote branches showed 
 marked arteriosclerosis. 
 
 The kidneys weighed 160 grams. ‘Those, of course, were very 
 small organs. (Normally 200-400 grams.) ‘The capsules were 
 slightly adherent in places and the surfaces were finely granular and 
 
474 FACTS ON THE HEART 
 
 red. The kidney tissue was tough, the markings more or less indis- 
 tinct, and there was decrease in the width of the cortex. Here and 
 there in the section surfaces the cut ends of the arteries showed scler- 
 osis. In the pelvis of the kidney the mucosa in a few places showed 
 small dark red hemorrhagic areas;—a small arteriosclerotic kidney. 
 It is in this type of nephritis that you are likely to get blood in the 
 
 urine. 
 Case 4327 
 
 An American carpenter of forty-two entered March 27, 1922, 
 complaining of difficulty in breathing of two months’ duration. 
 
 He had measles, mumps and chicken-pox in childhood, “typhoid 
 fever and pneumonia” at sixteen, prolonged attacks of rheumatic 
 fever at eleven years, nineteen and thirty-one. He had always uri- 
 nated twice atnight. Hehad sick headaches until he was twenty-two. 
 A years before admission he had a severe electric shock and was in 
 bed ten days with symptoms like those of the present illness. Best 
 weight 220 pounds, weight last September 195, present weight, 176. 
 
 on 
 }Q 
 E 
 
 ] 
 | 
 
 Midsternal 
 Nipple 
 
 w 
 ie) 
 5 
 
 TO.Cinee* fa -cna: 
 
 EIGo2: 
 
 Two months before admission, after excessive work in cranking an 
 automobile followed by a supper of oysters, he had dyspnea, somewhat 
 relieved by lying on the right side and using two pillows. He also 
 had palpitation and eructations of gas. During the following week 
 he had dyspnea on exertion and at night, with gas, distress and disten- 
 sion after eating. When he milked his two cows he had sudden 
 attacks of sharp pain with a sense of a heavy pressure across the front 
 of the chest radiating down the right arm, and a choking sensation 
 lasting half an hour and associated with dyspnea. After ten days of 
 complete remission he again ate oysters and had the same trouble as 
 before. The symptoms had persisted except for periods of two or 
 three days once a week. Three times he had had nausea and vomit- 
 ing at night. He had had hacking cough at night. For five weeks 
 he had been taking twelve digitalis pills a week. He had also taken 
 an average of three nitroglycerin tablets a day swallowed with water 
 for attacks of sharp pain in the chest and right arm. The pain was 
 relieved within half an hour. For three weeks he had been in bed. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 475 
 
 For two weeks he had had an external hemorrhoid. Three days 
 before admission he had a sudden onset of dull aching in the right 
 side of the head. The left side of the head and neck and the left 
 arm and leg became numb. His speech was mumbling, his jaw 
 sagged, and his pupils were dilated. He was able to move all his 
 muscles, though his limbs felt very heavy. In six hours this passed 
 off entirely except for the numbness under the right arm, which lasted 
 several hours longer. He had no edema. 
 
 Physical examination showed him to be well nourished. Cheeks 
 very high colored. Skin dry. Mucosae red. Tongue showed two 
 serpiginous white lines on the left edge. Apex impulse of the heart 
 
 i 
 
 Fic. 93.—Necropsy 4327. Hypertrophy and dilatation of the heart, primary. 
 Weight 703 grams. Mural thrombi in the right auricular appendix and the left ven- 
 tricle. X-ray shows the heart shadow very much enlarged, especially to the left. 
 Region of the right auricle also somewhat prominent. Enlargement appears somewhat 
 symmetrical and is more suggetive of dilatation than of hypertrophy. Supracardiac 
 shadow not abnormal. *(Roentgenological Department, Massachusetts General 
 Hospital.) 
 
 felt in the 5th space g cm. to the left. Percussion measurements as 
 shown in the diagram. Action regular, with very rare extra systoles. 
 P, slightly accentuated. No murmurs made out after slight exercise. 
 Pulses and arteries normal. B.P. 100/70—110/80-105/85. Electro- 
 cardiogram showed sinoauricular tachycardia. Rate tro. Small 
 complexes in all leads. P wave bifurcated and wide. Diphasic T. 
 Abdomen and genitals negative. Inguinal rings enlarged. Rectal 
 
476 FACTS ON THE HEART 
 
 examination: Dilated thrombosed external hemorrhoid. Extrem- 
 ites, pupils and reflexes showed nothing of significance. 
 
 Temperature. 96.4°—-98.9° until March 30, then 98.9°— 101.9° 
 rectal to April 6; afterwards 97.4°-100.9. Pulse, 89-120. Res- | 
 piration, 20-36. Urine: 312-28-6 in 24 hours. Sp. gr. 1034- 
 1030. Cloudy at one of three examinations, alkaline at.two, the 
 slightest possible trace to a slight trace of albumin at all. Renal 
 function 30%-50%. Blood: Hemoglobin 80%. Leucocytes 23,400— 
 12,000. Polynuclears 66%. Reds and platelets normal. Wasser- 
 mann negative. Non-protein nitrogen 33-40. mgm. Sputum 
 blood-streaked. Few organisms. X-ray, see Fig. 93. 
 
 When the patient was asleep the breathing was Cheyne-Stokes 
 with apneic periods of from five to fifteen seconds. At midnight 
 the night of admission he complained of very severe pain in the left 
 leg from the knee down. It was instantly relieved by sodium bicar- 
 bonate. Dr. Paul D. White found proto-diastolic gallop rhythm, 
 mitral facies, prominence of the left auricle by percussion, occasional 
 premature beats. ‘‘In the presence of the weak heart action there is 
 no mitral diastolic murmur evident to-day. The first sound has a 
 rumbling character.” 
 
 By the 31st the patient had difficulty in breathing during the day 
 and looked very ill. The morning of April 1 he fainted on slight 
 exertion. He was put on the “dangerous” list. The high leucocyte 
 count was unexplained. April 3 Dr. W. H. Smith found a suggestive 
 Broadbent. The right leg was markedly swollen, hot and painful, 
 the tenderness over the deep veins extending up to midthigh. April 
 6 the temperature was normal, but the next day rose again to 99.9. 
 The heart sounds were weaker. ‘The mental factor was very large. 
 He had prompt relief from bicarbonate of soda, which he thought 
 was morphia; no benefit from codein dissolved in milk. April to he 
 was very ill. There was gallop rhythm with a probable diastolic 
 rumble. That day he fell over, striking his head. He became 
 extremely cyanotic and the left arm seemed weak. His accounts 
 showed that he did not lose consciousness, and it was believed 
 that he complained largely to obtain sympathy. April 12 he had 
 to be catheterized because of edema interfering with micturition. 
 April 14 he suddenly died. 
 
 Clinical Diagnosis —Mitral stenosis. 
 
 Myocarditis. 
 
 Phlebitis of right popliteal. 
 
 Edema of the foreskin. 
 
—S 
 
 HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 477 
 
 Acute endocarditis. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Chronic adhesive pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Acute endocarditis? 
 
 Passive congestion, general. 
 
 Anatomical Diagnosis —Hypertrophy and dilatation of the heart. 
 
 Mural thrombi in the right auricular appendix and the left 
 ventricle. 
 
 Infarcts of the lungs. 
 
 Infarct of the left kidney. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, right. 
 
 Slight ascites. 
 
 Anasarca. 
 
 Chronic pleuritis, left. 
 
 Small mass of persistent thymic tissue. 
 
 Dr. OscaR RICHARDSON: We were not permitted to examine the 
 head. The face and ears were dusky to purplish, the skin generally 
 sallow with a faint yellowish tinge,—an appearance suggesting the 
 end conditions of heart cases. The dependent portions of the trunk 
 pitted, and the lower extremities were swollen and pitted on pressure. 
 
 There were 500 c.c. of fluid in the peritoneal cavity—slight ascites. 
 The gastro-intestinal tract was negative except for an astonishingly 
 good picture of chronic passive congestion. That is, all the mucous 
 membranes were dark red, velvety, oozing bloody fluid. The glands 
 were negative. The liver was 15 cm. below the costal border. The 
 diaphragm was at the sixth rib on the right and the sixth interspace 
 on the left. That means something in the pleural ‘cavities. We 
 found 2000 c.c. of fluid in the right cavity, and on the left about 50 
 c.c. There was a little fibrous pleuritis on the right, on the left a few 
 old adhesions. There was a bit of the thymus gland remaining. 
 There was nothing in the lungs except chronic passive congestion and 
 infarcts. That means of course that although there was chronic 
 passive congestion we should still look to see if we could find any 
 vessels plugged. 
 
 The pericardium contained 50 c.c. of fluid, and was smooth and 
 shining. The heart weighed 703 grams,— a very large heart. The 
 myocardium was of pretty good consistence, fair color, and I could 
 make out no definite myocarditis whatsoever. The cavities were 
 all markedly dilated and all contained a large amount of blood. If 
 that indicates anything, he died in diastole. In the right auricular 
 
478 FACTS ON THE HEART 
 
 appendix there were small thrombotic masses which with the condi- 
 tion of chronic passive congestion and emboli from them produced 
 the infarcts in the lungs. In the apical region of the left ventricle 
 there was a small adhering thrombotic mass. 
 
 The mitral valve measured 15 cm. ‘There were no definite lesions. 
 The aortic was 7 cm., the cusps 8 cm. ‘That means the ring where it 
 is attached to the lower end of the aorta,—what is called the aortic 
 ring. A peculiarity was that there were only two large cusps to the 
 aortic valve; there are usually three. In the regions of the conjoined 
 margins these two cusps presented a little roll of fibrous tissue which 
 might be a little fibrous endocarditis, small, chronic, only one cm. 
 long, two or three mm. in the other dimensions. The tricuspid 
 valve measured 16 cm. The mitral circumference was nearly as 
 large as the tricuspid. The pulmonic was 9 cm. The coronaries 
 were fairly capacious, free, negative. ‘The foramen ovale was closed. 
 The mitral and tricuspid valves except for great increase in their cir- 
 cumferences, were negative. 
 
 The ascending thoracic portion of the aorta showed a few small 
 fibrous plaques, the arch and descending portion a slight amount of 
 fibrosis. ‘The aorta and great branches on the whole were rather 
 small for the size of the man. That was the only thing about this 
 apparatus worth noting. 
 
 The liver weighed 2110 grams and showed typical nutmeg mark- 
 ings. The gall-bladder, pancreas and ducts were negative. The 
 spleen showed chronic passive congestion. The kidneys weighed 390 
 grams, were bluish-brown-red, large, and showed here and there one 
 or two infarcts. These were due of course to emboli from the throm- 
 botic mass in the left ventricle. 
 
 We put hypertrophy and dilatation of the heart first this time. 
 Presumably the condition in his leg was due to a bit split off from the 
 thrombus in the left ventricle passing into the vessels of the leg. 
 
 This heart was one of those to which we give the name of idio- 
 pathic hypertrophy. It is an extraordinarily good case,—a heart of 
 seven hundred odd grams giving out with no definite cause. 
 
 Dr. Casort: I was obviously wrong in supposing pericarditis as 
 the cause of heart hypertrophy. We found no cause. The valves 
 were all big but normal. They were part of the hypertrophy and 
 dilatation. We have no idea why this heart gave out. It does not 
 come into any of the classifications. Of course he may have had a 
 hypertension. It does not show in the arteries, does not show any- 
 where. ‘There was no evidence of it while he was here. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 479 
 
 Dr. RicHARDSON: He had a low blood pressure. 
 
 Dr. Casot: While here. We should have to say it was high 
 before he came here. 
 
 A PuysictaAn: What was the cause of the liver? 
 
 Dr. RrcHARDSON: It was due to the chronic passive congestion, 
 which was very great all the way through. [The assumption that 
 hypertension had existed before this patient was examined may be 
 false. Ifso the cause of cardiac enlargement and failure is a mystery. | 
 
 Case 3742 
 
 First entry. An American schoolboy of sixteen entered March 5, 
 two years before his final admission. 
 
 His mother died of Bright’s disease. 
 
 He had had mumps and a fracture of the left thigh at the age of six. 
 
 A week ago he began to have involuntary purposeless movements 
 of all his muscles, growing rapidly more violent. 
 
 He was well nourished. Restless, moving his head about occasion- 
 ally and making frequent grimaces and purposeless movements of the 
 body, arms, and hands; only slight movements of the legs and feet. 
 Breathing irregular. Small reddish scaling area on left side of the 
 lower jaw. Small palpable gland on right lower jaw. Glands the 
 size of peas in axillae. Palpable glandsin groins. Apex impulse of 
 heart seen and felt in 5th space 10 cm. to the left of midsternal line, 
 2 cm. outside the nipple line, corresponding with the left border of 
 dullness. Right border of dullness 3 cm. to the right of midsternal 
 line in 4th space. Slight palpable thrill at the apex. Action slightly 
 rapid. At apex first sound loud, sharp and reduplicated. With it 
 was heard a harsh low-pitched systolic murmur faintly transmitted 
 to the axilla. Much of the murmur was between the two first sounds. 
 At the base was heard a loud harsh systolic murmur slightly louder 
 in the pulmonic and transmitted to the neck. Second pulmonic 
 sound greater than the aortic and accentuated. Pulses slightly 
 rapid. Artery walls palpable. Lungs normal. Abdomen: Liver 
 dullness from 6th rib to costal margin. Edge not felt. Genitals: 
 Meatus reddened and swollen. Pupilsnormal. | Reflexes not recorded. 
 
 Temperature 97.4°—100.8°. Pulse 69-95. Respirations 18-28. 
 Urine normalamount. Sp. gr. 1013-1023. A large trace of albumin 
 to the slightest possible trace at all of six examinations. A very rare 
 red corpuscle at two. Blood: Hgb. 80%. Leucocytes 12,800—4200. 
 
 The patient threw himself about in bed, chafing his skin so that 
 it was necessary to pin his legs into a set of pillows and use a pneu- 
 
480 FACTS ON THE HEART 
 
 monia swathe on his chest and bandages on his arms. He was given 
 
 about 40 minims of Fowler’s solution daily. March 18 the loudest. 
 
 murmur at the apex was a presystolic and the first sound was no 
 longer reduplicated. A soft systolic murmur was faintly heard at 
 the apex, where a slight thrill was felt. There was a loud systolic 
 murmur at the base, loudest in the pulmonic area, transmitted to 
 theneck. Hehadafew boils. The chafing of the skin was now only 
 slight. By March 29 there were very few involuntary movements. 
 The excretion of urine was greater. The apex was 114 inches outside 
 the nipple line. ‘There were thrills and systolic and presystolic mur- 
 murs at the apex, a loud systolic murmur at the base, slightly louder 
 in the aortic area than in the pulmonic area, heard in the neck. 
 March 31 beside the murmurs of the apex a harsh systolic murmur was 
 heard at the aortic area and to a less extent at the pulmonic, trans- 
 mitted to the neck. The boils had healed, except one an inch and a 
 half in diameter on the back of the neck. Under staphylococcus 
 vaccine treatment this was practically healed by April 4. The urine 
 was almost normal, and he was quite free from twitching. April 6 
 the apex impulse was 334 inches to the left of midsternum. There 
 were definite double murmurs at the apex. That day he was 
 discharged. 
 
 Second entry. April 15, two years later, he returned. 
 
 Since leaving the hospital! he had felt absolutely well until six weeks 
 ago, when he began to vomit his breakfast. Five weeks ago his 
 face became bloated. This passed off in a week. Three weeks ago 
 he woke up so bloated that he could hardly see. In a few days his 
 legs swelled. His abdomen became distended, and at night the 
 edema came up out of his legs into his back and chest. He had 
 gained considerable weight. He had been living on milk, water and 
 other liquids. His eyes blurred at times. 
 
 Physical examination as before except as noted. No glands 
 palpable in axillae or groins. Apex impulse of heart in 5th space 
 12.5 cm. from midsternum, 2.5 cm. outside nipple line. Right border 
 4 cm. from midsternum. First sound at apex sharp and double. 
 At the apex and transmitted toward the base with increasing inten- 
 sity was a purring rough systolic murmur, loudest over the aortic 
 area, heard in the neck and axilla. A, markedly accentuated. Pulses 
 normal volume and increased tension. Abdomen full. Dullness in 
 flanks and over pubes shifting with change of position. Fluid wave. 
 - Liver dullness 5th space to costal border. Edge not felt. Genitals: 
 Penis and scrotum greatly swollen. Prepuce could not be retracted. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 481 
 
 Very marked swelling of face, arms, hands, and very great soft edema 
 of thighs and legs. Considerable edema of back and over abdominal 
 and chest walls. 
 
 Temperature 96.5°—-100°, with one rise to 1o1° May 24. Pulse 
 6o-101.. Respirations 11-31. Systolic blood pressure 135-210, 
 diastolic 100. Urine: 3 5-48. Sp. gr. ro14—1027. Smoky, cloudy 
 or turbid at all of thirty examinations. Albumin at all. Guaiac 
 questionably positive at five, red blood corpuscles at fifteen others. 
 Hyalin, granular and fatty casts. Stool: Guaiac strongly positive 
 (estimated 14-14 blood). Fundi apparently normal. 
 
 The patient sweat profusely in hot air baths and seemed to enjoy 
 them. The amount of albumin in the urine fell from 1% to .4% by 
 April 22. The edema slowly became less, though by May 4 the face 
 was still puffy and there was a thick pad of edema over the lumbar 
 region. The circumference of the abdomen was 78 cm., 7 cm. less 
 than at entrance. May 6 the temperature jumped to 100° and con- 
 tinued 99.8° for the next two days. The patient was very active 
 and delirious. Digipuratum was given. ‘The amount of urine rose 
 from 23 to 35 ounces. A little free blood now appeared in the urine 
 for the first time. It was very hard to keep the bowels moving. He 
 vomited a good deal. May 12 he was considerably better. The 
 chest showed less edema than ever before, but the amount of urine 
 was lower. The abdomen now measured 72.5 cm. He was somno- 
 lent and mentally confused. May 16 the amount of urine was 
 increased and he was much brighter. His face was more puffy, 
 perhaps because of the forcing of fluids. The twenty-four-hour 
 amount of urine remained about 3 xxx. Nevertheless he was gradu- 
 ally getting more and more edematous. Hot air baths were resumed. 
 May 24 the temperature rose to 1ror° in the morning, but was 99° by 
 night. The abdomen measured 78 cm. He gradually became more 
 somnolent. Four days later the twenty-four-hour amount had 
 fallen to 3 23. ‘There was a marked systolic murmur at the base. 
 On the 29th the abdomen was 71cm. ‘That day be became semicoma- 
 tose and quite noisy. His blood pressure rose to 210 and he seemed 
 to be going downhill. Venesection was done, 3 xvi of blood removed 
 and 400 c.c. of salt solution given intravenously. He began to rally 
 slowly. As his breathing became labored and he wheezed a good 
 deal, a tracheotomy layout was kept by hisbed. The urinary output 
 now averaged 3 20. June 5 the hot air baths were omitted because 
 they exhausted him. June 11 he vomited. June 13 the amount of 
 
 urine had jumped from § 15, where it had been for a week, to 3 30. 
 31 
 
482 FACTS ON THE HEART 
 
 The blood pressure was now 145. June 14 he vomited again. By 
 June 17 he had gained a pound and a half in ten days and seemed much 
 stronger. The blood pressure had risen to 155. The specific gravity 
 of the urine was 1016. ‘The patient was brighter than he had been 
 for weeks, but looked bloated and pasty. During the next week he 
 gained weight rapidly and his face and tongue became greatly swollen. 
 After a hot air bath June 25 he had a convulsion which was followed 
 by greatly increased respiration accompanied by loud stertorous 
 dyspnea. He was unconscious and the dyspnea rapidly increased. 
 Tracheotomy was done, relieving the dyspnea. In a short time he 
 recovered consciousness. Later he breathed well through his mouth 
 and no air came through the tube. He seemed very uncomfortable 
 at night and at midnight began suddenly to be very dyspneic. He 
 was resuscitated with difficulty, and the dyspnea was again relieved, 
 but only for a few moments. Then he became very dyspneic and 
 the wound leaked blood into the tube and trachea. The tube was 
 removed but he could not breathe even with the trachea and wound 
 wide open. A larger tube was inserted and through it an attempt 
 was made to swab out the trachea, but without avail. He ceased to 
 attempt to breathe. After fruitless attempts at artificial respiration 
 he died of asphyxiation. 
 
 Clinical Diagnosis —Chronic glomerulo-nephritis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Acute mitral and aortic endocarditis. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic mers nephritis 
 with acute exacerbation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Mitral stenosis. 
 
 Possibly aortic stenosis. 
 
 Passive congestion, general. 
 
 Ascites. 
 
 Hydrothorax. 
 
 Hydropericardium. 
 
 Possibly terminal infection, with acute endocarditis. 
 
 Terminal acidosis. 
 
 Anatomical Diagnosis —Chronic glomerulo-nephritis. 
 
 Chronic fibrous endocarditis of the aortic valve. 
 
 Verrucose endocarditis of the aortic valve. 
 
 Slight verrucose endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 483 
 
 Anasarca. 
 
 Septicemia, staphylococcus, terminal. 
 
 Chronic pleuritis. 
 
 Dr. Cazot: Was there any acute endocarditis? 
 
 Dr. RicHarpson: It does not seem to me so. The process was 
 a chronic one, involving the aortic valve mainly. 
 
 The heart weighed 305 grams, showing considerable hypertrophy 
 and dilatation for him. The lungs showed frank passive congestion. 
 
 Fic. 94.—Chronic glomerulo-nephritis with hypertrophy and dilatation of the heart. 
 Both kidneys are placed in the left ventricle. (Photograph by Lewis S. Brown. Dr. 
 Oscar Richardson.) 
 
 There was no fluid in the plural cavities, but considerable in the lungs. 
 
 Our best picture of chronic glomerulo-nephritis and hyper- 
 trophied heart is this one (Fig. 94), showing the contracted kidneys 
 easily resting within the left ventricle of the hypertrophied heart. 
 
 The stomach mucosa was thick, red and velvety, exuding thin 
 bloody fluid—a good example of chronic passive congestion. 
 
484 FACTS ON THE HEART 
 
 Dr. Casot: Was the blood shown by the guaiac test from that? 
 Dr. RicHArpson: I think so. 
 
 Case 4312 
 
 A Canadian barber of sixty-five entered February 18, 1922, com- 
 plaining of pain and blueness of the right leg of eight weeks’ duration. 
 
 His father and one brother died of ‘‘shock.” 
 
 His general health had been good. At fourteen he had a severe 
 fever of unknown cause. The same year a stone weighing six or 
 seven hundred pounds fell on his right leg and foot, leaving a bruise 
 which persisted for six months and pain lasting four months. He 
 had a recurrent abscess in the right ear for several years in his youth. 
 For many years he had had an attack of bronchitis of two or three 
 weeks’ duration nearly every winter. His teeth were soft and poor. 
 His bowels were slightly constipated for many years; now moved 
 regularly with cascara. Five years ago he had pneumonia. He had 
 once had piles, which hadnow disappeared. Occasionally he urinated 
 once at night. He denied venereal disease, though he admitted 
 frequent exposure. Average weight for the past ten years 170 pounds, 
 before that 140 pounds. He thought he had lost a little weight on 
 account of insomnia during the past three weeks. 
 
 He formerly took whiskey to excess at long intervals. He had 
 been an excessive pipe smoker all his life. 
 
 Eight weeks ago on stepping out of bed he felt a dull pain in the 
 lower right leg and noticed the foot was white. He felt no more 
 pain for three days. Ever since then he had had intermittent dull : 
 aching pain in the lower two-thirds of the leg and severe shooting 
 pain in the region of the great toe. The right leg and foot had been 
 purplish since a few days after the onset. The pain had been getting 
 worse week by week, although some days he was entirely free from it. 
 It was increased by cold and alleviated by warmth. The foot was 
 cold, numb and tingling all the time. During the past three weeks 
 the symptoms had grown very severe, so that he had been in bed, 
 unable to set the foot on the floor or to sleep at night, and had had to 
 take tablets to induce sleep and deaden the pain, during the past 
 three weeks as many as twenty-five tablets a day. During this time 
 his hands, feet and face had grown increasingly bluish. He had 
 had no treatment except that he had rubbed the leg and foot witha 
 liniment and later with mustard oil with only temporary relief. 
 The skin had been inflamed ever since this treatment. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 485 
 
 A poorly nourished man, dyspneic. Face and extremities slaty 
 gray. Mucous membranes reddish-gray. Sclerae slightly injected. 
 Teeth all missing. Chest slightly ‘““emphysematous.” Lung signs as 
 shown in the diagram. Motility of the spine limited. Apex impulse 
 of the heart not found. Measurements by percussion: midclavicular 
 line 9 cm., left border of dullness 8 cm., right border 4 cm., supracar- 
 diac dullness 5:cm. Actionnormal. Soundsdistant. Slight systolic 
 murmur at the apex in the left lateral position. Pulses poor volume 
 and tension. Artery walls palpable, brachials tortuous. 
 
 Slightly dull. 
 Expiration pro- 
 longed, Voice 
 increased. 
 
 Breathing emphysematous 
 
 Nerisdeete 
 throughout, 
 
 prolonged. 
 
 Old fracture, 
 
 FIG. 95. 
 
 Blood pressure 150/90. Abdomen distended, tympanitic. Genital. 
 and rectal examination negative. Extremities. Slight fine tremors 
 Finger markedly clubbed. Right foot blue gray and cold up to six 
 inches below the knee. Particulary intense blue in the foot, which 
 was very cold. Right dorsalis pedis not palpable. Skin scaling, 
 with several reddish-blue spots in the lower part of the shins. Veins 
 of both feet distended. Pupils and reflexes normal. 
 
 Before operation temperature 96.6°-100°, pulse 80-111, respira- 
 tion 20-31. Urine—norma] amount, sp. gr. 1028-1022, cloudy at one 
 of three examinations. Renal function 30%. Blood: Hgb. by 
 Tallqvist method chocolate colored. (See below.) No estimate 
 made. Leucocytes 13,400-22,800. Polynuclears 84%. Reds and 
 platelets normal. Wassermann negative. Non-protein nitrogen 
 61.8 mgm. Bleeding time 214 minutes. Clotting time 4 minutes. 
 Two throat cultures negative. 
 
 February 22 the patient felt considerably better. The foot was 
 kept warm and was much less painful. His physician reported that 
 he had given him not more than twenty-four tablets of ‘‘sel codeia’”’ 
 which may have contained acetanilid. Tests for methemoglobin 
 and spectroscopic examination negative. The 24th and 25th the 
 pains in the foot were very severe. ‘The foot became increasingly blue, 
 and by the 27th was very blue from toes to midshin. 
 
 February 28 amputation was done. The next day the heart 
 action was somewhat irregular. March 4 there was some slight 
 distension. The wound was surprisingly clean considering that 
 there was practically no bleeding at the time of operation. 
 
486 FACTS ON THE HEART 
 
 Dr. Hugh Cabot’s Pre-operative Diagnosis —Thrombosis of pop- 
 
 liteal artery from arteriosclerosis. 
 
 Pre-operative Diagnosis —Gangrene of the foot. 
 
 Operation—Spinal anesthesia. Amputation of the right leg 
 through mid-thigh for thrombosis. Anterior and posterior flaps 
 with muscle flaps. No bleeding from stump after tourniquet was 
 -removed. Femoral artery thrombosed as high as it could be traced. 
 Wound closed loosely with continuous catgut. 
 
 Pathological Report—The poplteal artery contains a solid throm- 
 bus. There is no necrosis of the toes or foot. | 
 
 Microscopic examination shows degeneration of the wall of the 
 artery with small round cell infiltration and thrombus formation. 
 
 Arteriosclerosis. 
 
 Thrombosis. 
 
 March 9g the patient had sudden right-sided paralysis involving 
 the face on the same side. He was semiconscious, but unable to 
 speak. He had clonic convulsions involving the whole right side 
 and left arm in very slow, deliberate movements. Any stimulation 
 of the right limbs resulted in slow contraction of the whole muscula- 
 ture, usually flexion. The pulse ranged from 92 to 120. March 12 
 he seemed improved. He was still unable to talk, but smiled and 
 seemed to understand what was said. ‘The facial involvement was 
 less, though the right-sided paralysis was still complete. March 16 
 the temperature rose to 101.2°. He grew gradually worse, showed 
 evidence of pain, March 18 became comatose, and March 1g died. 
 
 Clinical Diagnosis —Arteriosclerosis. 
 
 Embolisms of right leg. 
 
 Amputation of right leg, mid-thigh. 
 
 Dr. Hugh Cabot’s Diagnosis.—Arteriosclerotic gangrene (leg). 
 
 Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Cerebral embolism. 
 
 Anatomical Diagnosis —Arteriosclerosis. 
 
 Mural thrombus of the aorta. 
 
 Thrombosis of right femoral artery. 
 
 Thrombosis of the right iliac and femoral veins. 
 
 Embolism of splenic, hepatic and renal arteries. 
 
 Infarcts of brain. 
 
 Infarction of spleen and left kidney. 
 
 Infarcts of right kidney. 
 
 Focal pneumonia. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 487 
 
 Wet brain. 
 
 Recent amputation of left thigh. 
 
 Chronic pleuritis. 
 
 Obsolete tuberculosis, apices of lungs. 
 
 Emphysema of left lung. 
 
 The autopsy is interesting as showing the extent to which thrombi 
 and emboli may go and yet life continue. There was nothing about 
 
 Fic. 96.—Heart and aorta from case 4312. P, point of attachment of a pennant-shaped 
 mural thrombus of the aorta. 
 
 the condition of the urine to lead one to suspect the extent of the 
 
 interference with the circulation. 
 
 I do not see that they have anywhere accounted for the clubbed 
 fingers, and wonder whether it was a faulty observation. Clearly 
 he had enough things to die of, and it is surprising that he had not 
 done so before. 
 
 Necropsy 4251 
 
 First entry. An unmarried Irish laundress of twenty-seven 
 entered February 27, 1914, for relief of pain in the back. 
 
488 FACTS ON THE HEART 
 
 Her past history was negative except for frequent sore throats 
 and a run down condition in 1905. 
 
 Record of the Out-Patient Department, December, 1905. Com- 
 plaint, abdominal pain for two months, with headache and water 
 brash. Cheeks puffy in the morning with swelling of hands and legs. 
 Physical examination showed the eyelids puffy, but no edema of the 
 legs. Heart not enlarged. No murmurs. Slight dullness at the 
 right apex front and back. Urine negative. She did not stop work, 
 and was better after a few weeks. 
 
 Eight years later, a year before admission she began to have occip- 
 ital headache radiating to the orbital region, coming on early in 
 the morning and lasting all day, accompanied by frequent vomiting 
 and confining her to bed. ‘The attacks came about once a month, 
 without relation to catamenia. About this time she had swelling of 
 the feet and puffiness of the eyelids, which had increased. Four 
 months ago she was so much worse that she gave up her cooking 
 because of weakness, but chiefly because of pain in the left sacroiliac 
 region on walking. A week ago she gave up work altogether. She 
 had had dyspnea on much exertion for a long time, but worse recently. 
 For a few days she had had cough without sputum. Her bowels 
 moved only with medicine. She passed less urine than usual. She 
 had lost an unknown amount of weight. 
 
 She was well nourished, slightly pale. Palatal arch rather high 
 and narrowed. Teeth much decayed. Some pyorrhea. Tonsils 
 slightly enlarged. Heart: no enlargement made out. Apex 
 impulse forceful. Sounds of good quality. P2 accentuated. A soft 
 systolic murmur accompanied the first sound, heard best at the pul- 
 monic area, slightly at the apex. Pulses fair volume, good tension. 
 Right slightly greater than left. Walls not felt. Blood pressure 
 125/90. Abdomen normal. Edema of the sacrum and marked 
 edema of the lower legs and dependent portions of the thighs. Pupils 
 normal except that the right was slightly irregular. Reflexes. Left 
 knee-jerk somewhat sluggish. Right obtained only on reenforce- 
 ment. Plantars normal. 
 
 Temperature 97.2°-99°. Pulse61-80. Respiration 17-29. Urine: 
 3 17-32. Sp. gr. 1014-1024. Cloudy at one of six examinations, 
 a very slight trace to a trace of albumin at all, red blood cells and 
 many. leucocytes at all. Renal function 40%. Blood: Hgb. 80%. 
 Leucocytes 5200, polynuclears 79%. Wassermann negative. X-ray 
 of kidneys negative. Left antrum looked opaque, but there was 
 a good deal of distortion. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 489 
 
 By March 14 there was no edema. The other symptoms had 
 improved markedly, and she was up and felt strong. The urine 
 remained unchanged. She was discharged that day with advice as 
 to diet. 
 
 Records of the Out-Patient Department show a visit in March, 
 t9g15, to the Orthopedic Room, where her feet were strapped, and 
 one to the Throat Room in April 1918, for acute tonsillitis, strepto- 
 coccus. March 5, 1920, she came for headache, vomiting, and edema 
 of the face, the legs and perhaps also the abdomen. The urine was 
 cloudy, sp. gr. 1o1o, a large trace of albumin. Heart slightly 
 enlarged. Blood pressure 180/134. 
 
 Second entry, March 25, 1920. 
 
 Her father died of kidney trouble. 
 
 She had sore throats all her life until fourteen years ago; rarely 
 since then. Her bowels were always costive. Six years ago she had 
 considerable bilateral greenish discharge from the nose. Five years 
 ago she had a right earache and discharging ear. The ear had been 
 slightly deaf ever since. A year ago she had influenza. That year 
 she had occasional metrorrhagia for one or two days, never more 
 than twice a month. A few months ago while costive she noticed 
 a few specks of bright red blood in the stool. For five weeks she had 
 had frequency of urination. Occasional scalding. Her weight 
 gradually increased from 122 to 130 pounds, her present and best 
 weight. 
 
 Habits. Good. 
 
 She now gave a history of five months’ treatment at another Bos- 
 ton hospital in 1913 and three weeks in 1916 for the same complaint 
 treated here in 1914. In 1915 she was well. Three years ago she 
 came to the Out-Patient Department of this hospital with the same 
 complaint and was given a diet, but had never followed it. Since 
 that time she had been in the other hospital once and in the Out- 
 Patient Department several times. She had been fairly well for a 
 year until five weeks before admission, when she began to see specks 
 everywhere before her eyes. Her face, abdomen and legs began to 
 swell. She had been nauseated much of the time, and had vomited 
 once. She was getting a little dyspneic, had some palpitation on 
 exertion, and had used two pillows at night. Five weeks ago and 
 again at admission her urine was red. She had some scalding and 
 frequent urination in the day and dull ache in the lower abdomen 
 after eating, relieved by hot drinks and by passing gas by rectum. 
 She was occasionally dizzy and had a flushing sensation over the 
 
490 FACTS ON THE HEART 
 
 TABLE 107 
 
 Schlayer test, March 27 
 
 Nit 
 Volume S eres Sodium 
 
 Time | of urine : gm. per 
 
 in c:¢, a ea Total liter 
 liter 
 
 Chloride 
 
 .98 36 : Breakfast 8 a.m. 
 
 -73 
 Dinner 12 m. 
 
 Supper 6 p.m. 
 Night.... 
 
 Wotaleres 
 
 Intake... 
 
 head and neck. She had taken MgSO, at home every morning for 
 five weeks, during which period she had had practically constant 
 occipital headache. 
 
 She was well nourished. Slight edema of the face. Mucosae 
 slightly pale. Slight deafness of both ears. Pus pocket at roots of 
 lower incisors. No pyorrhea. Tonsils large, crypts prominent. 
 Lungs clear. Heart not enlarged.* A» accentuated. Pe. double. 
 A soft blowing systolic murmur heard all over the precordia, loudest 
 at the base. Blood pressure 190/120-150/100. Abdomen. Shift- 
 ing dullness in the flanks. Slight tenderness in the right upper 
 quadrant. Slight right costovertebral tenderness. Right kidney 
 questionably palpable. Extremities. Slight edema of the feet, legs, 
 thighs and lower back. Pupils and fundi normal. Knee-jerks 
 sluggish. 
 
 Temperature and respiration not remarkable. Pulse 65-95. 
 Urine: ward record 3 11-72. Cloudy at all of four examinations. 
 Neutral at one. Sp. gr. 1008-1024. A trace to a slight trace of 
 albumin at all. Loaded with red blood corpuscles at three exami- 
 nations, rare at the fourth, leucocytes at all. (No catheter specimen.) 
 Note on Schlayer test by Dr. Reginald Fitz. ‘‘Test appar- = 
 ently shows inability of kidney to excrete water and nitrogen. Chlo- 
 ride reactions show good concentrative powers of kidney and that 
 
 *The measurements were: midclavicular line 8 cm., left border of dullness 9.5 cm., 
 right border of dullness 3.5 cm., supracardiac dullness 5.5 cm. 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 4QI 
 
 total output approaches intake.’’ Renal function. March 25 25%, 
 April 5 15%. X-ray. Pus pocket at root of an incisor. Left 
 antrum hazy, also both frontal sinuses. Heart as shown in the 
 illustration. 
 
 Orders.. Salt free low protein diet. Limit fluids to 1200 c.c. 
 MgSO, 5 iss. 
 
 By April 4 the patient was much better, the edema was gone, 
 and there was no headache or visual disturbance. The urine and 
 
 ie 
 ee 
 
 Fic. 97.—Necropsy 4251. Chronic glomerulo-nephritis with hypertrophy of the 
 heart and subacute pericarditis. X-ray shows the heart apparently slightly enlarged. 
 There is unusual angulation in the border of the left ventricle; otherwise the shape of 
 the heart is not abnormal. Supracardiac dullness abnormally wide, and aortic area 
 shows generalized increase in size, suggesting a diffuse dilatation. (Roentgenological 
 _ Department, Massachusetts General Hospital.) 
 
 blood chemistry, however, were worse than at admission. She was 
 put upon the regular hospital diet and began to gain two poundsa day. 
 In four days edema appeared over the shins. Nevertheless she 
 insisted upon going home, and April g did so. 
 
 Third entry, September 13, 1921. 
 
 She had been married two years. Since leaving the hospital she. 
 had had slight edema of the ankles nearly every day, disappearing 
 at night, and headaches as often as once a week. She had not kept 
 to any diet or taken any medicine A year ago she had blurring of 
 vision, equal in both eyes, with gradual recovery. She considered 
 
AQ2 FACTS ON THE HEART 
 
 them nearly normal at present. Five weeks ago she began to have 
 smothering sensations, worse at night and on exertion, preventing 
 her from lying flat, and gradually increasing in severity and frequency. 
 The nocturnal frequency increased to every hour or half hour until 
 her doctor gave her some green liquid for her heart two weeks ago, 
 since when it had decreased to four times anight. The dyspnea had 
 remained the same. A week ago she had a slight nosebleed. About 
 this time she caught cold and had had slight cough ever since. For 
 four nights she had had very severe attacks of breathlessness accom- 
 panied by a sensation of great constriction in the chest and some shoot- 
 ing pains over the heart. During the attacks she thought she was 
 going to die. At the end she found that her hands and feet were 
 moving in an uncontrollable way. In two months she had lost 
 twenty-two pounds. | 
 
 Physical examination. A poorly nourished, pale, thin woman 
 sitting upright in some respiratory distress. Skin dry, icteric. 
 Mucous membranes pale. Sclerae injected. Chest expansion and 
 diaphragm excursion slightly greater on the left. Slight dullness at 
 both bases, more on the left. A few moist crackling rales at both 
 bases. Marked pulsation above the clavicle. Spine tender 
 over lumbo-sacral region. Heart action rapid (100). Sounds of 
 good quality. A» greater than Po, both accentuated. A» sharp and 
 ringing. Soft systolic murmur at the apex and over the precordia. 
 Pulses of poor volume and tension. Artery walls normal. Blood 
 pressure 220/140-170/110. Abdomen. Liver dullness from sixth 
 rib to costal margin. Edge not felt. Extremities. Slight edema of 
 shins and sacrum. Pupils slightly irregular, otherwise normal. 
 Fundi not abnormal except for greatly dilated veins. Reflexes. 
 Knee-jerks not obtained. 
 
 Temperature 98.5°—96.3° (by mouth); after September 26 96.5°— 
 99.6° (rectal.) Pulse 101-60. Respirations 31-9. Urine: § 18-6 
 (?). Sp. gr. roo6-1o12. Cloudy at four of six examinations, pink 
 at one, alkaline at all, a trace to a large trace of albumin at all. Red 
 blood corpuscles at one, leucocytes at one. Renal function O (two 
 tests). Blood: Hgb. 50%-40%. Leucocytes 24,000-11,800. Poly- 
 nuclears 71%. Reds 2,224,000-2,640,000. Smear and platelets 
 normal. Two Wassermanns negative. Non-protein nitrogen 
 September 13 95.1 mgm., September 20 133.2, and September 26 
 333 mgm. Bleeding time 2:10 minutes. Clotting time 6:45-8:45. 
 
 By September 15 the patient was vomiting practically all the food © 
 ingested. She was too ill for a Schlayer test. Two days later she 
 
HYPERTENSIVE HEART DISEASE—ILLUSTRATIVE CASES 493 
 
 was very weak and not clear mentally. Rectal taps were not well 
 retained. The night of the 17th there was pain in the upper half of 
 the left chest in front on deep breathing, and a definite pleural fric- 
 tion rub heard just to the left of the arch of the aorta. She grew 
 steadily more stuporous. By the 23rd there was edema of the left 
 hand and both feet. Morphia in 1@ gr. doses was used to control 
 the vomiting. There was some blood in the vomitus. Another 
 fundus examination showed a small hemorrhage in the left eye. Sep- 
 tember 26 the heart sounds were exaggerated. There was a friction 
 rub over the apex, which the following day was unusually loud and 
 grating all over the precordia, obscuring the heart sounds. Elec- 
 trocardiogram Sept. 29, showed arrhythmia, brady cardia, rate 55-80; 
 probably due to variation in site of pace maker; sometimes auricular 
 with upright P wave; sometimes auricular-ventricular or ventricular 
 escape with absence of auricular activity. Left ventricular pre- 
 ponderance. High T wave. 
 
 Against all expectations the patient lived in stupor until October 
 1, suffering some pain. | 
 
 Clinical Diagnosis —Chronic glomerulonephritis. 
 
 Uremia. 
 
 Hypertension. 
 
 Pericarditis. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic glomerulonephritis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Acute pericarditis. 
 
 Secondary anemia. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis —Chronic glomerulonephritis. 
 
 Hypertrophy of the heart. 
 
 Chronic passive congestion of the spleen. 
 
 Subacute pericarditis. 
 
 Ascites. 
 
 Edema of the ankles. 
 
 Dr. Oscar RicHARrDSON: The ankles pitted slightly on pressure. 
 Unfortunately the incision in this case was restricted to a six-inch 
 cut in the midline, but they found that the kidneys were small,—215 
 grams—and that the condition was chronic glomerulonephritis macro- 
 scopically and microscopically. Evidently there was some trouble in 
 getting the heart, but enough was seen to establish the hypertrophy, 
 —a hypertrophy of the left side. The wall of the left ventricle was 
 fifteen mm. thick, indicating hypertrophy of the wall of the left 
 ventricle. There was fibrinous pericarditis. 
 
CHAPTER V 
 MYOCARDITIS 
 
 1. CHRONIC FIBROUS MYOCARDITIS 
 
 Few terms have undergone so many vicissitudes or have been used 
 in more different senses within a century. In the years 1890-1910 
 we frequently heard the term used as a diagnosis to explain cardiac 
 weakness and arrhythmia in elderly people without evidence of val- 
 vular disease. When post-mortem examinations became more fre- 
 quent and their results were more often correlated with the clinical 
 findings, the term began to be abandoned, since, as I showed many 
 years ago,“ most clinical diagnoses of fibrous myocarditis made at 
 that time were demonstrably wrong post-mortem, and most of the 
 actual fibrous myocarditis discovered post-mortem had not been 
 suspected during life. I have therefore maintained for many years 
 that the diagnosis of myocarditis is impossible during life. Against 
 this it was for years contended, partly on the authority of Krehl, 
 that one could find myocarditis in most failing hearts if one searched 
 all parts of the heart muscle by microscopic examination. Since 
 this is rarely done the contention is difficult to refute. But even if 
 it were true it would not prove that such microscopic foci of fibrous 
 tissue caused any functional weakness of the heart. As a matter of 
 fact it can be demonstrated, as I shall show below, that even gross, 
 easily recognized patches of fibrous myocarditis in its extremest 
 form, may exist unassociated with any chronic passive congestion 
 demonstrable after death. 
 
 In view of these facts, the use by H. A. Christianf and others, of 
 the term ‘‘myocarditis”’ when there is clinical evidence simply of an 
 enlarged and weakened heart, seems to me unjustifiable. Any other 
 muscle in the body may become hypertrophied and then if over- 
 
 * A Study of Mistaken Diagnoses, Journal of the American Medical Assn., Oct. 15, 
 1910, Vol. LV. 
 + Chronic Myocarditis (Clinic). Med. Clinics of North America, January, 1918, 
 Vol. I, 813. 
 Chronic Myocarditis: A Clinical Study. Jour. Am. Med. Assoc., 1918, Vol. LXX,. 
 1909. 
 Chronic Myocarditis and Its Management. Southern Med. Jour., 1921, Vol. XIV, 
 587. 
 404 
 
THE MATERIAL HERE ANALYZED 495 
 
 worked may give out and cease to function. We call this giving out 
 “fatigue,” although its physics and chemistry are not yet clear. 
 Why should we not suppose that the muscle of an overworked heart 
 gives out from chronic and excessive “fatigue?” In such a heart 
 there may or may not be patches of fibrous myocarditis. But neither 
 their presence nor their absence is necessarily of any importance so 
 far as the work of the heart is concerned. 
 
 Of recent years, since the electrocardiograph has added so much 
 to our knowledge of cardiac physiology, there has been a tendency to 
 return to the practice of making clinical diagnoses of myocarditis, 
 now supposedly based on electrocardiographic findings. But it 
 has never been proved to my satisfaction that the presence of alter- 
 nation, or of heart block in any of its varieties, or of any other defect 
 demonstrable by the electrocardiograph, gives us no good grounds 
 for predicting that fibrous myocarditis will be found post-mortem. 
 Exception may perhaps be made of certain cases of complete heart 
 block. Nevertheless it still seems to me true that myocarditis has 
 little if any standing as a recognizable clinical syndrome. It remains, 
 I think, essentially an item of post-mortem anatomy. 
 
 THE MATERIAL HERE ANALYZED 
 
 Among the g1 necropsies which form the basis of this chapter, 
 there are two distinguishable groups, (a) those of acute cardiac infarc- 
 tion, making up 25 cases out of the total of 91, and (b) those of 
 chronic fibrous myocarditis, which in its pure, unmixed form, is 
 exemplified in 66 cases. Infarction and fibrous myocarditis were 
 present together in 18 cases. It is because of this latter association, 
 and also because of their anatomy that I have discussed the two 
 seemingly different entities together. It certainly appears to be the 
 fact that, in some cases, chronic fibrous myocarditis is an end result 
 of acute or subacute infarction. A coronary artery, usually the 
 descending branch of the left coronary, becomes narrowed or alto- 
 gether occluded, either by arteriosclerosis alone, by a thrombus, or 
 by a combination of both. The area of heart wall supplied by this 
 vessel becomes anemic, necrotic, and then is gradually replaced by 
 scar tissue. In some hearts different phases or stages of this process 
 can be found side by side. In others the acute infarction maims the 
 heart so seriously that death follows at once before any fibrous change 
 takes place. 
 
 I am well aware that this series of events will not account for all 
 cases of fibrous myocarditis. In 38 cases out of my series of g1 
 
496 FACTS ON THE HEART 
 
 there was no actual coronary obstruction or marked narrowing, 
 either at the mouth of the vessel (syphilitic aortitis) or in its course 
 (arteriosclerosis or thrombus). Most of these 38 cases have some 
 coronary sclerosis but no considerable narrowing of the vessels. The 
 origin of the fibrous myocarditis in these cases is obscure. They 
 appear, however, to be relatively common. Warthin’s belief that 
 most of them are due to syphilis may well be correct. 
 
 The cases of fibrous myocarditis may be further subdivided into 
 those which are diffuse and those which are limited to a small portion 
 of the heart, most often the left ventricle near its apex (18 cases out 
 of o1). These cases have no clinical peculiarities to distinguish them 
 from the rest of the series. The same may be said of our six cases of 
 cardiac aneurism. 
 
 One case in this series may be described separately under the 
 heading. 
 
 SYPHILITIC MYOCARDITIS 
 
 An ill-nourished male infant of four weeks lived one day in our 
 wards, with dyspnea, a bloody nasal discharge and a normal tempera- 
 ture. Post-mortem examination showed the lesions of congenital 
 syphilis (Necropsy 3346). On the posterior wall of the left ventricle 
 and the anterior wall of the right ventricle there were areas of 
 increased resistance and marked pallor. Inthese areas the heart’s wall 
 was about one anda half times as thick asin other parts of the ventricle. 
 The tissue was firm, homogeneous, and glistening, yellowish-gray in 
 color, like the uncooked white meat of chicken. The coronary arter- 
 ies appeared smaller than normal. ‘The heart weighed twelve grams. 
 
 In one other case of our series a single isolated area of necrosis in 
 the heart wall suggested gumma to the pathologist; and it may well 
 be that among the cases of fibrous myocarditis unassociated with 
 coronary disease, syphilitic lesions may have preceded the scar forma- 
 tion. The work of Warthin suggests this. (See also p. 424.) 
 
 ETIOLOGY OF FIBROUS MYOCARDITIS 
 
 Fibrous myocarditisis adiseaseofoldmen. 7omenout of 89 cases 
 in which the sex is known were above the fiftieth year at the time of 
 death, and only two were under thirty. In these eighty-nine cases 
 there were only nineteen females. It may be maintained with some 
 plausibility that the sex incidence argues in favor of a syphilitic 
 etiology. On the other hand, the duration of life argues somewhat 
 against this, unless we are to maintain that all coronary disease is 
 syphilitic in origin, whether we find any lesions of syphilis or not. 
 
ETIOLOGY OF FIBROUS MYOCARDITIS 497 
 
 The average age in this group is notably greater than in the cases of 
 syphilitic aortitis, or indeed in any other group of heart lesions known 
 to me. Certainly in the majority of cases, those associated with 
 coronary sclerosis, it seems safer to say that the cause of most cases of 
 chronic myocarditis, and of many if not most acute cardiac infarc- 
 tions, is arteriosclerosis, whatever further etiological mysteries may 
 be hidden behind this familiar term. 
 
 That infectious disease has any particular connection with fibrous 
 myocarditis, except in so far as infection may be supposed to favor 
 the development of arteriosclerosis, we have no evidence. There 
 was no special frequency of typhoid fever or of any other infection, 
 or of all infections taken together, in the histories of these patients. 
 They were not notably alcoholic or in any other respect different 
 from the old men dying of other causes at the Massachusetts General 
 Hospital. The znfarct group contains acute infectious cases with 
 coronary thrombosis, due to acute endocardial vegetations. 
 
 Cardiac hypertrophy was present in almost every case. Indeed 
 there were but five cases without some demonstrable enlargement 
 of the heart post-mortem. But since, as shown in Chapter I, myo- 
 carditis is usually associated with other lesions producing cardiac 
 enlargement, we cannot reasonably say that cardiac hypertrophy is 
 itself the cause or the result of myocarditis. 
 
 Only in six cases was hypertrophy linked with myocarditis alone 
 in the absence of other lesions suspected at least of being causes of 
 hypertrophy. The figures follow: 
 
 Myocarditis without cardiac hypertrophy.......... 5 
 Myocarditis with cardiac hypertrophy............ 86 
 Among these 86 cases we find but six in which myocarditis was the 
 only lesion. In the remaining eighty the associated lesions were as 
 
 follows: 
 
 TABLE 108 
 Chronic non-deforming endocarditis in... 0.0.00. 0.0... oe es oe (I 2 CASES 
 OR CI) ENS Ethie ea eg aan NMRA aA ae Nee et men 24 Cases 
 EST ae Cie | lr SSG gee ae Pea BA al oe ii) Ot ae a I5 cases 
 Prrerigsoicroric derenerationiof Kidneys. 517 cena oitacisie oh Ao“ 4 cases 
 BeriE OUMCHOCEILATULES 3h eet eas ote Ac eee hana gla Beat Ee A EN 6 cases 
 BREECH CEI) INS Pea tee Ui ce Beet hea, gee A OM MATA hs, eke sae 8 cases 
 UMULUNS UTICA ICs Mone yt Sein Ae ae gees oe ene wie hears 6 cases 
 ete eo met Set ek es ia ke. amie esa es Vi od SN, I case 
 CATE CEN SRT ca db Spee Rs AR Tea TEAR, OY Or Si me Dae I case 
 SUNT ATEDE gS OFEP aD a a ae A UR) Se Rh Ne I case 
 Sea et garth le a ear aie Meet Weel ig EAL EE or Oe 2 cases 
 
 80 cases 
 
408 FACTS ON THE HEART 
 
 The five largest hearts of the series show the following data: 
 TABLE I09 
 
 Age Necropsy | Heart 
 
 R k 
 Sex No. weight amis. 
 
 2603 No congestion. Anginoid death. Aortic 
 stenosis. Narrowed coronaries. 
 
 Mitral stenosis. Chronic nephritis, uremic. 
 Cardiac infarct. Left coronary descendens 
 
 blocked. Passive congestion. 
 
 Chronic passive congestion. Acute dila- 
 tation at end. 
 
 Prostatism. Chronic nephritis. B.P. 200/— 
 105. Chronic passive congestion. 
 
 Chronic passive congestion. Left coronary 
 blocked. B.P. 230/175. 
 
 In all these cases and in most of those in Table 108 we may 
 reasonably suppose that the hypertrophy is due to hypertension. — 
 There is no reason to believe that myocarditis causes cardiac hyper-_ 
 trophy. A truer statement seems to be that a small percentage 
 of enlarged hearts (86 out of 1209) get myocarditis. 
 
 It seems to me therefore that we may sum up the etiology of 
 myocarditis, so far as this series is concerned, as: coronary sclerosis 
 in most cases (five-ninths), syphilis (demonstrable) in a few. The 
 cases of suppuration in the heart wall, and of acute embolic myocardial 
 inflammation as a part of malignant endocarditis, are dealt with on 
 pages 512, 527. 
 
 DIAGNOSIS OF MYOCARDITIS 
 
 Only in the infarctive subgroup of cases can the diagnosis be often 
 reasonably suspected during life. Some such suspicion may arise 
 in any case of angina pectoris, expecially when it occurs in elderly 
 men. ‘This suspicion is justified, as has already been shown, because 
 we know that angina pectoris may be associated with obstruction 
 of the coronary arteries, either at their orifices or in their further 
 course, and that such obstruction often leads to myocarditis. But on 
 the other hand angina is often not connected with coronary disease 
 
DIAGNOSIS OF MYOCARDITIS 499 
 
 and this often fails to produce myocarditis; so that the surmise is 
 ill founded at best. 
 
 Angina was present in twenty-seven of our cases, and in this 
 group, therefore, some slight suspicion of myocarditis was justified. 
 But one can hardly say that our diagnostic right extends beyond a 
 vague suspicion. For, in the first place, there is the group of cases 
 on which great stress has been laid by Sir T. Clifford Allbutt, in which 
 angina pectoris is not associated with any form of coronary obstruc- 
 tion. Eleven necropsies in this series illustrate this. (See Chapter 
 VI.) Moreover, very marked narrowing of the coronary arteries, 
 amounting sometimes to a practical obstruction, may exist without 
 any myocarditis. Nevertheless the association of angina pectoris, 
 coronary obstruction, and fibrous myocarditis is sufficiently fre- 
 quent to justify some degree of diagnostic suspicion, under the condi- 
 tions mentioned, especially if there are signs of peripheral embolism, 
 of cardiac infarct or of acute pericarditis (see below). 
 
 Aside from the presence of angina and the favoring conditions of 
 age and sex, we have almost no clues to the diagnosis of fibrous myo- 
 carditis. Arrhythmia, which used to lead straight to a diagnosis of 
 myocarditis when the irregularity was present in an old man suffer- 
 ing from decompensated heart disease and without evidence of valve 
 lesion, was noted in only 23 out of g1 cases. Cardiac hypertrophy, 
 as has been already said, was present in 86 out of gi cases. The 
 blood pressure was measured in only 43 cases. It was high in 17 and 
 notably low in six, the remainder being approximately normal. 
 (See Tables 110, 111, and 112.) 
 
 TABLE 1I10.—SyYSTOLIC BLOOD PRESSURE 
 
 Not high 
 tiger (ae ye NEDA MET Y PE BRE a LR Oe A Ree oo S 
 TOT BLO. FGA ees. oe ieee ke tem a As 
 
 Wee eTA Oy Se he PE RCE tee ted cee 
 CATH OSs OE ce hoe ae 
 
 FGLET SO oe Wa ia ieee ce a aa Nae st 
 181—200 
 
 J 1a ag 4 Le, on de eee CO ee ah Tae! 59 Be Ra 
 92T=2AO) ws a 
 
500 FACTS ON THE HEART 
 
 TABLE I11.—PULSE PRESSURE 
 
 6 weeks (syphilitic) 
 
 20-30 years 
 
 31-40 years 
 
 41-50 years 
 
 SI=00 YearSsa: ae Ae eee ere 22 |. Males... fs2%.2)0) ee 
 61-70 years Females 
 
 71-80 years Sex unknown 1.45... .05 eee 
 SI=O0 "Vy GaSe a! seth ee endl ree i ae 
 
 “Elderly” 
 
 Unknown 
 
 Thrombi adherent to the ventricular endocardium were present 
 in thirty-two or about one-third of the cases. They are formed pre- 
 sumably on a patch of ill-nourished endocardium, this malnutrition 
 being due to the underlying myocarditis, especially when this is of 
 the acute or subacute type, closely related to infarct. Hence, if 
 during life we get evidences of embolism or peripheral infarct, we 
 may suspect that these are due to detached portions of an intracardiac 
 thrombus, and so if we are rash we may argue from this the presence 
 of a myocarditis beneath that thrombus. Occasionally such a guess 
 may come out right. But (1) the other sources of peripheral embol- 
 ism or infarct and (2) the cases of intracardiac thrombus without 
 myocarditis, are so many that unless there were associated evidence 
 of angina, cardiac infarct or pericarditis (due to the infarct) the guess 
 at a diagnosis of myocarditis would be largely unfounded. 
 
be 
 
 DIAGNOSIS OF MYOCARDITIS 501 
 
 TABLE 114.—10 CASES OF EXTREME DIFFUSE FIBROUS MyocarDITIS 
 
 Chronic 
 Necropsy | Heart |passive| Blood 
 No. weight | conges-| pressure 
 tion 
 
 Age—sex Remarks 
 
 + I yr. ago dysp. and cyan. 3 wks. 
 Last 2 mos. dysp. and cyan. 
 Died with acute dilatation. 
 
 Palpit. r yr. ago. Signs as of 
 mitral stenosis. 3 weeks dys- 
 pnea now. 
 
 Syph. aortitis obliterating one 
 coronary orifice. Died in attack 
 of angina. Aortic regurgitation. 
 
 5 yrs. gradual decompensation. 
 Infarction at end. 
 
 Senile gangrene. Chronic neph- 
 ritis. No cardiac symptoms. 
 
 2 weeks epigastric pain (infarct?) 
 2 weeks orthopnea. 
 
 160/120 | 3 yrs. dyspnea. Renal stone. 2 
 mos. orthopnea. Died on way 
 to cystoscope room. 
 
 too/70 | 3 yrs. angina. Actinomycosis of 
 lung. No decompensation. 
 
 Cancer of stomach. No cardiac 
 symptoms. 
 
 200/120 | Dyspnea 4 mos. (since pneumonia). 
 Angina. 
 
 In Table 114 I have separated out ten cases in which the fibrous 
 myocarditis was of the extremest grade, diffused throughout the 
 whole heart. The table shows that this group does not differ in any 
 important essential from the remaining 81 cases. One of the most 
 remarkable features about it is that in four of the ten cases there was 
 no discoverable passive congestion post-mortem, which means that 
 relatively good cardiac function must have been carried on to the end 
 of life, despite a very extensive replacement of muscle tissue by fibrous 
 
502 FACTS ON THE HEART 
 
 tissue in the walls of the heart. Evidently it is not this replace- 
 ment alone or in itself that makes the disease serious tolife. Patients, 
 even with extreme grades of fibrous myocarditis may have no cardiac 
 symptoms and may die (as in this group) of cancer or nephritis. 
 
 With this I have contrasted, in Table'115, a small group of seven 
 cases in which the amount of fibrous myocarditis was very notably 
 slight, only a few patches here and there. In this group one might 
 expect that the passive congestion would have been very slight, and 
 indeed this seems to be somewhere near the truth, since in four out 
 of seven cases no such congestion could be demonstrated. This 
 gives us some contrast with the whole group, in which passive con- 
 gestion was demonstrated post-mortem in 41 out of 66, or two-thirds 
 of the cases of uncomplicated fibrous myocarditis. Nevertheless 
 the difference is not very striking. The weight of these seven hearts 
 averaged distinctly less than that of the ten serious cases of Table 114, 
 averaging 477 grams in the slight cases as against 554 in the extreme 
 cases. 
 
 TABLE 115.—7 CASES OF NOTABLY SLIGHT FIBROUS MyYocarDITIS 
 
 Chronic passive 
 
 Necropsy No. | Heart weight ‘ 
 congestion 
 
 Blood pressure 
 
 MODE OF DEATH 
 
 In only a few cases, mostly of the infarct group, was the weaken- 
 ing of the heart wall itself apparently the cause of death. If we 
 separate out the cases in which neither angina pectoris nor the infarct 
 syndrome was present during life, we find (see Table 116) that death 
 resulted from chronic passive congestion in only three cases, in other 
 words, that death usually has very liitle to do with the myocarditis. 
 
MODE OF DEATH 503 
 
 Chronic nephritis was apparently the main factor in the fatal result 
 in twelve cases, streptococcus sepsis in eight, pneumonia in four, 
 valvular disease in five. Arteriosclerotic gangrene and its results 
 brought about the fatal issue in at least three cases, gastro-intestinal 
 cancer in two, prostatic disease, pernicious anemia, cerebral hemor- 
 rhage, delirium tremens and cirrhosis of the liver were apparently 
 the chief factors in other cases. Only in three out of forty-eight cases 
 could one say that the myocarditis may well have been an important 
 cause of death. In these three cases the heart weights were 413, 545, 
 and 807 grams respectively, and as the lightest of these belonged to 
 a wizened old woman it, like the rest, was considered to be hyper- 
 trophied. But all these cases may well belong to the hypertensive 
 group and their deaths may be attributed primarily to hypertension 
 and its results, one of which, for all I know,.may be myocarditis. 
 
 I have already referred above to the very considerable hypertro- 
 phy which was present in almost all the hearts of this group. In the five 
 largest hearts, nephritis was apparently a factor in four. The 
 remaining case presumably represented one of those examples of 
 hypertrophy associated with a hypertension of unknown cause. 
 From these as from the whole group one gets the impression that 
 these patients have acquired an enlargement of the heart from the 
 usual causes which lead to arteriosclerosis as well as from chronic 
 nephritis or from hypertension of unknown origin; that in the course 
 of this disease they have acquired also a certain amount of fibrous 
 myocarditis; but that, in the absence of coronary disease and espe- 
 cially of coronary infarct, this myocarditis has been of very little 
 clinical importance. 
 
 TABLE 116.—Main Factor IN DEATH IN 48 CASES WITHOUT ANGINA OR CARDIAC 
 
 INFARCT 
 ECOMI Ce NCONIILIS: px acid 3 aexsheet. Great eee Peers GNA i wake aah a? bk she 12 
 Benuicentia, OF acute endocarditis ce muee mt meee a, eet ete eee ey ane ee 8 
 ME ELA RM IGCASE SR, yaa DIT a LRM Amd ct), salem clit too e ee ieled ce 5 
 Eelam ne reed ee iyo re PR aR etl ie een ciel Wachtel e dixie Sa 4 
 Peariprane, Omer tretaity yc as fain | A Rate ees out ny Menai eve e 3 
 Beer Rt ONGESOI Ste rhs Or eichate is vadiad «tie kein Aol ahd oti Sony eats 3 
 Ae els aie a a et By Td: oat SS nae URE ns Hk ant a 2 
 Sg CART Degen Cog Se gD PRE ty gh RE co. Pd ih ea MRE Ne Rea cet 2 
 PUREE LUSEITS tai tia dak he ots a kee Eins Crk he Rls rahe aime 2 
 
 COT TST ST ee tome aia hie he MRR er anal ticbe a coats pamerht hs aie aed 7 
 
 Necropsy No. 2291 is unique in our series in that it showed an 
 extreme degree of fibrous myocarditis in a boy of twenty years, 
 
504 FACTS ON THE HEART 
 
 without important previous illness. A year before his death, he had 
 his first attack of dyspnea and cyanosis and went to bed for three 
 weeks. Two months before death dyspnea, cyanosis and edema of 
 the face reappeared and continued. They were severe for the last 
 _ three days, preventing sleep and accompanied by vomiting. ‘There 
 was also edema of the legs and ascites with intense cyanosis of the 
 face, hands, and feet. 
 
 The heart’s impulse was in the fifth interspace, two and a halt 
 inches outside the nipple. The right border of dullness extended 
 three inches to the right of midsternum, and there was a moderate 
 increase of the supracardiac dullness. The heart was irregular and 
 rapid, its sounds often obscured by noisy respiration. No murmurs. 
 The pulses were equal, synchronous, irregular, of fair volume and 
 low tension. The pulmonic second was sharply accentuated. 
 
 He collapsed on his way to the ward and was bled three ounces, 
 apparently with good effect, but attacks of tremendous cyanosis 
 and extreme dyspnea continued. The outlines of cardiac percussion 
 suggested pericardial effusion but the action of the heart was forcible 
 and the dullness did not extend beyond the impulse to the left. He 
 died in one and a half hours. 7 
 
 Necropsy showed a huge, gristly, fibrous heart weighing 807 
 grams. On cutting through the myocardium of the left ventricle 
 great resistance was offered by the tissues which were everywhere 
 tough and gristly to the touch, though more so in some places than 
 in others. Section surfaces showed replacement of the muscle by 
 gray-white homogeneous, apparently fibrous tissue in larger or 
 smaller confluent areas. Microscopic examination confirmed these 
 impressions. 
 
 The coronaries were free and smooth. The left ventricle was 
 twelve mm. thick, the right eight. The valves were normal. The 
 other organs were normal save for chronic passive congestion. No 
 evidences of nephritis or syphilis. 
 
 Here was a tremendous hypertrophy and dilatation quite unex- 
 plained and in a boy of twenty without any history to throw light on 
 it. Wasthe myocarditis here a cause forhypertrophy? What caused 
 the myocarditis? Icannot answer. In most of our cases myocarditis 
 was apparently only an incident in the hypertensive cardiovascular 
 disease of arteriosclerotic old people. But here the conditions are 
 wholly different. One suspects syphilis but no evidence of it was 
 obtained in the necropsy. 
 
FIBROUS MYOCARDITIS—-ILLUSTRATIVE CASES 505 
 SUMMARY AND CONCLUSIONS 
 
 1. Fibrous myocarditis is an item of post-mortem anatomy, occur- 
 ring especially in elderly men with arteriosclerosis, nephritis, and 
 hypertension. 
 
 2. It is not clinically recognizable, though its presence may be 
 vaguely suspected when angina pectoris is present and especially 
 when this symptom is associated with evidence of cardiac infarction, 
 of peripheral embolism, and of acute pericarditis. 
 
 3. It is rarely the cause of congestive heart failure. 
 
 4. Only in one case had we adequate evidence of syphilis. 
 
 5. Coronary narrowing was present in about five-ninths of our 
 cases and is the most clearly recognizable factor in etiology. Syphilis 
 may also play a part. 
 
 6. Fibrous myocarditis is rarely the only cardiovascular lesion 
 present. 
 
 7. It is usually associated with cardiac hypertrophy (present in 
 86 out of or cases) but since such lesions as chronic nephritis, valve 
 lesions, chronic pericarditis are also usually present, we have no 
 evidence that the myocarditis is the cause of the hypertrophy. 
 
 8. Evidence of chronic passive congestion was found in 51 of g1 
 cases, but when present need rarely be attributed to the myocarditis. 
 
 g. Since fibrous scars in the myocardium—even when numerous 
 and extensive, are not always associated with evidence of heart 
 failure in life or of passive congestion after death, there seems no suffi- 
 cient reason to believe that they interfere with the heart’s action in 
 any material way. There is all the more reason to suspect that 
 fibrous myocarditis is usually harmless, because in the cases which 
 are associated with heart failure and passive congestion causes other 
 than the myocarditis are almost always present. 
 
 19. Myocarditis is an obvious danger to life only when it leads to 
 cardiac aneurism or rupture (see below) or when it causes intracardiac 
 thrombosis and acute pericarditis. 
 
 FIBROUS MYOCARDITIS FOLLOWING INFARCT—ILLUSTRATIVE CASES 
 Necropsy 2871 
 
 A Scotch engineer of sixty-five entered June 20. His father and 
 mother both died of ‘‘heart disease,’ one brother of brain trouble. 
 The patient had all the diseases of childhood, then vigorous health 
 until he was fifty-seven. He had taken no alcohol for five years. 
 Before that he had whiskey before breakfast and half a pint during 
 
506 FACTS ON THE HEART 
 
 the day. He drank to excess three or four times a year. A year 
 before admission he was advised in the Out-Patient Department to 
 enter the wards because of obstructing prostate. 
 
 For eight years he had had occasional nausea and vomiting, usu- 
 ally attributed to excesses in food and drink. He had occasional 
 epigastric distress an hour or two after meals, relieved by food. On 
 a restricted diet without meat he did well. His vomitus was never 
 bloody or coffee-colored. Two weeks before admission he was shovel- 
 ling coal as well as tending his engine. He felt severe general abdom- 
 inal pain, vomited, and fainted. Distress persisted for, four days. 
 Since this attack he had had increasing dyspnea and orthopnea. 
 For four days his feet had been slightly swollen. His urine was 
 scanty. He had no nycturia at entrance, though formerly he had 
 had frequency by day and several times at night. His bowels 
 required catharsis. 
 
 Examination showed a fairly well nourished, orthopneic man with 
 many dilated venules on the face. The mucosae were cyanotic. 
 The apex impulse of the heart was not found. The left border was 
 not made out. The right border was 1 cm. to the right, the upper 
 border at the third rib. The sounds were of very poor quality, 
 almost inaudible in the mitral and tricuspid areas, apparently normal 
 at the base. The pulses were of fair volume and tension. The 
 artery walls were not felt. The systolic blood pressure was 115. 
 Both lungs showed dullness increasing toward the bases, from the 
 fourth rib in front to a little below the scapula in the back. Breath- 
 ing and vocal fremitus were much diminished at the bases. Many 
 medium and*coarse moist rales were heard, most numerous in the 
 axillae and the angles of the scapulae. The abdomen, extremities, 
 genitals, pupils, and reflexes were normal. 
 
 The temperature was normal, the pulse 80 to go, the respirations 
 30 to 34. The urine is not recorded. The hemoglobin was 90%, 
 the leucocytes 16,000, the smear normal. 
 
 The patient continued to have dyspnea and sat up almost all the 
 time. June 21 just after midpight he died. 
 
 Clinical Diagnosis (from Hospital Record) —Myocardial weakness. 
 
 Dr. William H. Smith’s Diagnosis —Arteriosclerosis. 
 
 Possibly angina pectoris with coronary occlusion and myomalacia 
 cordis. 
 
 Much less probably rupture of the aortic arch. 
 
 Anatomical Diagnosis.—Arteriosclerosis. 
 
 Arteriosclerotic occlusion of the coronary arteries. 
 
FIBROUS MYOCARDITIS—ILLUSTRATIVE CASES 507 
 
 Myomalacia cordis. 
 
 Chronic interstitial myocarditis. 
 
 Thrombi of the left ventricle. 
 
 Hypertrophy and dilatation of the heart. 
 
 Infarcts of the kidneys. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax, double. 
 
 Chronic perisplenitis. 
 
 Diverticulum of the duodenum. 
 
 Hypertrophy of the prostate. 
 
 Hypertrophy of the trabeculae of the bladder with small diver- 
 ticula. 
 
 Cholelithiasis. 
 
 Dr. RicHsrpson: There was arteriosclerois of the aorta and great . 
 branches and marked arteriosclerosis of the coronary arteries. The 
 sclerosis was more pronounced in the left artery than in the right, so 
 pronounced, in fact, that it presented points of occlusion with corre- 
 sponding areas of degeneration and softening in the myocardium. 
 There was only a small strip of myocardium left that was fairly 
 normal in appearance, but the greater portion of the wall of the 
 left ventricle showed marked changes due to the sclerosis of the coro- 
 nary artery and presented, on the whole, a typical picture of 
 degenerative changes in the myocardium. ‘That is, it showed 
 degeneration of the muscle tissue and replacement by areas of 
 necrosis and fibrosis. The muscle of the right ventricle was 
 in fairly good condition, because the lumen of the right artery 
 was sufficient to give a fair blood supply. The thrombi in the left 
 ventricle were erected, of course, onan endocardium which had become 
 degenerated. Beneath it the wall showed chronic interstitial 
 myocarditis. 
 
 The heart weighed 600 grams (normally 200-300), showing con- 
 siderable enlargement. The cavities showed considerable dilatation. 
 The valves, with the exception of a slight increase in their circum- 
 ferences, were negative. From middle to old age the valves of the 
 heart usually show a certain amount of fibrosis, because they are 
 lined with endocardium, which plays the same réle on the valve that 
 ‘the endothelium intima plays in the blood vessels. 
 
 The kidneys weighed 427 grams (normally 200-400). When a 
 pair of kidneys weighs more than 400 grams you are suspicious of 
 glomerulo-nephritis. There are other conditions, however, which 
 cause increase in size of these organs. In this case the man probably 
 
508 FACTS ON THE HEART 
 
 had fairly large organs to start with. Then there is a certain amount: 
 of chronic passive congestion which has increased the size, mainly 
 due to edema. Sometimes edema is the only thing found in kidneys 
 of 400 or even 500 grams. Aswe have pointed out before, the increase 
 occurring in glomerulo-nephritis is due to the obstruction of the 
 glomeruli and the capillaries. These kidneys were plump, were of 
 the so-called ‘‘hog-back”’ type, and were pale to dark brown-red in 
 color, in some places cyanotic-looking. The infarcts to the kidneys 
 were due to small pieces from the thrombi in the left ventricle which 
 were brought by the blood stream. With the exception of the condi- 
 tions described, the kidneys were very good for a man of sixty-five. 
 It is rather striking in persons over fifty years of age that the kidneys 
 stand the wear and tear of life remarkably well, as a rule. The 
 kidney is a very resistant organ, and works to the best of its ability 
 whether there be much or little of it left. The kidneys usually show 
 at this man’s age some areas of arteriosclerotic atrophy. When the 
 condition present is sufficient to be called ‘‘arteriosclerotic nephritis” 
 the kidneys, unless the process is very extensive, are of extra good 
 size, in marked contrast to those affected with glomerulo-nephritis. 
 The development of the classification of kidney diseases into these 
 two groups has come about, within the last ten or fifteen years. 
 There was some hypertrophy of the prostate. With this there 
 was, of course, back pressure. The bladder worked to expel the 
 urine, with more or less consequent hypertrophy of the trabeculae. 
 
 Necropsy 2787 
 
 A Prussian lithographer of sixty-six entered December 16, 1904, 
 He had never been ill in bed. He had taken no tobacco or alcohol 
 for the past six months. Formerly he used both in great excess— 
 ‘“‘used to be a high liver.”” He drank ten to fifteen cups of coffee a 
 day. 
 
 For twenty years he had had “‘indigestion,’’—gas, sour stomach 
 and pain two to three hours after meals. The attacks at first came 
 on only after indiscretions of diet or drinking, but for the past two 
 weeks he had had dull pain all of the time which at intervals became 
 much worse and crampy in character. He had never felt nauseated 
 and had never vomited. He had lost twenty-five to thirty pounds 
 within the past three months. His bowels, usually regular, had 
 been constipated for four weeks. His appetite had always been 
 good until the past month. 
 
FIBROUS MYOCARDITIS——_ILLUSTRATIVE CASES 509 
 
 Examination showed a poorly nourished man with normal heart, 
 lungs, and abdomen except for liver dullness from the sixth rib 
 to an inch and a half below the costal margin where the edge was 
 felt. The reflexes were normal. There was no edema. 
 
 The temperature was 98° to 99°, the pulse 64, the respirations 22, 
 the leucocytes 5900. A test meal showed free HCl 0.06%, total 
 acidity 0.14%. At asecond test there were no fasting contents and 
 no residue of the test meal after an hour. 
 
 The patient was discharged on January 5, 1905, with a diagnosis 
 of neurasthenia. 
 
 He was well until the middle of January, 1906, when he “‘caught 
 cold riding horseback.’”’ Cough kept him awake, and he raised con- 
 siderable white or yellowish sputum, sometimes blood-stained. 
 February 3 he reentered the hospital. 
 
 Examination showed a systolic murmur all over the precordia, 
 loudest at the apex. The lungs were slightly hyperresonant, with 
 occasional moist rales. Expiration was faint, especially in the backs. 
 
 The temperature was 98° to 99°, the pulse 66, the respirations 25, 
 the leucocytes 8800. The sputum showed no tubercle bacilli. 
 
 By February 7 his cough was much better and he was discharged 
 with a diagnosis of subacute bronchitis. 
 
 After leaving the hopsital he ‘‘never felt better in his life.” But 
 early in June, 1906, he found that he could not walk uphill or rapidly 
 without dyspnea and a sense of oppression in the chest. June 5 
 he drank a glass of ale when tired and shortly afterwards had con- 
 siderable discomfort rather than pain in the epigastrium and much 
 nausea. He vomited for the first time in his life. He had some pain 
 in the epigastrium relieved by sodium. phosphate and sodium car- 
 bonate. He slept very little the next three nights. He got up five or 
 six times anight tourinate. Hehadlostnoweight. June8at4p.m. 
 he was suddenly seized with sharp pain in the epigastrium spreading 
 into the chest, through to the back, down both arms, especially the 
 left, and very marked in the precordia. At its onset “‘he burst into 
 a cold sweat,’’ panted for breath, and had “terrible nausea”’ without 
 vomiting. Gastric lavage did not relieve the pain. 
 
 Examination at his third admission, June 8, 1906, showed the car- 
 diac impulse and dullness in the fourth space just inside the nipple line. 
 There was no enlargement to the right. The action was regular, 
 the sounds distant, the aortic second sound greater than the pulmonic 
 second. A soft systolic murmur was heard in the aortic area trans- 
 mitted upward but not heard in the neck, a soft systolic in the mitral 
 
510 FACTS ON THE HEART 
 
 area and the axilla. The arteries were sclerosed and tortuous. The 
 lungs showed a few rales at the bases, hyperresonance throughout, — 
 prolonged, low pitched expiration. The liver dullness extended 
 from the fourth space to the costal margin. The edge was felt one | 
 inch below the costal margin. The temperature was 98° to 101.5°, 
 the pulse 70, the respirations 20, the leucocytes 10,900. The sputum 
 showed no tubercle bacilli. 
 
 About 10 p.m. June 9 the patient had a sudden attack of cardiac 
 weakness following a small dose of trional and sulphonal. Sub- 
 sequently his pain did not return, his appetite returned to normal 
 and the heart sounds improved in quality under treatment with digi- 
 talis. June 21 he was discharged relieved. 
 
 After leaving the hospital he was comparatively well. He walked 
 seven to eight miles daily, but did nothing more violent. He had 
 practically no ‘‘stomach trouble.” Taking care not to overdo, he 
 had no cardiac symptoms. December 29, 1906, he caught cold in the 
 head and thought he spat up a quart of yellow sputum. He was 
 unable to sleep, worried considerably over financial difficulties, and 
 lost ten pounds in ten days. January 8, 1907, he entered the hospi- 
 tal for the fourth time. 
 
 Examination showed the impulse of the heart forceful, corre- 
 sponding with the dullness in the fifth space just inside the nipple 
 line. ‘There was a soft systolic murmur at the apex, not transmitted. 
 The arteries were palpable, slightly tortuous. The lungs showed 
 scattered coarse rales. The temperature was 98.4° to 99°, the pulse 
 80, the respirations 24, the leucocytes 13,400. 
 
 On January 14 the patient was discharged with a diagnosis of 
 bronchitis. 
 
 After leaving the hospital he had only slight dyspnea and cough. 
 He had however some gastric distress. On January 8, 1911, he 
 cought cold; his dyspnea and cough became worse and soon his spu- 
 tum became bloody. He had no definite thoracic pain. January 
 tg he was seized with severe gastric pain and vomited once. After 
 this he felt very weak and helpless and had a good deal of abdominal 
 pain, chiefly in the region of the stomach and the right costal margin. 
 He had some pain in the region of the bladder, some frequency, and 
 burning on micturition. January 20 he entered the hospital for the 
 fifth time. 
 
 Examination showed a well nourished man with Cheyne-Stokes 
 respiration lying propped up in bed, The mucous membranes were 
 pale. The apex impulse of the heart was seen and felt in the fifth 
 
FIBROUS MYOCARDITIS——ILLUSTRATIVE CASES She 
 
 space just outside the nipple. The retrosternal dullness was slightly 
 increased. ‘The upper border of flatness was at the third rib, the 
 lower at the fifth space. The sounds were practically inaudible. 
 There were no murmurs. ‘The systolic blood pressure was 140. The 
 pulses were of very poor quality. The artery walls were tortuous 
 and showed fibrous thickening. The lungs posteriorly showed many 
 coarse and fine moist rales. The patient was coughing considerably 
 and raised blood-tinged sputum. The reflexes were normal except 
 for a double Babinski. There was no stiffness of the neck, no edema, 
 and no paralysis. 
 
 The temperature was 99° to ror°, the pulse 80, the respirations 
 28, the leucocytes 15,000, the polynuclears 93%. The sputum 
 showed thin mucus with fresh blood and a few pus cells. The spe- 
 cific gravity of the urine was 1.026 to 1.032. There was the slightest 
 possible trace of albumin at two of four examinations. The sedi- 
 ment showed a few coarsely and finely granular casts and an occa- 
 sional red blood corpuscle. 
 
 Following admission the pulse was very weak and the patient’s 
 condition extremely grave. January 24 the apex of the heart was 
 just outside the nipple line in the sixth space. The action was heav- 
 ing and forceful. The sounds were very distant. There was gallop 
 rhythm. No murmurs were heard. The pulmonic second sound 
 was greater than the aortic second, not accentuated. The aortic 
 second sound was sharp and ringing. January 29 the patient 
 appeared somewhat improved. A systolic murmur was heard all over 
 the precordia, loud over the aortic area, but loudest at the apex 
 and transmitted a short distance to the axilla. The aortic second 
 sound was greater than the pulmonic second. February 3 he became 
 pulseless and suddenly died. 
 
 Clinical Diagnoses (from Hospital Records). 
 
 First entry. Dec. 1904. Neurasthenia? 
 
 Second entry. Jan. 1906. Subacute bronchitis. 
 
 Third entry. June 1906. Myocarditis with dilatation. 
 
 Fourth entry. Jan. 1907. Arteriosclerosis. 
 
 Fifth entry. Jan. 1911. Arteriosclerosis. 
 
 Coronary sclerosis with thrombosis. Myomalacia cordis. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Narrowing of the coronary arteries, very possibly with 
 
 Myocarditis. 
 
 Terminal infection? 
 
512 FACTS ON THE HEART 
 
 Anatomical Diagnosis.—Arteriosclerosis. 
 
 Arteriosclerotic occlusion and thrombosis of the coronary arteries. 
 
 Infarct of the myocardium. 
 
 Chronic interstitial myocarditis with slight aneurismal dilatation 
 of the wall of the left ventricle. 
 
 Mural thrombi, left ventricle. 
 
 Fibrous and fibrocalcareous endocarditis of the mitral and aortic 
 valves. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic interstitial hepatitis. 
 
 Hyperplasia of the spleen. 
 
 Chronic pleuritis. 
 
 Obsolete tuberculosis of the lungs. 
 
 Emphysema of the lungs. 
 
 Dr. RicHarpson: The chronic interstitial hepatitis was not very 
 marked. 
 
 Dr. Cazsot: A point of great interest in this last case is that the 
 symptoms pointing to coronary occlusion and cardiac infarction 
 apparently showed themselves as much as seven years before the 
 patient’s death. They are more definite and recognizable in the 
 later years of his illness, but still are spaced by long intervals of very 
 fair health e.g. between 1907 and 1911. Perhaps this case exempli- 
 fies a group intermediate between some of those ordinarily classed 
 as chronic fibrous myocarditis (without acute seizures) and the more 
 acute infarction next to be described. 
 
 Il. MYOCARDIAL INFARCTION 
 
 Since the studies of Herrick, Wearn*, and others the clinical 
 picture corresponding to the blocking of a coronary artery with necro- 
 sis and infarction of the heart wall has been emerging more and more 
 clearly. 
 
 The present series contains twenty cases of acute cardiac infarction, 
 fifteen of them with blocked coronary. ‘There were nineteen males 
 and one female. The ages varied from thirty-five to seventy-nine 
 but only three were under fifty, and the average age was sixty years. 
 Considering that it is the arteriosclerotic coronary lesions which pro- 
 duce the infarction in most cases, this age is what one would expect. 
 The extraordinary excess of males in this as in all the various series 
 of cases either of infarct or of angina pectoris so far reporteaaay has 
 
 * Wearn: Amer. Jour. Med. Sciences, February, 1923. 
 
MYOCARDIAL INFARCTION 513 
 
 not so far as I know been satisfactorily explained. In Wearn’s 
 nineteen autopsied cases there were but nine women. 
 
 Chronic passive congestion was present in life and after death in 
 twelve of our twenty and in eight of Wearn’s nineteen. There had 
 been previous anginoid attacks in six of Wearn’s nineteen cases and in 
 seven of our twenty cases. The interval between the first attack 
 and the fatal seizure varied from two weeks to six months in five of 
 our seven recurrent cases. But in one, the anginoid attacks began 
 two years before death and in two others (men of seventy) there 
 had been numerous anginoid attacks scattered through the seven 
 years preceding death. One of these men described his sufferings as 
 beginning in the left upper chest sometimes with ‘“‘rheumatic”’ (dull?) 
 pain, somtimes with ‘‘twisting pain.” With this was a sense of 
 tremendous pressure in the precordia and a feeling “as if his left arm 
 was being torn off from his body.’’ These seizures lasted three or 
 four hours and had no definite relation to exertion, but seemed to 
 him connected with ‘‘catching cold” (i.e. perhaps with cough due to 
 passive congestion?). The attacks had been increasing in intensity, 
 so that the patient said he knew he was “‘playing with death” (often 
 near death?). 
 
 In the hospital ward December 11, 1902, he had prolonged pre- 
 cordial distress not relieved by nitroglycerin. December 17 an acute 
 conjunctivitis appeared. The patient had been up and about the 
 ward until the 25th, when slight dyspnea appeared. On the 27th 
 there came a sudden sense of suffocation without pain but with great 
 pallor and dyspnea. The heart was slow and regular but the chest 
 rapidly filled with rales and he died in fifteen minutes from the onset 
 of the attack. 
 
 At necropsy there was arteriosclerosis of the aorta and coronaries 
 with thrombosis of the left descendens and some of its branches, 
 fibrous myocarditis and an area of acute infarction in the left ven- 
 tricle. Syphilitic hepatitis. Chronic passive congestion. 
 
 The occlusion of the coronaries was in places due to calcareous 
 material, in other places to blood clot more or less organized. 
 
 The other long case which lasted from 1904 to 1911 has been 
 described above (p. 508). 
 
 Histories like this and the frequent association of chronic fibrous 
 scars with the acute infarction, as in twelve of our twenty cases, 
 make it reasonable to assume that some at least of the older fibrous 
 patches are due to previous infarcts which have accompanied earlier 
 attacks and have healed so as to make recovery possible. 
 
 33 
 
514 FACTS ON THE HEART 
 SITE OF PAIN 
 
 A point of great importance is the epigastric localization of the 
 initial pain in ten of our twenty cases. Such pain is rarely thought 
 of by physicians as having any possible relation to coronary occlu- 
 sion, but is often attributed to “acute indigestion,” especially when 
 it begins after a meal and is associated with vomiting. Probably 
 this explains many of the sudden deaths reported in daily papers under 
 the diagnosis of ‘‘acute indigestion” or ‘‘ptomaine poisoning,” espe- 
 cially when the seizure occurs at a banquet, perhaps at the end of an 
 exhausting address. 
 
 In Wearn’s series the acute epigastric pain caused several patients 
 to be operated on with diagnosis of perforated peptic ulcer, acute 
 pancreatitis or acute cholecystitis. Others were mistaken for 
 pneumonia or pleurisy. 
 
 Epigastric pain may be the beginning of attacks of ordinary angina 
 pectoris without infarction. Moreover seven of the infarcted hearts 
 in this group were associated with precordial and never with epigas- 
 tric pain. Three were free from pain altogether, one dying after an 
 operation for cancer of the sigmoid, the other two of diabetic coma 
 with gangrene. In four cases the pain began in the epigastrium but 
 was later felt in the precordia and in the left arm. 
 
 In distinguishing the epigastric pain due to cardiac infarct from 
 the pain of acute peritonitis, it is of value to note that the pain of 
 infarction is often accompanied by sudden pulse failure and fainting 
 which are not signs of an early acute peritonitis. Pulse failure, i.e. 
 a sudden rapidity, irregularity, then partial or complete disappearance 
 of the radial pulse, was noted in nine of our twenty cases. Sudden 
 faintness with or without nausea and vomiting was recorded in four 
 cases. There was arrhythmia, usually auricular fibrillation, noted in 
 nine cases. 
 
 The duration of the attacks of pain was for hours or for days in all 
 our 20 cases. ‘This point together with the lack of any relation to 
 exertion or of any considerable relief from nitrites, give us the most 
 important clues to the exclusion of ordinary angina pectoris. 
 
 The coronary arteries were arteriosclerotic in all our cases and one 
 or more were occluded in fourteen of twenty cases. In the remaining 
 six cases the coronaries are described as: 
 
 1. Sclerotic but not occluded (one case). 
 
 2. Sclerotic but, free (one case) 
 
 3. Sclerotic and narrowed but free (three cases). 
 
 4. Sclerotic and capacious (one case). 
 
SITE OF PAIN 515 
 
 In four cases the occlusion was due to thrombosis (as well as to arte- 
 riosclerosis) ; in sixteen there was arterioslerosis alone. 
 
 The systolic blood pressure was over 165 in three cases (highest 
 250), 160/100 in one, normal in seven, not recorded in nine. Hyper- 
 trophy and dilatation of the heart was present in nineteen out of twenty 
 cases, as would be expected from the age and the arteriosclerosis. 
 Five of the hearts weighed 600-680 grams, eight from 500-600, two 
 from 400 to 500, and five less than 400 grams. 
 
 Intracardiac thrombi were recorded in eleven of twenty cases. 
 
 Fever was present in eight cases, slight Jeucocytosis in thirteen; 
 but neither of these was sufficiently constant or marked to be of diag- 
 nostic value in patients so acutely and desperately ill. 
 
 Syphilitic aortitis was found in three out of 20 cases (1816, 2488, 
 3759) and in two of these the mouths of the coronaries were obstructed 
 by the syphilitis process though there was some sclerosis in the 
 coronaries as well. In addition to these three there was evidence of 
 syphilis in the liver of a fourth patient (992). The Wassermann 
 reaction was tried for in 2 cases and was positive in neither. 
 
 As to physical signs of cardiac infarction we may say that there are 
 none. No characteristic electrocardiographic changes are present, 
 though peculiar complexes have been noticedinsomecases. Arrhyth- 
 mia may be present especially near the end of life but is not con- 
 stant or characteristic. Systolic murmurs are often to be heard 
 and never significant. In one of our cases (667) during the last seven 
 hours of life (tortured with dyspnea and pain) there was audible over 
 the precordia a series of short sharp sounds spaced at equal intervals 
 and all exactly alike—apparently all first sounds. In the pulmon- 
 ary area a faint ticklike suggestion of a second sound was to be 
 heard after each of the first sounds. The latter corresponded in 
 rhythm with these sounds. There was no arrhythmia. At the end 
 the heart stopped suddenly. 
 
 Necropsy showed a thrombosed right coronary (sclerotic) and an 
 area of acute infarction in the right ventricle. The thrombus 
 extended down from a large clotin the sinus of Valsalva. Correspond- 
 ing with the infarcted area there was a mural thrombus inside the 
 
 heart and an acute pericarditis outside. 
 _ The patient’s symptoms had begun six weeks ago with a sudden 
 vertigo and a ‘“‘feeling that his heart had stopped,” together with 
 severe precordial pain unrelated to exertion. These attacks recurred 
 several times in the next six weeks. 
 
516 FACTS ON THE HEART 
 
 This case is the only one in our series in which the right coronary 
 alone was affected. In the other cases either the left coronary alone 
 (9 cases) or both coronaries were affected (5 cases), or there was no 
 actual occlusion (5 cases). » 
 
 Clearly the diagnosis of coronary occlusion with infarction of 
 the heart must depend chiefly on the history and course of the disease, 
 not on physical examination. Hence it may be well to quote a few 
 more of the patients’ stories. 
 
 1. ‘A week ago I got a terrible pain at the pit of my stomach and 
 an awiul pressing in along withit. A while after I felt it in my heart 
 and inside my left arm.”’ 
 
 Two days after that on which he told us this, the patient (a man 
 of sixty-three) woke at 2:50 a.m., suddenly sat up, gave a cry and 
 fell back dead. Necropsy showed that the apical part of the left 
 ventricular wall and about one-third of the ventricle above this was 
 thinned to five or six mm. and showed much fibrous change in the 
 midst of which there were, here and there, small dirty-yellowish 
 homogeneous soft necrotic areas. The right coronary was free but 
 showed much fibrous or fibro-calcareous change. The left was like 
 a beaded pipe-stem or a solid cord, its lumen gone. In places this 
 was owing to the sclerosis, but the vessel contained also a recent 
 thrombus. There was an intraventricular thrombus over the site 
 of the fresh infarction. 
 
 During the last two days of his life his cardiac impulse was regular 
 and forceful though the heart sounds were weak. No cardiac mur- 
 murs were detected. His blood pressure was 120/85. 
 
 As he had dyspnea and palpitation for seven years, we may con- 
 jecture that the coronary thrombus originated from the intraventri- 
 cular thrombus, though the sequence may have been in the opposite 
 direction. 
 
 2. For seven or eight years a man of sixty-five had had occasional 
 epigastric distress one to two hours after meals. ‘Two weeks ago he 
 had severe abdominal pain lasting most of four days, with dyspnea, 
 orthopnea and edema. He lived forty hours in the hospital with 
 orthopnea and double hydrothorax. I could hear almost no heart 
 sounds at the apex. At the base they were normal though faint. 
 No murmurs. Pulse regular, fair volume and tension. From his 
 usual position leaning forward over his knees he suddenly fell back 
 against the bed-rest. The interne went to him immediately, found — 
 
SITE OF PAIN 517 
 
 him pulseless and could hear no heart sounds. Apparently his 
 sudden death was not preceded by pain. 
 
 Necropsy showed that the left coronary was practically occluded 
 by arteriosclerosis. The right showed a moderate amount of fibrous 
 and fibrocalcareous change and a reduction of its lumen at one point. 
 The left ventricle was everywhere reduced in thickness except for a 
 strip about 2.5 cm. wide where its wall measured fifteen mm. In 
 the thinned portions it often came down to one mm. The wall 
 (except for the strip just described) showed opaque discrete or conflu- 
 ent dull grayish-yellow areas. Also grayish-white streaks and patches 
 of fibrous tissue. ‘Towards the apex the wall was like thin leather. 
 The changes extended into the region of His’s bundle. 
 
 3. A man of sixty-eight had suffered for five years with attacks 
 of epigastric pain and faintness. For a year he had felt soreness in 
 the precordia, worse on exertion. Ten days ago he suddenly began 
 to have pain limited to the epigastrium, severe, non-radiating (dura- 
 tion?). For four days he has had dull pain and “weakness” in the 
 middorsal region. 
 
 During his first two days under observation he had ‘‘three dis- 
 tinct attacks of angina, with dyspnea and phlegm in his throat.” 
 The heart showed no enlargement clinically, was regular and not 
 rapid. No murmurs. For most of the time during the last days of 
 his life his pulse was strong and regular. In some of his anginal 
 attacks his heart continued to be regular though the sounds became 
 weak. In other attacks it was absolutely irregular with a large pulse 
 deficit. Blood pressure 130/90. He died in a week. 
 
 Necropsy: Coronary sclerosis without occlusion. The myocar- 
 dium of the left ventricle was reduced to one to five mm. in thickness 
 with streaks and patches of fibrous tissue and indefinitely bounded, 
 dull, dark brownish red, homogeneous areas. A mural thrombus in 
 the left ventricle could only with difficulty be distinguished from the 
 softened myocardium beneath it. The wall of the left ventricle 
 was generally boggy and yielding. It tore easily and in places bulged 
 (cardiac aneurism). There was subacute and also chronic pericardi- 
 tis. The heart weighed 600 grams, though no enlargement was 
 detected in life. Valves normal. 
 
 4. A woman of sixty-one was seized six days before she entered 
 the hospital with very severe epigastric pain, faintness and vomiting. 
 These symptoms recurred twenty-four hours before her entrance with 
 
518 FACTS ON THE HEART 
 
 vomiting, and did not afterward abate. The heart was moderately 
 enlarged, rapid and regular, with a rough apical systolic murmur 
 replacing the first sound. The pulse was barely perceptible and 
 disappeared soon after she reached the ward. Seen by Dr. Maurice 
 H. Richardson who wrote: ‘“‘There is a very strong indication for 
 operation—probably to reheve pancreatic hemorrhage—but her 
 general condition is too bad to warrant any interference.” Dr. 
 Hugh Cabot concurred in this diagnosis. A definite mass palpable 
 in the epigastrium lent support to the idea of pancreatitis. The 
 leucocytes were 17,000, the temperature normal. She died on the 
 day of her arrival at the hospital. 
 
 At necropsy there was arteriosclerotic occlusion of the left coro- 
 nary with softening and necrosis of the wall of the left ventricle. The 
 heart weighed 307 grams, its valves normal. The epigastric mass 
 was a congested liver. The thymus was persistent. 
 
 6. A medical army officer of fifty-two had been in excellent health 
 and had done very strenuous work at Camp Devens in the spring of 
 1917. From May 3 to 13 he was prostrated with an obscure type of 
 fever, thought to be typhoid or paratyphoid but without cardiac 
 symptoms. (Wassermann negative, syphilis denied.) Recovery 
 seemed complete, but June 3d and 4th he had several attacks of 
 palpitation and irregular pulse, with belching but no pain. The 
 attacks came soonaftereating. Electrocardiogram June 14thshowed 
 a flat T-wave in Lead II; otherwise normal. June 24th at 8:10 he 
 suddenly cried, ‘I can’t get my breath,” clutched the region of his 
 heart, became very cyanotic, and died in a few minutes. 
 
 At necropsy the left coronary was practically occluded by arterio- 
 sclerosis, the right considerably narrowed. The left ventricle showed 
 chronic fibrous myocarditis and fresh infarcts. 
 
 I have allowed a good deal of space for the description of myocar- 
 dial infarct because it is certainly not uncommon as a cause of sudden 
 death yet is not often considered at all in the differential diagnoses 
 attempted in life. A skillful and conscientious medical examiner 
 tells me that about 10% of all the medico-legal cases of sudden death 
 examined by him in the last few years have proved to be cases of 
 coronary occlusion with infarct. 
 
 We may distinguish four types: 
 
 (1) Sometimes death follows the occlusion so rapidly that there is 
 no time for the formation of aninfarct. This was true in four cases of 
 
519 
 
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520 FACTS ON THE HEART 
 
 our series (1537, 2371, 2566, 3177). Here the clinical picture may be 
 exactly the same as in those with infarct. For example a woman of 
 forty-two, with syphilitic aortitis which at necropsy occluded both 
 coronary orifices, had suffered from typical attacks of angina pectoris 
 for six months before her death. In the first of these she fainted and 
 was unconscious for half an hour. Her second and fatal attack of 
 faintness came on suddenly with clutching pain in the precordia. 
 The heart beat feebly a few times and stopped. Post-mortem there 
 was no infarct. 
 
 A second case of the same type but without evidence of syphilis 
 occurred in a woman of sixty who had had one severe attack of angina 
 pectoris three years previously and been dyspneic ever since then, 
 with orthopnea for the past three weeks. Nevertheless a plastic 
 operation on the abdominal wall was undertaken for the relief of 
 enteroptosis then (1902) just beginning to become a fashionable 
 diagnosis. She was cyanotic at the beginning of the operation and 
 after it had a weak but regular pulse of 120. The heart was 
 negative. On the second day after the operation vomiting and 
 pulse failure suddenly supervened at 5:45 a.m. and she died in 
 twenty minutes. _ 
 
 Necropsy showed that the left ventricle was only four mm. in 
 thickness; its muscle largely replaced by fibrous tissue. The branch 
 of the coronary running toward this thinned portion was more or less 
 occluded by a reddish-gray translucent thrombus. The wall of 
 the vessel showed a yellowish discoloration. The right coronary 
 was slightly sclerosed. There was an acute pericarditis and infarcts 
 of the liver and spleen. The heart weighed 435 grams, valves normal. 
 No cardiac infarct. 
 
 Aortic Stenosis with Acute Vegetations Blocking the Coronary 
 Orifices —There was extensive fibrous myocarditis but no infarct and 
 in life no pain or other symptoms beyond those of aortic stenosis, 
 until one hour before her death when she suddenly began to have 
 extreme dyspnea and became pulseless. (Necropsy 2238.) 
 
 (2) The second type, represented by seven cases of this series, 
 shows acute infarction without chronic fibrous myocarditis and death 
 follows the first coronary blocking. 
 
 (3) The third or recurrent type shows post-mortem both acute 
 infarction and chronic fibrous myocarditis. The clinical picture 
 and the history of these cases allows us to suppose that the fibrous 
 myocarditis (or part of it) corresponds to previous occlusion of coro- 
 nary branches, the infarct having become organized. Later a larger 
 
MYOCARDIAL INFARCTION—ILLUSTRATIVE CASES 521 
 
 branch is blocked and this results in an infarction which leads to 
 immediate death. 
 
 (4) There are also occasional infarctions without demonstrable 
 occlusion of an artery and without clinicalsymptoms. For example: 
 
 Typical Cardiac Infarct without Any Symptoms in Life (Necropsy 
 2183).—The patient died after an operation for diabetic gangrene and 
 sepsis, without any particular heart symptoms and without any 
 noticeable suddenness. 
 
 SUMMARY AND CONCLUSIONS 
 
 1. Cardiac infarction is a frequent cause of sudden death in 
 elderly men. As the patient may vomit in his attack, such deaths 
 are often explained as due to “‘acute indigestion.”’ 
 
 2. When death does not follow so swiftly, the severe epigastric 
 pain often complained of may lead to an operation for pancreatitis, 
 perforated peptic ulcer, etc. 
 
 3. An infarction may heal and another may occur months or 
 years afterwards. 
 
 4. Sudden, severe, prolonged epigastric pain (often lasting for 
 hours without relief by nitrites), especially if associated with faint- 
 ness and pulse failure, should always lead us to suspect cardiac 
 infarction. If in an elderly man there are prior, concomitant or sub- 
 sequent “‘gastric” or anginoid attacks of the ordinary type, the 
 diagnosis of infarct is probable. 
 
 5. Only about half the cases show any evidence of passive conges- 
 tion before or after death. 
 
 6. Four types may be distinguished: 
 
 (a) Potential infarction (blocked coronary and sudden death 
 before an infarct has time to form.) 
 
 (b) Rapidly fatal infarct. 
 
 (c) Recurrent infarct with an interval of weeks months or 
 years between the first attack and death. 
 
 (d) Symptomless acute infarct. 
 
 MYOCARDIAL INFARCTION—ILLUSTRATIVE CASES 
 Case 4138 
 
 First.entry. An American factory girl of twenty-two entered 
 November 7, 1895, for treatment of an abscess of the thigh which 
 had discharged for seven years. Four operations had already been 
 done. 
 
 At the fifth two discharging sinuses were enlarged and the abscess 
 cavity curetted out. After a somewhat troublesome convalescence 
 
522 FACTS ON THE HEART 
 
 she was discharged January 22, with a diagnosis of osteomyelitis 
 
 May 20, 1896, she wrote that she had gained a great dealand was 
 
 able to walk about the house without crutches. 
 
 Second entry. January 29, 1920. Age: 47. 
 
 Both parents died of heart disease. Her mother had several 
 miscarriages. One living brother was very ill during childhood, had 
 black skin, which peeled off, and was said to have inherited “bad 
 blood.” Several relatives died of cancer. 
 
 Additional past history. Measles and scarlet fever in childhood. 
 Bronchitis for about six weeks every winter. Typhoid fever thirty- 
 one years ago. Injured the right leg just above the knee thirty years 
 ago. The disease described in the first entry followed. The knee 
 was opened thirteen times and discharged constantly for nine years. . 
 Twenty-five years ago she had a sudden eruption of erysipelas over 
 the legs several times. Twelve years ago she had tonsillitis. Nine 
 
 Mid sterual ( 
 5 
 Nipple 
 
 3cm. 8.5 cm. ° 4 cm. 
 
 Fic. 98.—Measurements by percussion. 
 
 years ago the right leg was amputated. For a number of years she 
 had throbbing headache every two weeks, better for the last twelve 
 years, when she had worn glasses. For ten years, with the attacks 
 of bronchitis, she had slight cough, palpitation, sharp localized pre- 
 cordial pain, and occasional attacks of orthopnea. She urinated 
 five or six times at night. For the past few years there was occasional 
 burning. Catamenia began at fifteen, but after one period ceased 
 until eighteen. Since then it had been very regular, at times rather 
 profuse. Slight brownish yellow discharge, especially after the 
 periods. Four years ago she weighed 160 pounds, her best weight. 
 Usual weight 150. 
 
 Three days ago, during the ten minutes’ walk to the office where 
 she was now a telephone operator, she had a feeling of depression and 
 intense pain under the upper part of the sternum and suprasternal 
 region. After sitting down for a short time she felt normal, but on 
 resuming her walk had the same feeling until she sat down in her 
 office. For the next two days she had the same pain on the way to 
 the office. The day before admission it was more severe. In the 
 late afternoon she had another attack, this time very severe, and — 
 for the first time radiating to the left shoulder and down the whole 
 
MYOCARDIAL INFARCTION—ILLUSTRATIVE CASES 523 
 
 left arm to the finger-tips. This lasted more than ten minutes, 
 relieved by small white pills given by a physician. In the evening 
 she had morphia, which kept her awake the greater part of the night. 
 She vomited several times. 
 
 The patient was well nourished. Head and throat negative. 
 Apex impulse of the heart not found. Action slow. Sounds of 
 good quality. P. greater than A». Electrocardiogram showed 
 normal rhythm, inverted T wave in Lead II. Pulses and arteries 
 normal. Systolic blood pressure 1oo-125, diastolic 50-80. Abdo- 
 
 Fic. 99.—Necropsy 4138. Arteriosclerosis of the aorta with coronary occlusion. 
 Thrombus of the left coronary artery. Mural thrombus of the left ventricle. Hyper- 
 trophy and dilatation of the heart. Measurements by X-ray the day before death. 
 (Roentgenological Department, Massachusetts General Hospital.) 
 
 men: Liver dullness 5th rib to costal margin. Edge just felt on 
 inspiration. Genital, rectal and pelvic examinations not made. 
 Extremities and reflexes normal except for amputation of right leg 
 above the knee. Pupils normal except for sluggish reactions to light 
 and distance. 
 
 Temperature normal except for rise to 100° the day after entrance. 
 Pulse 68-100. Respirations 15-28. Urine: Normal amount, 
 except one record of J10. Sp. gr. 1020-1030. Cloudy at one of 
 three examinations, a very slight trace to the slightest possible trace 
 
524 FACTS ON THE HEART 
 
 of albumin at two. Renal function 60%. Blood: Hgb. 75%, 
 leucocytes 8600-6400, polynuclears 79%. Wassermann negative. 
 X-ray. Heart shadow enlarged downward and to the left. Promi- 
 nence also in region of left auricle and pulmonary artery. Diameter 
 across base of heart not particularly increased. Aortic knob promi- 
 nent. (See Fig. gg.) 
 
 The patient was given the usual hospital diet and codeia gr. Ws. 
 Shortly after entrance she had an attack of pain in the chest referred 
 down the left arm, relieved by nitroglycerin gr. 499. The same 
 dose was given on ten out of fifteen days until February 13. Aspirin 
 gr. v was ordered on four occasions for headache; also phenacetin 
 gr. v once, and pantopon gr. 14 in four doses at one-hour intervals. 
 February 21 and 22 pyramidon gr. v. was given. She had had no 
 recent attacks at that time, had been up and about in a chair and able 
 to walk a few steps. February 24 she was discharged to stay for a 
 week in the country before returning to work. 
 
 Third entry, November 14, 1920. Since her discharge she had 
 been very comfortable until two weeks ago, except for occasional 
 precordial pains, easily and immediately controlled by sodium nitrite 
 tablets. Two weeks ago she had a sudden sharp pain in the epigas- 
 tric region, thought at first to be acute indigestion, somewhat 
 relieved by eating toast and taking soda. Two days later the painful 
 attacks were higher in the precordial region and occasionally radiated 
 to both arms. ‘The nitrite tablets had less effect, the attacks lasting 
 five minutes or more and occurring on any exertion. She had taken 
 
 On5 Cm. 
 3 
 A 
 o ro 
 = A, 
 7c Ao, 
 S rae 
 7G, Shletaey OF Sorjerercaie 
 Fic. 100. 
 
 as many as twelve tablets a day. The morning of entrance a severe 
 attack began at five o’clock and lasted until after eight without relief 
 from codeia or morphia. She brought a note from her physician 
 saying that she had had no treatment until two days ago. The 
 morning of entrance she had had 34 of a grain of morphia. Amyl 
 nitrite made her vomit and increased her pain. She had been on © 
 sodium nitrite gr. i 4 id. for months and digitalis leaves gr. i.b.i.d. 
 for two days. The present attack came on without any unusual — 
 exertion. 
 
MYOCARDIAL INFARCTION—ILLUSTRATIVE CASES 525 
 
 Physical examination. Obese. Complained of precordial pain 
 after every movement. Grayish pallor with slight cyanosis of 
 skin and mucosae. Lungs: Many fine and coarse bubbling rales 
 at both bases behind, on the left rising to the angle of the scapula. 
 Apex impulse of heart not found. Action slightly rapid. Faint 
 tic-tac rhythm. Sounds of very poor quality. Ps doubled and 
 accentuated. Pulses of poor volume and tension. Arteries normal. 
 Abdomen: Liver dullness from 5th rib to 3 cm. below costal margin, 
 where a smooth non-tender edge was felt. Very slight edema of 
 left ankle. Pupillary reactions very slight. 
 
 Temperature 97°-100.5°. Pulse 100-109. Respiration 20-27. 
 Blood pressure 85 /60-80/65.. Urine not recorded. Blood: Hgb. 
 go%. Leucocytes g600. Polynuclears go%. Wassermann negative. 
 
 The patient was given soft solids. Fluids were limited to 1500 
 c.c. Morphia in 1 grain doses, once with atropin gr. 1490, was given 
 p.r.n. every three hours, whiskey 3 2 b.i.d., digitalis leaves gr. iss t.i.d. 
 She had a rather poor night and complained of soreness over the lower 
 sternal region. Next day she suddenly became cyanotic, complained 
 of sharp pain in the precordial region, had Cheyne-Stokes breathing, 
 and died. 
 
 Clinical Diagnosis.—Angina pectoris. 
 
 Myocardial insufficiency. 
 
 Coronary occlusion? 
 
 Amputation of right leg. 
 
 Dr. Richard C. Cabot’s Diagnosis —Arteriosclerosis. 
 
 Arteriosclerosis of the coronary arteries with occlusion. 
 
 Myocardial infarction (probably). 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis —Slight arteriosclerosis of the aorta. 
 
 Arteriosclerosis of the coronary arteries with occlusion. 
 
 Thrombus of the left coronary artery. 
 
 Infarct of myocardium. 
 
 Mural thrombus, left ventricle. 
 
 Hypertrophy and dilatation of the heart. 
 
 Edema of the lungs. 
 
 Fatty metamorphosis of the liver. 
 
 Soft hyperplastic spleen. 
 
 Fibromyomata of the uterus. 
 
 Edema piae. 
 
 Old amputation right thigh. 
 
. 2 
 
 526 FACTS ON THE HEART 
 
 Dr. Oscar RicHARDSON: The brain was frankly negative, the 
 vessels of Willis negative. The abdominal organs were out of the 
 picture. 
 
 The heart weighed 415 grams. She wasa strongly built, muscular 
 woman, and the hypertrophy is moderate in amount. If she had a 
 heart that weighed 325 grams we should not think anything about 
 it. The cavities showed slight dilatation and the valves were nega- 
 tive. The left ventricle wall was 13 mm. and the right 3. That is 
 about right. The myocardium generally showed no chronic myocar- 
 ditis. But in the region of the left apex there was an area about two 
 inches across where there was some thinning. In places it was some- 
 what fibrous and in other places rather soft. The right myocardium 
 microscopically was negative. There was possibly a little fatty 
 infiltration. 
 
 The left coronary showed considerable sclerosis, and about 
 two cm. from the region where the coronary breaks up into 
 branches one of the branches was occluded by a small thrombus. 
 Of course the area in the left ventricle was connected with that 
 occluding thrombus. Whether that was the last thing that occurred 
 I do not know. 
 
 The vessel generally showed considerable sclerosis, and although 
 the first portion of the right coronary artery was in pretty good ~ 
 condition, still it showed some sclerosis. Looking on a little further 
 we found a marked pipe-stem artery. These coronaries had been 
 diseased for a long time, and the left had been occluded by the small 
 thrombus, which was the source of the infarct in the myocardium in 
 the region of the apex. 7 
 
 The remarkable thing is that we should not have found more 
 frank myocarditis. But every once in a while for some reason the 
 tissues maintain their condition under the decreased supply of the 
 blood. In the left ventricle, over the area of thinning and infarction, 
 there were several frank thrombotic plaques, thrombi arising on the 
 endocardium over that area of degeneration, in this case a perfectly 
 frank cause for them. Somtimes we find them and really cannot 
 state anatomically why they are there. There was no pericarditis 
 and no growth from the blood, so that if there was any temperature it 
 must have been due to the thrombi. 
 
 There was only a very slight amount of arteriosclerosis in the 
 aorta. In this case it seemed to be particularly of the coronaries 
 and no other vessels in the body. We took some tissue to be sure — 
 there was no syphilitic taint, and there was none. 
 
MYOCARDIAL ABSCESS 527 
 
 The lungs showed some edema, otherwise nothing. The lym- 
 phatic apparatus was negative. 
 
 The anatomical diagnosis is essentially the basis for the clinical 
 picture in this case. 
 
 A PuysiciAn: Do you often find arteriosclerosis so localized as 
 that? 
 
 Dr. RICHARDSON: Yes; that is one of the strange things about 
 arteriosclerosis. 
 
 Dr. Casot: That is one of the common things and one of the 
 tragic things. We may have arteriosclerosis somewhere else and it 
 will do no harm, but if we have two or three inches of it in this little 
 place in the heart, that sclerosis will kill. This was a typical case of 
 its kind. I think everyone sees cases of its exact counterpart. They 
 run very much alike. 
 
 A PuystctaAn: How common Is it at that age? 
 
 Dr. Casot: Not very uncommon. We expect it later. 
 
 A PuysictANn: Are the coronaries more prone than other arteries 
 to arteriosclerosis? 
 
 Dr. Casort: I don’t think I could say that. I should say the 
 abdominal arteries get it most, and then the big arteries like the 
 aorta. Ishould say the brain arteries suffer as often as the coronaries. 
 
 Dr. RICHARDSON: Yes, it seems to hit the coronaries or the vessels 
 of Willis. 
 
 Ill. MYOCARDIAL ABSCESS 
 
 In our 4000 necropsies there were fifteen cases in which genuine 
 abscess of the myocardium was found. Cases of myomalacia 
 (infarction) without true pus are here excluded. Only five of these 
 fifteen cases were over the twenty-fourth year. One case occurred in 
 a baby only eighteen months old, and excluding this case there were 
 six others at or under the fifteenth year. There were thirteen males 
 (seven boys) and two females in this group. 
 
 In all cases the cardiac abscess was only a minor item ina general 
 septicemia. This septicemia originated in osteomyelitis in four 
 cases. The septic focus in two cases was the heart valves, in one 
 case a carbuncle, in one case the middle ear, and in two cases a small 
 incised wound of the forearm. In four cases no primary focus could 
 be distinguished. | 
 
 In one case an actinomycosis of the chest wall was the beginning of 
 the disease which in this case ran a much more chronic course than 
 any of the others, corresponding to the difference in etiology. 
 
528 FACTS ON THE HEART 
 
 The micro-organisms present were staphylococcus aureus in nine 
 cases, streptococcus in three cases, both of these organisms in one 
 case, actinomycosis in one case, while the remaining case remains in 
 doubt. 
 
 Ten acute septic cases ran a rapid course lasting from two to 
 eighteen days from the first symptom to death. One case of actino- 
 mycotic abscess lasted four months and really belongs to a different 
 group from the rest. 
 
 The symptoms are ihose of a general septicemia without anything 
 to call attention to the heart. Chills, ‘‘picket-fence temperature,” 
 marked leucocytosis (90,000 in one case), and increasing stupor 
 (‘‘typhoidal state’) are the main features. One of our cases was 
 mistaken for typhoid fever. In the rest the diagnosis of a general 
 septicemia was made, but there was no suspicion of any cardiac 
 involvement. 
 
 Nor were there any physical signs of tmportance. The heart 
 was not enlarged, clinically or at necropsy, in twelve of the fifteen 
 cases; in three cases (aet. 28, 40, and 46) there was slight enlargement 
 (345,429 and 450 grams). No murmurs were heard in thirteen cases, 
 systolic apical murmurs in two. There was no arrhythmia. 
 
 Suggestions of embolism were noted in one case in which one radial 
 pulse disappeared and the spleen increased rapidly in size during 
 observation—an event pointing always (in my experience) to an 
 infarct, whether bland or septic. In two other cases a double septic 
 parotitis gave evidence of the diffuseness of the septic processes, if 
 not of embolism. 
 
 At necropsy the following metastatic infectious processes were 
 Presen: 
 
 TABLE 118.—LOCAL SEPTIC PROCESSES ACCOMPANYING CARDIAC ABSCESS 
 
 Renal abscess i. oy «ss inj dave ee ten cs Set ck None mae 12 
 Pericarditis... 5 cs o8 islets vind givadniacnel ceo kte ance oe ee 9 
 Lung abscess; 05. SAV or ee ae eh ag 8 
 EMpyemag oe Pe odin ea oe Me dient ane allege es ee 5 
 Splenic abscess icws. ii. ae oe, cag ai wee as 0 yee cer 4 
 Subcutaneous abscess’...c . oan. eh vale sole cio lath ait cn eet eee 3 
 Multiple synovitis... eo... lec bees ae ee a nl 3 
 Liver abstess es -weciiiices oo ee. 5 log ib ee ee 2 
 Brain abscess/%, + 2..05;. 2s v6 4s seve dy ee eee 2 
 Abscess.of :the prostate..: .4o5s- 4.5 tt 2-9 go ty ea I 
 Abscess of the: thymus ..2.$20o%ud 4.890. ho 5 Ceo I 
 Abscess of the rectus musclé. 2. 32 05. ee eae Soe I 
 
 Retroperitoneal abscess) a, init. ee ies 2 a ete ae I 
 
MYOCARDIAL ABSCESS——ILLUSTRATIVE CASES 529 
 
 During life there were, as has been said, identifiable foci of sepsis, 
 most often in the bones, in peripheral wounds, or on the heart valves. 
 
 The coronary arteries showed nothing of note in thirteen cases. 
 In one case (Necropsy 59) the branches of the coronary artery in 
 the left ventricle contained grayish-red plugs. In another, one 
 of the arteries was disorganized. One of the abscesses extended to 
 the region just beneath the epicardium. They were usually covered 
 with patches of fibrous exudate. Outside the well marked abscesses, 
 there was often invasion of the spaces between the muscle fibers by 
 polynuclear leucocytes, and masses of cocci. 
 
 SUMMARY 
 
 Our general conclusion, from these cases, is that it is hopeless to 
 make any attempt to diagnose or to treat myocardial abscess. It 
 may be suspected, like renal abscess and pericarditis, as a frequent 
 ~ complication of staphylococcus sepsis, and especially of osteomyelitis, 
 in boys. 
 
 One wonders whether healing and recovery ever take place in 
 such cases. I see no reason why this is not possible. Perhaps some 
 of the patches of scar tissue—which we find in the myocardium 
 without any close relation to the main branches of the coronary— 
 are the remains of healed myocardial abscesses. 
 
 MYOCARDIAL ABSCESS—ILLUSTRATIVE CASES 
 Necropsy 3167 
 
 A nine-year-old school boy came to the Accident Room March 2. 
 His father said that except for measles and whooping cough the boy 
 had been perfectly well until a week before admission, when he 
 bruised his shin. That evening when his shoe was taken off he 
 complained of pain just above the ankle. The next morning he was 
 unable to stand on the foot and complained of pain in the lower 
 leg. This had persisted. February 24 the leg was red and swollen. 
 February 25 the left arm became sore, and the following day the 
 lower arm and elbow were red and swollen. The day of admission 
 the right arm began to be sore. The boy had complained chiefly 
 of pain, most severe in the leg. He had eaten and slept very little. 
 
 Examination showed a fairly well nourished, rather pale boy. 
 The throat was somewhat reddened. The tonsils were slightly 
 enlarged. The heart and abdomen were normal. There were rales 
 
 throughout both lungs. The right leg from the knee, including the 
 34 
 
: 
 . 
 
 , = 
 
 530 FACTS ON THE HEART 
 
 ankle, was much swollen and red. About the lower part of the foot 
 and ankle, there were many blebs filled with serum. There was 
 exquisite tenderness on pressure over the tibia. The left arm from 
 the elbow to the wrist was swollen, very tender, and in the lower 
 half somewhat reddened. There was an indefinite sense of fluctua- 
 tion in the soft parts. The right elbow was somewhat swollen and 
 very tender to pressure and passive motion. X-rays showed nothing 
 definite. The temperature at admission was 104°, the pulse 120, 
 the leucocytes 22,000. 
 
 Operation was done the day of admission. ‘The periosteum of the 
 right tibia was dissected entirely free the length of the bone by a 
 large abscess. There were pockets of pus in the popliteal space and 
 about the ankle. Other abscess cavities were found on the right 
 ulna and the right humerus. Trephine holes into all these bones 
 showed pus. The boy was in poor condition after the operation. 
 The next day the pulse and general condition seemed a little better. 
 March 5 there was tender swelling in the region of the right parotid 
 and the boy seemed worse. ‘The following day this swelling was very 
 marked and was extending upward over the scalp. There was also 
 some swelling in the left parotid region. March 7 both sides were 
 opened and pus was obtained from inside both parotid sheaths. 
 March 9g the boy died. ; 
 
 Clinical Diagnosis —Osteomyelitis, right tibia, right radius, left 
 ulna. 
 
 Double septic parotitis. 
 
 Sepsis. 
 
 Exhaustion. 
 
 Dr. Young’s Diagnosis —Septicemia, staphylococcus. 
 
 Osteomyelitis. 
 
 Multiple abscesses. 
 
 Anatomical Diagnosis.—Septicemia, staphylococcus pyogenes 
 aureus. | 
 
 Osteomyelitis. 
 
 Pyemia, abscesses of the lungs, myocardium, thymus, kidneys, 
 and anterior thoracic wall. 
 
 Serofibrinous pericarditis. 
 
 Fibrinopurulent pleuritis, double. 
 
 Septic spleen. 
 
 Operation wounds. 
 
 Dr. RICHARDSON: We were not permitted to examine the head. 
 In these cases abscesses and meningitis are found at times. 
 
 ." 
 
MYOCARDIAL ABSCESS—ILLUSTRATIVE CASES 531 
 
 Dr. YouncG: There were no mental symptoms mentioned. 
 
 Dr. RICHARDSON: One each side of the neck just below the angle 
 of the jaw an open wound extended into the deep tissues. In the 
 region of the left forearm an open wound extended down to the ulna, 
 in which there was a small surgical opening. In the region of the 
 inner aspect in the lower part of the right upper arm an open wound 
 extended down to the humerus, in which there was a small surgical 
 opening. In the region of the right leg an open wound extended 
 down to the tibia, in which there was a small surgical opening. 
 
 There was a small amount of subcutaneous fat. The muscles 
 were pale and soft. At one place in the subcutaneous tissues of the 
 anterior thoracic wall there was a small collection of pus. 
 
 The peritoneal cavity and gastro-intestinal tract showed nothing 
 to record. Once in a while in these septicemias we do find lesions in 
 the mucosa of the gastro-intestinal tract. They vary from hemor- 
 rhagic areas to areas of hemorrhagic necrosis, and may go on to 
 perforation. In one case along the mucosa of the small intestine 
 there were small collections of pus,—abscesses. In this case although 
 there was a marked infection the gastro-intestinal tract escaped. 
 
 The lungs were weakly bound to the parietal pleura by yellowish 
 fibrinopurulent material,—abscesses of the lungs which had extended 
 through and involved the pleura. The bronchial lymphatic glands, 
 the trachea and bronchi were negative. 
 
 The pericardium showed a frank acute pericarditis. The heart 
 welghed 125 grams. In the myocardium here and there were small 
 collections of pus,—abscesses. The circulatory apparatus otherwise 
 was negative. The kidneys were dotted over with minute abscesses. 
 The culture from the spleen, which was soft, gave a good growth 
 of the staphylococcus aureus. There were some small abscesses in 
 the thymus. All told a frank case of pyemia, the portal of infection 
 debatable. 
 
 Dr. Younc: He hit his shin and it started immediately after that. 
 
 Dr. RIcHARDSON: That is the usual story. 
 
 Dr. Casort: I should like to say a word on the modern hope of 
 finding some sort of chemical treatment for these cases. He applied 
 that only to the very serious cases like this. I venture to prophesy 
 that if we develop valuable drugs of the gentian violet type, we shall 
 apply them not only to the apparently hopeless case but to the early 
 case which, if left alone, becomes appendicitis, becomes cholecys- 
 titis. We do not often take our histories from the point of view 
 of the hypothesis that those supposed local lesions are septicemias 
 
532 FACTS ON THE HEART 
 
 first. We know that typhoid, pneumonia, meningitis are first septi- 
 *cemias and later local, because those have all been proved. I believe 
 that appendicitis and cholecystitis are the same. I believe that with 
 careful history-taking and especially with this point of view behind 
 that history-taking, we are going to be able to recognize these cases in 
 the septicemic stage before they become appendicitis and chole- 
 cystitis, and, if we get any sterilizing drug, to put it in early as we 
 do with tetanus now whenit has much more chance of doing good. 
 
 I feel that we are going to have a rearrangement of our ideas 
 about the so-called local lesions, which I believe are not first local and 
 then general, septicemia coming from the local, but general septi- 
 cemia first and then the local lesion. 
 
 A Puysictan: Do you think that principle might apply to 
 furunculosis? 
 
 Dr. Casot: I think so. I do not believe furunculosis is a lesion 
 that comes in from the skin in most cases; it comes from a weakening 
 of the powers of resistance against the bacteria which are constantly 
 in the skin or in the blood. Adami and others have shown how com- 
 mon it is to have bacteria circulating in the blood, how common to 
 have mild septicemias which we never complain of at all, the bacteria 
 being excreted by the kidney and never making any localizations. 
 That sort of work and the work of Dr. Frank Kidd* seem to 
 me to show how mild septicemias often are. I think, we often do not 
 find them out. Whereas we have thought of septicemia as a terrible 
 disease almost invariably fatal, I think it is a common disease often 
 mild and in most cases not recognized at all. 
 
 Dr. Younc: The trouble is that up to the present the drugs are 
 themselves very upsetting. There is no question but that there is a 
 considerable risk of mercurial poisoning in using mercurochrome. I 
 think the drug has to be of guaranteed harmlessness to have it used in 
 the majority of cases. But I do believe what Dr. Cabot has said 
 about the large number of these cases at least starting as septicemias. 
 
 Necropsy 3575 
 
 An American reporter of twenty-two entered March 26. Two 
 years before admission he stayed out of work for two months because 
 he was run down and had lost weight. Otherwise he had always 
 been well until six weeks before admission, when he was ill in bed for 
 two weeks with “grippe.’’ He was feverish, coughed a little, and 
 lost fifteen pounds. A week before admission he had a swelling on 
 
 * Common Infections of the Kidneys—London, 1920. 
 
MYOCARDIAL ABSCESS—ILLUSTRATIVE CASES 533 
 
 the back of the neck. This became increasingly large, painful and 
 tender. He had hardly been able to move his neck, had had a 
 temperature of about 103°, and had felt very ill. For the past two 
 days the pain had prevented him from swallowing. 
 
 Examination showed a fairly well developed, poorly nourished 
 man looking ill and holding his head turned stiffly to one side. He 
 was unable to open his mouth more than half an inch. The skin 
 was moist and pale, the tongue thickly coated. On the back of the 
 neck was a sloughing area the size of a nickel, surrounded by brawny 
 induration extending half-way around the | 
 neck. The edema completely encircled the [pence 
 neck. The heart was normal except for a gogukas 
 systolic murmur at the apex. The rest of fowss™=| 
 the physical examination is not recorded. aie 
 
 The temperature and pulse are shown in 
 Fig. tor. The respirations were 23-28. 
 The urine was normal in amount, the 
 specific gravity 1.030. There was a slight 
 trace of albumin. The blood was not ex- 
 amined until after operation. A_ throat 
 Ponsultant, reported, -“I- cannot... see’ the 
 ghottis, but as far as I can see there is no 
 edema. Thesymptoms of inspiratory without 
 expiratory dyspnea, esophageal obstruction, 
 and good phonation point to an obstruction 
 between the larynx and the sternal notch 
 affecting both trachea and esophagus. The 
 only possible pharyngeal neurosis would be 
 a bilateral abductor paralysis, which is very 
 improbable except in cases of tabes.” 
 
 Operation was done the day of entrance. 
 A T-incision was made through the sloughing 
 area deep into the muscles of the neck. No 
 pus ornecrotic tissue was obtained. Acultureshowed staphylococcus. 
 
 The patient made a good post-operative recovery and was some- 
 what relieved, being able to open his jaws about an inch. There 
 was a fair amount of staining. He complained of some difficulty 
 in breathing. The edema and induration on the back and sides of 
 the neck were somewhat increased. The leucocyte count was 
 23,400. March 28 he was distinctly worse, unable to separate his 
 jaws more than a quarter of an inch. 
 
 Fic. 101.—Temperature 
 and pulse in Case 3575. 
 
534 FACTS ON THE HEART 
 
 March 29 a two-inch incision was made in the right post-cervical 
 region. Finger dissection revealed no free pus. The tissue was 
 brawny, red, and indurated. A similar incision was made on the 
 other side of the neck, but no free pus was obtained. The wounds 
 were left wide open and packed with iodoform gauze. He was 
 very comfortable during the afternoon, but early in the evening 
 began to grow rapidly worse, with difficulty in breathing, princi- 
 pally inspiratory stridor. March 30 he suddenly died. 
 
 Clinical Diagnosis (from Hospital Record).—General septicemia. 
 
 Carbuncle of neck. 
 
 Cardiac failure. 
 
 Incision and drainage, March 26. 
 
 Wider incision and drainage of neck, March 29. 
 
 Dr. Hugh Cabot’s Diagnosis——Deep cervical abscesses not 
 satisfactorily drained. 
 
 General septicemia, staphylococcus. 
 
 Anatomical Diagnosis—1. Primary fatal lesion. Septicemia, 
 staphylococcus. . 
 [ Abscesses of the lungs, 
 | myocardium, kidneys, 
 | and rectus muscle. 
 | Small mural thrombus of 
 the right ventricle. 
 
 Acute pericarditis. 
 | Acute peritonitis. - 
 Subacute interstitial 
 heptatitis. 
 Soft hyperplastic spleen. 
 
 2. Secondary or terminal lesions. 
 
 Operation wounds. 
 Slight chronic pleuritis. 
 Dr. RicHArpson: I would not be sure that there was no free pus 
 in the neck. So far as I could dissect there was not any. There 
 was no edema of the larynx. 
 Typical staphylococcus infection with abscesses everywhere, 
 pericarditis, and peritonitis,—a profound infection. 
 
 3. Historical landmarks. 
 
 IV. CARDIAC ANEURISM 
 
 In twenty-five out of g1 cases of myocarditis there was a 
 thinning of the left ventricular wall near the apex. Cardiac aneu- 
 rism occurred in seven of these, associated with fibrous myocarditis 
 or cardiac infarcts. The lesion caused no recognizable signs in life 
 
CARDIAC ANEURISM 535 
 
 and is of no practical importance to clinical medicine. Ordinarily 
 the weakened tissues bulge outward but in one peculiar case (No. 
 2413) the myocardium was split and bulged inward so as to produce 
 a narrowing of the mitral orifice. 
 
 The patient, a woman of thirty-nine, had suffered with cough and 
 palpitation for a year but had had no dyspnea till three weeks before 
 we saw her, when it led rapidly to orthopnea and prevented sleep. 
 Edema and other evidence of stasis were obvious at the time of her 
 admission to the hospital. The heart showed moderate enlargement 
 with a weak diffuse impulse over which was heard a loud harsh sys- 
 tolic murmur replacing the first sound and ending in a feeble second 
 sound. There was no arrhythmia. The pulmonic second sound was 
 accented, the aortic second not remarkable. Edema _ persisted 
 despite rest and digitalis. The pulse rose steadily in rate, reaching 
 160 in ten days. After that there were occasional extra systoles at 
 regular intervals but no fibrillation. The patient in most respects 
 seemed to be holding her own during the month of her stay, but on 
 the twenty-eighth day she suddenly screamed, turned blue, and died 
 in a few minutes. 
 
 Necropsy showed a heart weighing 426 grams, the right ventricle 
 four mm. in thickness, the left eleven mm. The valves were normal. 
 With the heart laid open and held apex down, the anterior cusp of 
 the mitral valve was continuous witha projection from the left ventric- 
 ular wall forming a sort of shelf which roofed over a cavity in the 
 ventricular wallitself. The floor of this cavity consisted of the myo- 
 cardium of the left ventricle and papillary muscle. Its roof was 
 formed by the elevated endocardium, the mitral valve, and the left 
 auricle which skirted over and slightly around it. The cavity 
 measured six cm. in greatest diameter and during life, when full of 
 blood, must have caused quite a little obstruction of the mitral orifice, 
 though the valve was itself normal. 
 
 The myocardium showed fibrous scars. The coronaries were 
 normal. 
 
 Among the other cases of this series, four showed no signs or 
 symptoms during life by which they could be differentiated from the 
 ordinary senile failing heart of the hypertensive-arteriosclerotic type. 
 Two cases showed no passive congestion post-mortem, one being 
 clinically pneumonia without heart symptoms, the other senile 
 dementia. Either angina pectoris or symptoms suggesting cardiac 
 infarction or both were present in five out of seven cases. ‘There 
 was coronary occlusion in three. 
 
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CARDIAC ANEURISM—ILLUSTRATIVE CASES eer 
 
 On the whole it seems probable that the myocarditis and thinning 
 of the apex (left ventricle) with or without an aneurismal bulge, 
 represents the healing of an old cardiac infarct. 
 
 There are no clinical manifestations corresponding to such a 
 thinning, whether it bulges (aneurism) or not. 
 
 ILLUSTRATIVE CASES—CARDIAC ANEURISM 
 
 Necropsy 3842 
 
 An unoccupied American of sixty-eight entered May 27 for relief 
 of weakness and abdominal pain. His father died of enlarged liver, 
 possibly cancer, one sister of cancer of the stomach. One child died 
 of throat trouble at ten days. The patient had the usual diseases 
 of childhood, including scarlet fever. In youth he often had tonsil- 
 litis. Fifteen or twenty years before entrance he was operated upon 
 for hemorrhoids, and since that time had had them two or three times 
 for short periods. He had had no gastric symptoms except very 
 occasional burning indigestion easily relieved by mint tablets. For 
 a year he had had uncomfortable soreness over the precordia, worse 
 on exertion. He rarely used tobacco, and had taken very little 
 alcohol for six years. Before that he was for years a steady drinker, 
 three or four times a day, and was occasionally slightly intoxicated. 
 Eight years before admission he weighed 180 pounds, his best weight; 
 a year ago, 140. He had not lost during the six months preceding 
 admission. 
 
 Except for the soreness over the precordia he had had no cardiac 
 symptoms until May 15, when after no unusual exertion but rather 
 indigestible food he had sudden severe non-radiating pain limited to 
 the epigastrium, with marked dyspnea and orthopnea. He described 
 the pain as a sense of “‘a ball in his stomach acting as a shut-off to 
 his breath.’”’ He became markedly constipated and during ten days 
 had not had a normal movement, though he had passed flatus freely 
 and had belched some gas. One enema gave a partial result, two 
 others very meager results. The stools were straw-colored, like 
 his former stools. For three or four days at the onset he had marked 
 dull constant pain and weakness in the middorsal region and lower 
 in his back near the midline, relieved by massage and catharsis, 
 which also somewhat relieved the epigastric pain. For three days 
 after the onset he had flashes before his eyes and dizziness.. Since 
 the onset he had had slight nausea and marked repugnance to food. 
 
538 FACTS ON THE HEART 
 
 Examination showed a fairly well nourished man, cyanotic, with 
 moderate inspiratory distress. The eyelids were puffy, the skin dry, 
 the mucosae slightly cyanotic. The few remaining teeth were poor. 
 The heart was normal in size and position. The action was regular, 
 not rapid. The sounds were of poor quality. The aortic second 
 sound was accentuated and was heard in the neck. The artery walls 
 were palpable, the brachials tortuous. The lung signs were as shown 
 in Fig. 102. There was slight tenderness over the liver. The liver 
 dullness extended 5 to 7 cm. below the costal margin, lower on deep 
 inspiration. The edge went deep into the flank. The extremities, 
 genitals and reflexes were normal. The pupils were equal, irregular, 
 especially the right, and reacted to light and distance. 
 
 Hyperresonant,. Breath 
 
 sounds and tactile 
 
 fremitus increased. Ax 
 
 Expiration —=. Avs 
 prolonged. Bp 
 ANS 
 Dull. Conson- D BSN f 
 eting r@les. , ZS 
 Tactile frem- “GEA Sy 
 
 SA itus diminished. Ze Dili eRarees 
 SSH / Dull to flat. Dimin- sa Sage a8) consonating on 
 
 ished breath,voice, Lars inspiration. 
 whisper and tactile S 
 
 fremitus. Paraverte- \ WE 
 bral dullness. No aR 
 egophony. 
 
 eG 
 
 Fic. :102:—Physical signs in Case’ 3842. 
 
 The temperature was 96.6° to 99.2° until May 30, then 98.1° 
 to 102.8° until June 2, falling to 95.4°. The pulse was 88 to 130, the 
 respiration 78 to 36. The systolic blood pressure was 135, the dias- 
 tolic go. The urine was normal in amount, the specific gravity 
 1.028 to 1.014. There was the slightest possible trace of albumin 
 at two of three exminations, pus at two, rare red blood corpuscles, 
 hyalin and granular casts at the last. The hemoglobin was 80%. 
 There were 17000 to g200 leucocytes, 80% polynuclears. The smear 
 showed achromia and slight variation in size. A Wassermann was 
 negative. 
 
 The patient had three distinct attacks of anginoid pain accom- 
 panied by difficulty in breathing and in the pharynx and the trachea 
 a sense of phlegm which he felt would cause suffocation if he did not 
 raise it. He coughed hard, producing nothing. ‘The effort precip- 
 itated a real attack with great sense of constriction of the chest and 
 
CARDIAC ANEURISM—ILLUSTRATIVE CASES 539 
 
 a feeling of suffocation, horror and air-hunger. During the attacks 
 his pulse became absolutely irregular. There was marked pulse 
 deficit with real delirium cordis. The heart sounds were weak, the 
 face ashen-gray. ‘The heart became regular several hours after the 
 attacks, and remained regular during the last one. It was doubted if 
 amyl nitrite helped him. June 1 he became very much worse, his 
 chest was full of rales, and he was expected to die. The therapy 
 was continued, however, digitalis by mouth, digifolin, morphia, and 
 also large doses of caffein, gr. v, at frequent intervals. He at once 
 showed improvement, which continued until the night of June 3. 
 Then his pulse became very weak and rapid, his temperature sub- 
 normal. He coughed considerably. His breathing was very diff- 
 cult, though there were fewer rales than previously. June 4 he died. 
 
 Clinical Diagnosis (from Hospital Record) —Chronic myocarditis. 
 
 Arteriosclerosis. 
 
 Angina pectoris. 
 
 Chronic nephritis. 
 
 Chronic bronchitis. 
 
 Chronic decompensation. 
 
 Dr. William H. Smith's Diagnosis —Arteriosclerosis. 
 
 Arteriosclerotic heart. 
 
 Probably coronary occlusion. 
 
 Passive congestion, pneumonia, or infarction of the lungs. 
 
 Arteriosclerosis and infarctions of the kidneys. 
 
 Anatomical Diagnosis.—Arteriosclerosis. 
 
 Arteriosclerotic occlusion of the left coronary artery. 
 
 Chronic myocarditis with aneurism and infarction. 
 
 Mural thrombus, left ventricle. 
 
 Chronic pericarditis. 
 
 Subacute pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Purulent bronchitis. 
 
 Edema of the lungs. 
 
 Hydrothorax, right. 
 
 Arteriosclerotic degeneration of the kidneys, very slight. 
 
 Slight chronic interstitial hepatitis with hyaline degeneration of 
 branches of the hepatic artery. 
 
 Chronic pleuritis. , 
 
 Obsolete tuberculosis of bronchial lymph nodes. 
 
 Focus of obsolete tuberculosis, apex of the right lung. 
 
 Chronic perihepatitis and splenitis. 
 
540 FACTS ON THE HEART 
 
 Cholelithiasis. 
 
 Cysts of the right kidney. 
 
 Slightly defective closure of the foramen ovale. 
 
 Dr. RicHARDSON: The background in this case was arteriosclerosis, 
 and the various lesions in the organs were the end-result of it. The 
 aorta and great branches were rather capacious, but in the first 
 portion of the aorta there was only a slight amount of fibrous sclero- 
 sis. When we came to the arch, the descending portion of the tho- 
 racic aorta and the abdominal portion of the aorta, we saw that the 
 great artery and its branches were the seat of marked fibrous, fibro- 
 calcareous and atheromatous sclerosis, a good anatomical basis for 
 the clinical condition. 
 
 The heart weighed 600 grams (normally 200-300). The valves 
 showed nothing worthy of discussion. The right coronary artery 
 showed a moderate amount of fibrous sclerosis. It was rather capa- 
 cious, and the areas of sclerosis were scattered. The left one, how- 
 ever, showed an entirely different picture. Along a length of three 
 or four cm. of the first portion, the wall showed marked fibrous thick- 
 ening with much fibrocalcareous change which occluded the artery 
 at one point. From this point on the sclerosed artery and branches 
 are lost in an area of myocarditis. Asa result of these changes in the 
 coronary artery, which had of course gone on for years, there was 
 present in the wall of the left ventricle a well established chronic 
 myocarditis in a large area supplied by the branches of the left coro- 
 nary artery. There were also numerous dirty brownish-red areas 
 which resembled areas of infarction, and the probability is that some 
 of the branches running to that area of myocarditis had become 
 occluded, with resulting softening and necrosis in the areas of chronic 
 myocarditis. On the endocardial surface which rested along the 
 area of myocarditis just described, there was erected within the ven- 
 tricle a large thrombus, so intimately associated with the wall, which 
 was thinned out and bulging, that in the necessary manipulation in 
 the examination, the heart wall tore off with pieces of the clinging 
 thrombus attached to it. There we have the whole process, a slow- 
 growing one due to the gradual decrease in the supply of blood and 
 later more or less sudden occlusion of some of the branches with 
 areas of infarction and the production of a mural thrombus. It is 
 interesting to note that while ordinarily pieces of thrombus sweep 
 off into the blood stream with the erection of infarcts in different 
 organs, in this particular case there were no infarcts anywhere. 
 A possible reason is that the thrombus developed beneath the smooth 
 
CARDIAC ANEURISM—ILLUSTRATIVE CASES 541 
 
 membrane which rested over the exposed surface in the ventricular 
 cavity and prevented it from fracturing. 
 
 The pericardium showed at one place a broad band of fibrous 
 adhesions, and in addition a general coating of grayish-red granular 
 material which weakly bound the two layers of the pericardium 
 - together; that is, a band of chronic pericarditis and a more or less 
 extensive subacute pericarditis. 
 
 There was a moderate amount of chronic pleuritis and some few 
 areas of obsolete tuberculosis both in the bronchial lymph nodes 
 and in the apex of the right lung. These pleural adhesions plus the 
 adhesions of the pericardium, together with the arteriosclerosis, are 
 sufficient in themselves to cause the extensive hypertrophy of the 
 heart. 
 
 About the liver and spleen there were numerous old fibrous adhe- 
 sions, chronic perihepatitis and splenitis. The liver showed slight 
 cirrhosis along the portal canals with some hyalin degeneration of 
 branches of the hepatic artery. 
 
 The gall-bladder contained about seventy small stones, but the 
 mucosa was negative. The bile ducts and pancreatic ducts were also 
 negative. 
 
 The kidneys weighed 340 grams (normally 200-400) and were in 
 very good condition. 
 
 Necropsy 4283 
 
 An Irish laborer of sixty entered January 7, 1922, for relief of 
 dyspnea and cough of twenty-five years’ duration. He was in 
 considerable respiratory distress and not cooperative. He had 
 measles, mumps and scarlet fever in childhood. His teeth had 
 always been bad. In general his health had been very good until 
 he was thirty-five. He was ill in bed at forty with pneumonia. He 
 had typhoid fever at forty-five. For a year he had had some diffi- 
 culty in starting the urinary stream and some burning on urination. 
 He formerly drank a pint of whiskey a week. For the past few years 
 he had taken none. 
 
 For twenty-five years he had had “asthma,” ‘bronchitis,’ and 
 frequent palpitation accompanied by slight dizziness and _ slight 
 cough with thick brownish sputum. He had slight dyspnea on 
 moderate exertion with the asthma until 1917. During the past 
 twenty years he had had attacks of precordial pain, numbness and 
 soreness over the precordial region, and sharp pain in the pit of the 
 stomach and the left arm. These attacks had no relation to meals, 
 
542 FACTS ON THE HEART 
 
 A 
 
 were accompanied by gaseous eructations, considerable belching of 7 
 gas, and marked nausea. Soda had always relieved the pain! For 
 five years his dyspnea had occurred more easily and he had urinated _ 
 fifteen times at night and frequently by day. During the past year 
 
 he had had to rest for several periods of half an hour each during the 
 day to relieve the dyspnea, and to use five pillows at night. Six 
 months ago he visited a Boston hospital for relief of “indigestion 
 and cough,” and was given pills and powders which relieved the 
 “indigestion” and made him bring up a “ quart of sputum at a time.” 
 
 He worked until two weeks before admission taking care of horses. 
 His last attack of pain occurred a few days before admission and |. 
 lasted two hours and a half. 
 
 sy 
 
 Emphysematous, 
 Crackling and groan- 
 ing respiratory rale 
 throughout. Moist 
 rales at bases on 
 
 inspiration, 
 
 Liver edge, 
 slightly 
 tender, 
 
 Fic. 103.—Physical signs in Case 4283. 
 
 Examination showed a well nourished man with marked respira- 
 tory distress. The skin was dry. The mucous membranes were 
 slightly cyanotic, the sclerae injected. There were many broken 
 tooth roots and marked pyorrhea. The lung signs were as shown 
 in Fig. 103. The chest expansion was small, the diaphragm excur- 
 sion limited. The apex impulse of the heart was seen and felt in the 
 sixth space 11 cm. to the left, 2.5 cm. outside the midclavicle. The 
 right border of dullness was 5.5 cm. to the right of the midster- 
 num, the substernal dullness 8 cm. The action was rapid, regular, 
 with tic-tac quality. The pulmonic second sound was equal to the 
 aortic second. The artery walls were negative. The pulses were of 
 fair volume and tension. ‘The systolic blood pressure was 120, the 
 diastolic 90. The abdomen was distended. The liver dullness 
 extended from the fifth rib to two centimeters below the costal mar- 
 gin. There was reducible right inguinal hernia. The fingers and 
 toes were clubbed. The rectal examination showed the prostate 
 enlarged. The pupils and reflexes were normal. | 
 
 The temperature was 99° to 1ro1°, the pulse 81to 111, the 
 respirations 20 to 45. The amount of urine is not recorded. The 
 specific gravity was 1.030. The urine was alkaline at the single 
 
 " 
 
CARDIAC ANEURISM—ILLUSTRATIVE CASES 543 
 
 examination and showed the slightest possible trace of albumin; 
 no sugar. ‘The hemoglobin was 75%. ‘There were 22,000 to 29,600 
 leucocytes, 82% polynuclears, 4,568,000 reds, slight achromia. The 
 platelets were increased. A Wassermann was negative. 
 
 The morning after admission the patient was evidently much 
 worse. He had Cheyne-Stokes respiration with apneic periods as 
 long as fifteen seconds. During these periods he would not respond 
 to questions, though he was rational during the times of active 
 breathing. That afternoon when apparently in about the same 
 condition he suddenly died. 
 
 Clinical Diagnosis (from Hospital Record) —Emphysema. 
 
 Chronic bronchitis. 
 
 Myocarditis. 
 
 Pericarditis. 
 
 Arteriosclerosis. 
 
 _ Dr. Richard C. Cabot’s Diagnosis. —Arteriosclerosis of the coronary 
 arteries, with obstruction. 
 
 Myocarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 General arteriosclerosis. 
 
 Chronic bronchitis? 
 
 Bronchiectasis? 
 
 Bronchopneumonia? 
 
 Chronic passive congestion. 
 
 Anatonuical Diagnosis —Arteriosclerosis of the coronary arteries. 
 
 Arteriosclerotic thrombotic occlusion of the right coronary artery. 
 
 Myocarditis and cardiac aneurism. 
 
 Mural thrombosis of left ventricle. 
 
 _ Arteriosclerosis. 
 
 Chronic adhesive pericarditis. 
 
 Chronic passive congestion. 
 
 Acute pericarditis. 
 
 Hypertrophy and dilatation of heart. 
 
 Slight ascites and anasarca. 
 
 Chronic pleuritis. 
 
 Dr. RicHarpson: This man was rather short, well developed and 
 fairly well nourished. We were not permitted to examine the head. 
 The skin in the region of the base of the neck and the upper part of 
 the chest presented a sallow appearance, with possibly a little 
 underlying yellowish tinge. I notice that color in these old cases of 
 heart disease. I don’t know what kind of jaundice it is. It is slight 
 
544 FACTS ON THE HEART 
 
 in amount, and nothing that would be put down in the anatomieal 
 diagnosis. 
 
 The peritoneal cavity contained a small amount of thin pale clear 
 fluid,—a little ascites. The appendix was negative. The gastro- 
 intestinal tract was out of the picture except that it showed a well 
 marked velvety, juicy mucosa,—passive congestion. 
 
 There was a little fluid in the pleural cavities—a few c.c——and 
 pleural adhesions on each side. The trachea and bronchi showed 
 some reddening of the mucosa and a moderate amount of reddish 
 mucus; otherwise they were negative. The apices of the lungs were 
 frankly negative. ‘There were no areas of consolidation. The tissue 
 generally was spongy and a little leathery, and yielded more or less 
 reddish frothy fluid,—a little congestion, no definite emphysema. 
 
 The pericardium contained about fifty c.c. of thin dirty reddish 
 cloudy fluid and a little fibrin, and there was some reddening of the 
 pericardial surfaces,—a frank acute pericarditis. In the region of 
 the anterior half of the left ventricle a band of fibrous adhesions 
 extended between the visceral and parietal pericardium, a broad 
 band of old adhesions tying the two surfaces together pretty strongly, 
 —an old band of chronic adhesive pericarditis besides the acute 
 pericarditis. 
 
 The heart weighed 585 grams, considerably enlarged. ‘The myo- 
 cardium, except in places to be spoken about, was pretty fair, but in 
 these places presented an entirely different picture. The right 
 ventricle in the good places was three mm. and the left ventricle 
 eleven mm., so that where it was more or less normal in appearance it 
 was about as thick as usual. In the region of the band of adhesions 
 on the left ventricle wall, section showed marked fibrosis and thinning 
 of the wall. Above and extending well up the wall of the heart the 
 sections of the heart wall showed fibrosis and in places areas of brown- 
 ish-yellow more or less necrotic looking tissue,—altogether a marked 
 myocarditis, fibrous, with areas of necrosis, of course suggesting that — 
 somewhere some coronary had been blocked to produce the condition. 
 This marked thinning of the ventricle wall in the region of the lower 
 half of the ventricle produced what we call cardiac aneurism, some- 
 times called aneurismal dilatation. ‘The valves themselves were out 
 of the picture, showing a moderate amount of the usual sclerosis, but 
 otherwise negative. The circumference of the tricuspid was a little 
 increased. 
 
 Now for the real condition which underlies all the others. The 
 orifice of the left coronary was free, but a short distance from that 
 
CARDIAC ANEURISM—ILLUSTRATIVE CASES 545 
 
 point there was an area of marked fibrosis with marked diminution 
 of the lumen. Then going down from that point along the artery 
 and its branches, there were places here and there where there were 
 small fibrous plaques with diminutionof the lumen. But in between, 
 the vessel was in pretty good condition. In the right coronary the 
 orifice was free. But about two cm. from that point there was an 
 area of sclerosis with marked thickening of the wall and diminution 
 of the lumen, and on the intimal surface a small columnar thrombus 
 plugging the artery. The right artery beyond this area was much 
 like the left. We have here again an example of the peculiar local- 
 ization of sclerosis within a given set of arteries. The condition 
 of the heart from a pathological standpoint furnishes a basis for 
 Dr. Cabot’s diagnosis, coronary sclerosis, the background for angina. 
 
 The first portion of the aorta was pretty good. There was slight 
 sclerosis in the arch and a small fibrocalcareous area. The other 
 portions showed more or less fibrous sclerosis with some atheroma. 
 The great branches showed a small amount of sclerosis. 
 
 The liver showed chronic passive congestion. The gall-bladder, 
 bile ducts, pancreas were negative. The spleen was chunky and 
 thick, the issue elastic; chronic passive congestion. The adrenals 
 were out of the picture. 
 
 The kidneys weighed 350 grams and were typical, grossly and 
 microscopically, of passive congestion. They were bluish-brown-red, 
 with a good cortex, the vessels rather engorged. Except for passive 
 congestion they were out of the picture. 
 
 The prostate, seminal vesicles and testes were negative. 
 
 On the surface of the area of myocarditis in the wall of the left 
 ventricle, up just beneath a papillary muscle there was an area of 
 roughening to which a small frank thrombus was adherent. 
 
 An interesting thing from the pathological point of view is the 
 peculiar localization of the sclerosis in the coronary arteries and the 
 great amount of change in the left ventricle wall. Not infrequently 
 we find cases where there is marked sclerosis all along the coronaries 
 with diminution of the lumen, leavmg only a slender channel, and 
 with the myocardium showing no definite changes. 
 
 Dr. Casot: Was there more change in the right than in the left? 
 
 Dr. RicHarpson: There was more change in the wall of the left 
 ventricle, but there was considerable change in the right ventricle wall 
 also. There was much change in the region of the interventricular 
 septum. 
 
 35 
 
546 FACTS ON THE HEART 
 
 Dr. Cazot: I suppose that long two-hour pain he had was when 
 that thrombus formed. The acute pericarditis we missed as we 
 usually do. We recognise one out of five cases here. 
 
 Dr. E. L. Younc: I think it is interesting, the number of cases 
 we see here with urinary symptoms and the prostate put down as 
 enlarged, which show nothing post-mortem, as in this case. 
 
 V. RUPTURE OF THE HEART 
 
 In one case the cardiac infarction resulting from a much narrowed 
 left descendens led to a rupture of the heart. ‘‘The probe passed 
 easily through the center of an opening four mm. in length with 
 irregular blood-stained margins. This opening is the center of a 
 dark red boggy area in which some branches of the much narrowed 
 
 ¥ 
 
 left coronary are lost. Cross section of the heart wall in the region - 
 
 of the perforation shows a slender ragged channel which extends 
 through into the left ventricle. The tissues about the channel are 
 blackish red and slightly soft; itis margined by a small area of grayish 
 firm fibrous-like tissue.” 
 
 Despite all this, the clinical diagnosis is “‘ Acute Bronchitis, Psy- 
 choneurosis, Weak Heart.’’ She was not thought to be much ill 
 and was on the danger list for only a few minutes before her death, 
 when she was noticed to be breathing slowly and soon after to be 
 unconscious and pulseless, with great pallor. Until that time the 
 heart and pulse had shown nothing abnormal, but on account of 
 three months’ complaint of prickling sensations in the finger-tips, 
 abdomen, legs and back Dr. James J. Putnam had considered her 
 psychoneurotic. 
 
 With this may be compared a case of ‘“‘traumatic rupture of the 
 heart” (No. 2249) occurring in a young man of twenty-seven who 
 one hour before he entered the hospital had fallen backward with a 
 heavy iron bar on top of him, sustaining a compound fracture of the 
 left leg with wounds on the scalp and right hand but no injury to the 
 chest. The heart was normal in size and valves but ‘‘over the left 
 ventricle, midway between the auriculoventricular junction and the 
 apex was an ecchymosis in the middle of which was a linear tear 
 2.5 cm. long with closely approximate edges running diagonally 
 across the ventricle. The rent entered the interior of the heart 
 to the left of and behind the anterior papillary muscle. Below 
 the opening the heart wall showed hemorrhagic infiltration and at the 
 extreme apex there was some laceration and disorganization over the 
 septum beneath ecchymoses. ‘There was also hemorrhagic infiltra- 
 
RUPTURE OF THE HEART 547 
 
 tion of the wall of the right auricle with a ragged laceration 2.2 cm. 
 by i cm. 
 
 There was hemopericardium. 
 
 During the hour of his life at the hospital the heart sounds were 
 very irregular and rather faint, with periods of complete standstill 
 lasting several seconds. The radial pulse could be obtained only 
 occasionally and was very faint and irregular. The patient was in 
 muttering delirium and did not answer questions. 
 
 Necropsy 1897 was a similar case. A man of twenty-three was 
 struck by a falling telegraph pole. His chest was crushed and his 
 lung ruptured. Death followed swiftly. At necropsy beside the 
 lesions mentioned there were pneumopericardium and rupture of the 
 epicardium. 
 
CHAPTER VI 
 ANGINA PECTORIS 
 
 It is not to be expected that anatomical studies will ever throw 
 much light on the clinical manifestations which we call angina 
 pectoris. At the outset it seems improbable that so elusive and 
 transient a phenomenon, varying as it does with some of the most 
 evanescent of vital changes—such as exertion, emotion, and the 
 effects of the nitrites—could be explained by a permanent anatomic 
 lesion. Anything so closely connected as angina is with temporary 
 physiological phases of the body’s activities cannot so far as I can 
 see be adequately explained by anatomical lesions which must be 
 present before and after the attack, i.e. in the absence as in the pres- 
 ence of angina itself. Hence hypotheses such as vascular spasm or 
 cardiac fatigue naturally suggest themselves. The difficulty with 
 such theories is that it is hard to see how they can be either proved or 
 disproved. 
 
 I am not disappointed therefore that the 138 cases studied here 
 throw no new light on the nature or the origin of angina pectoris. 
 The controversies regarding the relationship of this disease (or 
 symptom) to occlusion of the coronary arteries seems to me to depend, 
 in part, on the similarity of the symptoms following cardiac infarction 
 —the “‘infarction syndrome”—with those of true angina pectoris. _ 
 
 The long and especially the fatal attacks of heart pain unrelated 
 to exertion, unrelieved by rest or nitrites, we certainly must associate 
 with coronary block and its effects. We can hardly suppose any 
 unusual state of things in the aorta as causal here. 
 
 But before or after these terrible seizures there are often milder 
 and properly anginoid attacks, typical in the location of pain, in 
 its relation to exertion, emotion and rest and in the relief by nitrite 
 medication. It is certainly tempting to think that some similar 
 mechanism, some cause for insufficient blood flow through the coro- 
 _ naries is at work also in these cases. But the inference is not neces- 
 sary. There may be some anginoid attacks due to coronary disease 
 and others of a different origin. On the whole I incline to this opinion. 
 
 There can be no question, I take it, that the pain of cardiac 
 infarction is due not to any changes in the aorta but to the infarct 
 
 548 
 
ANGINA PECTORIS 549 
 
 itself and its results. It is true that a similar syndrome may occur 
 without infarct as in the following case (No. 3527): An Irishman of 
 seventy-four while being treated in the ward for dermatitis exfolia- 
 tiva associated with aortic regurgitation and without any evidence 
 (post-mortem) of arteriosclerosis or of syphilitic aortitis, complained 
 one evening of slight dyspnea and abdominal distress. At one a.m. 
 he had an attack of sharp pain in the precordia. In half an hour the 
 pain had become an intense agony. (Pulse 140, respirations 50.) 
 Morphia 16 gr. and nitroglycerin 499 gr. had no effect and the pain 
 continued until 5:40 a.m. when 1 gr. of morphia was again given 
 and the pain ceased. 
 
 On being questioned he now said that he had similar but milder 
 attacks for three or four weeks. He vomited frequently in the final 
 twenty-four hours of his life and after this attack became Irrational, 
 restless, dyspneic, with Cheyne-Stokes breathing leading to death. 
 Necropsy showed no cause for the pain. 
 
 In spite of occasional cases like this it remains true that there is a 
 group of clinical facts by which we can predict the finding of a cardiac 
 infarct post-mortem with a percentage of diagnostic success equal to 
 that now attainable in most other diseases. 
 
 But from the existence of angina in the sense of a Sacral pain, 
 preceded or followed usually by pain in the left arm (or both arms), 
 always produced in the early stages of its development by emotion 
 or exertion and ceasing after a few minutes’ rest, often linked with 
 a sense of constriction and an anticipation of immediate death,*— 
 from this what can we predict as to the post-mortem? 
 
 In our series if we had predicted that esther coronary sclerosis or 
 syphilitic aortitis would be found post-mortem, we should have been 
 right in this prediction 32 times and wrong 11 times, apparently a 
 respectable showing of 75% success. 
 
 But if we analyze this success it crumbles. Most of the patients 
 here studied were at an age when arteriosclerosis (including some 
 coronary sclerosis) is common and sometimes extreme, without 
 angina. Among our 72 cases of coronary sclerosis without angina 
 there were four in which both the main coronaries were nearly 
 occluded by arteriosclerosis. I have looked over the necropsies and 
 clinical records of all cases which contained in their anatomical 
 diagnosis a note of marked sclerotic changes in the coronaries, 127 
 cases in all. To these I have added r1 cases suffering from anginoid 
 
 * T make no attempt to enumerate here a// the phenomena or varieties of angina. 
 
550 FACTS ON THE HEART 
 
 pain without coronary disease of any considerable degree, making 
 138 cases in all. The whole group can be subdivided into: 
 
 (1) Coronary narrowing without angina.... 94 cases 
 
 (2) Coronary narrowing with angina....... 33 cases 
 
 (3) Angina without coronary narrowing.... 11 cases 
 138 
 
 Of the first group—narrowed coronaries without evidence of 
 angina in life—there is little to say save that the number of cases, 
 94, is far beneath the true number.* Among the 94 cases which I 
 have come across, there were eleven in which the arteriosclerotic 
 process was so extreme that the lumen of one or more arteries was 
 nearly or quite obliterated (see below). 
 
 As in all the cases studied in this section there was an enormous 
 preponderance of elderly males,—ten males to every female. The 
 average age was 54. Theheart was usually enlarged but in two-thirds 
 of the cases was quite competent, the patients dying of pneumonia, 
 prostatic disease, apoplexy, cancer, etc. Less than one-half showed 
 some fibrous myocarditis but no acute infarctions occurred in this 
 group. } 
 
 The absence of more damage to the myocardium may be explained 
 by supposing that the collateral circulation, which varies in different 
 hearts, was in these cases sufficient to nourish the heart wall despite 
 the narrowing of certain vessels. 
 
 In two of these cases there was syphilitic aortitis, one with 
 gumma of the heart wall, yetno pain. In another, one coronary was 
 occluded at its mouth, yet there was no pain and death was not sud- 
 den. In three there was arteriosclerotic occlusion of the left coronary; 
 in three others a clot or a vegetation had practically if not absolutely 
 closed the left coronary. 
 
 When the pain is not relieved by rest but lasts on for hours and is 
 associated with pulse failure and fainting, we can much more confi- 
 dently assert that an organic obstruction of the coronary by syphi- 
 litic aortitis, arteriosclerosis or thrombosis is present and is the main 
 cause of the symptoms. But when the painis brief and not associated 
 
 * Had I read over all the 4000 necropsies looking for the descriptions of coronary 
 arteries I should have found many,more cases of coronary sclerosis. The 94 cases which 
 I found represent merely those with coronary changes marked enough to be mentioned 
 in the anatomical diagnosis or summary of the findings. Since the accumulation of 
 more cases would merely reiterate a fact already established by many observers (that 
 coronary sclerosis without angina is common), I have not thought it worth while to pile 
 up more of this cumulative evidence, 
 
ANGINA PECTORIS é 551 
 
 with evidence of heart failure we cannot say, so far as our material 
 goes, that the coronary arteries are any more diseased than in many 
 elderly individuals who are free from angina. Coronary arterioscle- 
 rosis may be present yet insignificant. 
 
 Again coronary disease may be wholly absent in patients with 
 definite angina, as is shown in eleven cases of this series. In 6 of 
 these the whole aorta, carefully examined macroscopically, was normal,* 
 and I see no reason to believe that the microscope would have 
 revealed anything of importance. 
 
 These eleven cases without coronary disease were in other respects 
 very much like the cases of this series with coronary disease. There 
 were ten men to one woman, three over seventy years and three under 
 forty (30, 32, 39). The hearts averaged 508 grams in weight. In 
 one the aorta showed syphilitic aortitis without any narrowing of 
 the coronary orifices; four others showed an arteriosclerotic aortic 
 arch (without coronary disease), and six showed no changes whatever 
 in the aorta. Chronic passive congestion was present in ten of the 
 eleven post-mortem. Blood pressures, in one case high, in three cases 
 were normal, in the others not measured. 
 
 Some of the phrases used to describe the pain are as follows: 
 
 1. For six months sharp piercing pains about the heart. 
 
 2. Occasional sharp piercing pains about the heart. 
 
 3. For two years sharp sudden pains about the heart on exertion. 
 
 4. Burning pains in left chest and down the left arm and wrist 
 on exertion, came one to five times a day and lasted from five minutes 
 to two hours. 
 
 5. Severe paroxysmal precordial pains up to and on the day of 
 death despite chronic passive congestion. 
 
 6. Precordial pain and pressure for two or three months Oe 
 fifty times in a night, ceasing with onset of edema. 
 
 7. ‘Typical attacks of angina pectoris” in the ward relieved 
 by nitroglycerin. Chronic passive congestion ante and post-mortem. 
 
 8. Intense agony in the precordia lasting five hours despite 
 morphia gr. 1%, finally ceasing with another 1é. Similar but milder 
 attacks for three or four weeks. (Necropsy: chronic passive conges- 
 tion, hypertrophy and dilatation of the heart. Aorta smooth, 
 coronaries free. No history of syphilis. Chronic perisplenitis 
 and perihepatitis.) 
 
 9. For five months attacks of sharp precordial pain lasting a few 
 minutes. (Blood pressure 160/130.) 
 
 * One showed a single smooth yellowish patch. 
 
552 FACTS ON THE HEART 
 
 10. Two years ago attacks of nocturnal precordial pain for three 
 months. (Chronic passive congestion ante and post-mortem.) 
 
 Syphilitic aortitis with narrowing of the coronary orifices in the 
 aorta certainly seems to have a closer relation to angina than arterio- 
 sclerosis does. It was present in twelve cases of this series, ten of 
 which suffered from angina. In our g2 cases of syphilitic aortitis 
 there were fifteen with angina and several others with epigastric 
 pain, possibly of the anginoid type. ‘This frequency is apparently 
 about the same as in coronary sclerosis, which out of 127 known 
 
 + 
 4 ’ 
 y. 
 i. 
 , 4. 
 
 cases is associated with angina in 33. But the actwal number 
 
 of cases of coronary sclerosis in this series is presumably far more 
 than 127. For out of tro5z cases recorded as arteriosclerotic 
 in the necropsy records, we can scarcely believe that the coronaries 
 were spared in 970. 
 
 But granting that syphilitic aortitis and angina are not infre- 
 quently associated, the question still remains, what is the relation 
 between the two? The partisans of the coronary theory of angina 
 can point to a good many cases of angina in which post-mortem the 
 mouth of one or more coronaries was found narrowed or occluded by 
 the syphilitic process. But still more common is the coincidence of 
 syphilitic aortitis and angina when the disease has not blocked the 
 coronaries at all, and when these vessels are free, smooth, and dilat- 
 able throughout. 
 
 In our series, among 15 cases of syphilitic aortitis with angina 
 there are four showing narrowed or occluded coronary openings and 
 six in which these openings are free. My chief impression is this: 
 Syphilis has something to do with angina pectoris, more to do with tt 
 than arteriosclerosis has. But the syphilitic disease certainly does 
 noi act in all (or in most) cases by any demonstrable effect on the coronary 
 arteries. It may exert its effect in the way described by Sir T. 
 Clifford Allbutt or in some other way, but certainly not in all cases 
 by way of the coronaries. | 
 
 Of the 33 cases of angina pectoris with coronary changes, 23 were 
 above the fifty-first year, 21 were men and 12 women. The pain 
 disappeared with the advent of chronic passive congestion in three, 
 and did not disappear in twelve; as to the other cases the record is 
 not clear. . 
 
 Syphilitic aortitis was present in nine of the 33, fibrous myocardi- 
 tis in fourteen, cardiac hypertrophy in most. The blood pressure 
 showed no rule; it was high, low, or normal. 
 
ANGINA PECTORIS 550 
 
 Among the phrases used to describe the pain fourteen could be 
 classified as typical of angina: Other non-typical phrases are recorded 
 as follows: 
 
 t. ‘In bad weather sharp pain shooting from chest down left 
 arm.” 
 
 2. ‘Frequent attacks of precordial pain for two months.” 
 3. “Much pain around the heart July 3” (during hospital obser- 
 vation one week before death). 
 
 4. ‘‘Constant pain in right breast, worse with exertion. Some- 
 times shoots down left arm.” 
 
 5. In ward “‘attacks of great weakness and precordial distress 
 relieved by amyl nitrite or morphia; two to four attacks in twenty- 
 four hours, especially at night.” 
 
 6. Severe epigastric pain with smothering. 
 
 7. Sense of painful constriction in the chest. Sudden death. 
 Arteriosclerotic occlusion left descendens with myocarditis. 
 
 8. Shooting pain in right arm with slight tightness in chest. 
 
 g. ‘“‘Dyspnea and constriction in the chest at night.” (Perni- 
 cious anemia.) 
 
 to. “Sharp pain in chest radiating to left nipple.” 
 
 tz. “‘Substernal pain.” Arteriosclerosis of coronaries with 
 fibrous myocarditis and intracardiac clot in corresponding region. 
 
 12. Dull precordial pain with exertion, radiating down left arm. 
 
 13. Severe stabbing pain at cardiac apex following attacks of 
 paroxysmal dypsnea. Sudden death. Acute endocarditis with 
 coronary thrombosis. 
 
 14. For three years attacks of sharp non-radiating momentary 
 precordial pain on exertion. 
 
 15. Dull throbbing precordial pain radiating to chest and 
 shoulders. Right coronary closed by syphilitic aortitis. 
 
 16. Male, sixty-seven years. Eight years epigastric pain in 
 half-hour attacks both with and without exertion, radiating to both 
 arms. Marked arteriosclerosis of the aorta and coronaries. 
 
 The following cases are of interest. 
 
 No. 3424. Housemaid of sixty. For five years she has suffered 
 from attacks of severe precordial pain and intense dyspnea brought 
 on by exertion, worry, or anger, two or three times a year. Pain 
 usually starts in precordia and is as though she were being crushed. 
 Radiates to left shoulder and hand. Lasts about anhour. Followed 
 by intense dyspnea and cough, which last for about a week after the 
 attack. 
 
554 FACTS ON THE HEART 
 
 Last May she had an exceedingly sharp cutting pain starting in 
 the region of the left biceps, radiating across the back to the shoulder 
 and arm and finally to the precordia. Since then (it is now Decem- 
 ber) she has had no more pain but progressively increasing dyspnea, 
 orthopnea and cough. 
 
 Physical examination showed aortic stenosis and regurgitation, 
 hypertrophy and dilatation, chronic passive congestion. Necropsy 
 confirmed these. The aorta and coronaries showed marked 
 arteriosclerosis. | 
 
 No. 3259. Carpenter of fifty-five with diabetes and abscess of 
 right lung. October 5th: ‘‘On this date a carbuncle of the back 
 appeared and he began to feel an ache down his left forearm when he 
 walked. A year later he made many visits to the Out-Patient 
 Department on account of precordial pain which began nine minths 
 after the first hospital visit. He describes it as ‘‘a dead heavy feeling 
 over the heart, coming on with exertion and lasting ten to fifteen 
 minutes.” In attacks he has also headache, vertigo and dizziness 
 and feels as if he was going to die. The pain radiates down both 
 arms, especially the left. The attacks now come on with less exertion 
 and last longer, sometimes an hour. 
 
 Sudden death in the hospital. Arteriosclerotic occlusion of the 
 coronary arteries with fibrous myocarditis, chronic pneumonitis 
 and abscess of the lung. 
 
 No. 3607. A colored fireman of thirty-four complains that for 
 eight years he has noticed a sickening fainting feeling under the 
 sternum with nausea on exertion. Three years ago he began to have 
 constant pain of varying severity in both forearms. This left the 
 right arm after a month but has continued in the left. For the past 
 year it has radiated up the arm and across the back. Mercury gives 
 relief. 
 
 Necropsy: syphilitic aortitis. Coronaries not obstructed. 
 
 ANGINA AND MYOCARDITIS 
 
 Beside the two familiar but still mysterious associates of angina, 
 aortitis and coronary narrowing, it is inked up with fibrous myocardi- 
 tis which was present in fifteen of the forty-four cases of angina. The 
 most obvious explanation that suggests itself is that coronary disease, 
 which is certainly responsible for some cases of fibrous myocarditis 
 and myomalacia, may be also the cause of angina and so link the two 
 sets of facts together. But as both angina and myocarditis are noto- 
 
 bd 
 
THE CESSATION OF ANGINA 555 
 
 riously diseases of elderly people, their association with sclerotic 
 coronaries proves nothing as to the cause of angina. 
 
 Aortic stenosis without mitral disease also appears rather fre- 
 quently as an associate of angina. The latter was present eight times 
 among 28 cases of aortic stenosis. But here as with myocardial 
 fibrosis, we must take account of the factor of age. Aortic stenosis 
 (uncomplicated) is a disease of elderly people, 22 of 28 cases occurring 
 in persons past their fortieth year, and 15 of 28 after the fiftieth year. 
 It may be that influences dominant in elderly people act to favor 
 both the slow emergence of the symptoms of aortic stenosis and the 
 appearance of angina pectoris. ‘There need be no more direct con- 
 nection between the pain and the valvular lesion. 
 
 I have seen three cases of intense and typical angina associated 
 with pernicious anemia and without coronary change. One showed 
 moderate sclerosis of the aorta, the others none. All were strictly 
 
 dependent on exertion and relieved by rest. Such cases, like those 
 
 seen in convalescence from pneumonia and from other infections, 
 certainly make us skeptical of any etiology based wholly on organic 
 and permanent changes either in the coronaries or in the aorta. 
 
 BLOOD PRESSURE AND ANGINA 
 
 Although the recorded data furnished as to blood pressure are 
 scanty in this series of patients with angina pectoris, they are sufh- 
 cient to support the usually accepted idea that angina has no definite 
 relation either to hypertension or to hypotension. High, low, and 
 normal pressures are found and the high pressures are no more 
 common than in any set of people past middle life and free from 
 angina. 
 
 Cardiac enlargement is present in a considerable majority of the 
 cases, but like hypertension, myocarditis and aortic stenosis, bears no 
 discernible causal relation to the angina, which can and does exist 
 in persons with hearts of normal size. 
 
 THE CESSATION OF ANGINA WITH THE ADVENT OF GENERAJ 
 PASSIVE CONGESTION 
 
 It has been noticed by many that angina pectoris often ceases 
 when cardiac compensation fails. Our experience presents three 
 striking instances in confirmation of this. But out of fifteen cases in. 
 which this point was especially studied there were twelve in which 
 the angina persisted, despite all the evidences of chronic congestive 
 
550 FACTS ON THE HEART 
 
 heart failure. Evidently it is only certain types or phases of con- 
 gestive failure which give relief to angina. 
 
 Death from angina without congestive failure is I believe a decided. 
 rarity, if we exclude the cases of cardiac infarction with blocked 
 coronary. ‘There were but thirteen cases in this series of 44 in which 
 no congestive failure was found post-mortem. This represents all 
 the known deaths from angina in a series of 1906 individuals dying 
 with cardiovascular lesions. 
 
 CORONARY THROMBOSIS AND ACUTE BLOCKING OF THE CORONARY 
 
 I. Cases without Pain. 
 
 1. In No. 2393, a boy of twenty suffering with acute endocarditis; 
 the orifices of the coronaries were partly occluded by soft vegetations 
 attached to and above the aortic valve. ‘There were no symptoms 
 corresponding to this obstruction in life, the patient dying of chronic 
 passive congestion and sepsis. 
 
 2. No. 2578 is a similar case of acute endocarditis occurring in 
 a man of forty-six, who died with symptoms of a general septicemia 
 and without any pain. His death was not sudden or in any way 
 remarkable. 
 
 3. In No. 2727 a woman of forty-three dying of a widely dissem1- 
 nated lymphoma with no symptoms calling attention to the circula- 
 tory system (the diagnosis was lethargic encephalitis in life) was 
 found at necropsy to have a thrombus in the descending branch of the 
 left coronary. 
 
 IT. Cases with Pain. 
 
 t. In No. 3389 a man of fifty-two suffered from typical angina 
 and also from sharp paroxysmal epigastric pain with dyspnea. Post- 
 mortem the left descendens was not only sclerotic but occupied by an 
 organizing thrombus. Death was not sudden or painful but is to be 
 counted I suppose as, on the whole, of the anginoid type, since there 
 was no chronic passive congestion or other cause for death discovered. 
 
 2. Necropsy 3921 was performed on a woman who died at thirty- 
 one of acute endocarditis and chronic passive congestion. She had 
 had many attacks of severe stabbing precordial pain immediately 
 following on spells of dyspnea and weakness. Death was sudden 
 and was associated with intense pallor and a slight general convulsion. 
 The post-mortem examination showed in addition to the acute endo- 
 carditis a partial obstruction of the left descendens by a clot. 
 
CORONARY THROMBOSIS 557 
 
 In the painless cases we may suppose, I take it, that death followed 
 the coronary obstruction too swiftly for the production either of 
 pain or of myocardial infarct. 
 
 Outside of the 4000 cases here analyzed I have records of the 
 following cases which seem of sufficient interest to be added here. 
 
 1. No. 4116. A married Scotch woman of forty-seven was seen 
 in the autumn of 1915 with the history of seven years of attacks of 
 severe epigastric pain with vomiting and headache. She had had 
 seven such in the last five weeks, relieved only by morphia. Explor- 
 atory laparotomy showed no disease in the biliary tract, stomach, 
 duodenum, pancreas, kidney or spleen. An appendix thought to be 
 slightly inflamed was removed. The attacks of pain continued. 
 In September 1920 she had sudden severe substernal distress 
 following exertion and lasting twenty minutes. That night she 
 had another attack while lying quiet in bed. This time the pain 
 radiated to the back, to both shoulders and down the left arm, espe- 
 cially to the fourth and fifth fingers. Dyspnea and orthopnea came 
 with the pain which she said lasted twenty-four hours this time, and 
 had recurred several times since. Orthopnea persisted and six days 
 ago the feet became swollen. 
 
 There were paroxysms of fibrillation and at times an apex rate 
 of 190 with a large pulse deficit, but no arrhythmia. Electrocardio- 
 gram showed only sino-auricular tachycardia with a somewhat 
 inverted T-wave (digitalis?). 
 
 She died in diabetic coma. | 
 
 At necropsy there was very slight general arteriosclerosis; very 
 marked coronary sclerosis with occlusion of the left descendens, with 
 a corresponding area of fibrous myocarditis, and a degeneration and 
 perforation of .the interventricular septum. There were mural 
 thrombi in the ventricle, slight hypertrophy and dilatation, chronic 
 passive congestion. Streptococcus sepsis with abscess in a bronchial 
 lymph gland. Also hyalin degeneration of the islands of Langerhans 
 and a few minute concretions in the gall-bladder. 
 
 The most natural interpretation of these data seems to’be that 
 the patient had survived an infarct of the heart in or before 1915; 
 that the infarct became transformed into a fibrous myocarditis, but 
 that a few days before her.death in 1920 the interventricular septum 
 became necrosed and perforated owing to the degeneration of a 
 fresher cardiac infarct. 
 
 2. A Finnish laborer of thirty-nine had suffered for three years 
 with attacks of precordial pain and dyspnea, accompanied by severe 
 
558 FACTS ON THE HEART 
 
 pain in the left elbow. The attacks lasted about two minutes. Three 
 months before he came under observation he had an attack which he 
 said lasted nine days without intermission or change in intensity. 
 He sat doubled up and could not sleep or eat. The elbow was not 
 swollen. 
 
 Later chronic passive congestion appeared and the pain ceased. 
 X-ray suggested a mitral lesion with dilatation. Blood pressure 
 105/80. Heart enlarged, regular, 80, soft systolicat apex. Wasser- 
 mann negative. Electrocardiogram showed a broad notched P-wave 
 in Lead II. The R-wave in all leads was low. Sinoauricular 
 tachycardia: Sudden death after nine-days’ observation. 
 
 Necropsy.—Heart 590 grams. Left coronary occluded for 3.5 cm.; 
 this artery led directly to a large area of fibrous myocarditis with 
 great thinning of the wall (5-1o mm.). Mural thrombus over this. 
 Moderate arteriosclerosis of aorta. A branch of the pulmonary 
 artery occluded by arteriosclerosis with resulting infarct. A broad 
 band of old pericardial adhesions at the cardiac apex. No sign of 
 syphilis. 
 
 3. No. 4170. A Swiss woman of sixty-five, divorced, had had two 
 still-births and three living children. Was seen in decompensation 
 with attacks of precordial pain and “‘tightness”’ relieved by nitro- 
 glycerin. Blood pressure 160/65, 175/85, 180/100, 100/45, 96/65. 
 Auricular fibrillation. Heart not apparently enlarged. Parkinson’s 
 disease. Died of congestive failure. 
 
 Necropsy—Heart 440, moderately enlarged with dilatation 
 confined to the auricles; left coronary sclerosed with considerable 
 diminution of its lumen. Right less so. Myocardium no lesions. 
 Arterioslcerosis of aorta with small dissecting aneurism. 
 
 4. No. 4200. A married woman of forty with a negative past 
 history began to suffer two weeks before we saw her from excruciating 
 knife-like midepigastric pain radiating to the back beneath the right 
 scapula and lasting two days; morphia alone gave any relief. On the 
 second evening she became unconscious. Next morning the right 
 hand and right facial muscles were weak and the speech thick. But 
 after a week in bed she felt and seemed well and was up for two days. | 
 Then dyspnea and orthopnea. 
 
 When seen there was a loud friction rub synchronous with the 
 heart’s action, heard over and on both sides of the sternum. Blood 
 pressure 120/60. Heart irregular, rapid, no mumurs. Moderate 
 cardiac enlargement. Right hand weak. Staphylococcus albus — 
 cultivated from the blood. Death in two days. 
 
SUMMARY AND CONCLUSIONS 559 
 
 Necropsy.—Subacute pericarditis with moderate hypertrophy and 
 dilatation (430 grams) and mural thrombus in the left ventricle. 
 Circumflex coronary occluded by an embolus and an infarction of the 
 corresponding area of the heart. Also embolism of superior mesen- 
 teric and of iliac arteries. A small amount of fibrous sclerosis in the 
 aorta, none elsewhere. 
 
 The pain might conceivably be due to pericarditis, but its inten- 
 sity, sudden onset, its radiation and the coma soon after it, make the 
 coronary embolism a more probable cause. 
 
 5. A man aged forty-eight when seen, had had four years pre- 
 viously an attack of sharp precordial pain radiating to the left shoulder 
 and down the left arm. Physical examination was negative and ina 
 short time he seemed quite well and remained so until during an 
 attack of peritonsillar abscess, which did not disable him from work, 
 he was suddenly seized with terrible pain in the abdomen and legs 
 which caused him to fall to the floor. He died a week later with signs 
 of general peritonitis and gangrene of the legs. 
 
 Necropsy showed old myocardial scars and complete arteriosclero- 
 tic closure of a small branch of the left coronary. Intracardiac 
 mural thrombi on the old myocardial scars had led to mesenteric and 
 iliac thromboses. 
 
 SUMMARY AND CONCLUSIONS 
 
 1. If we take care to distinguish the group of symptoms and signs 
 known as angina pectoris from the syndrome accompanying cardiac 
 infarct, we must confess that there are many cases of angina without 
 adequate anatomical basis or explanation. 
 
 2. Coronary sclerosis and occlusion is certainly a cause of the 
 pain and collapse seen in cardiac infarction, but bears no clear or 
 stable relationship to angina pectoris proper. 
 
 3. The same may be said of disease in the aortic arch of which 
 there is no evidence macroscopically in a considerable group of 
 anginoid cases. 
 
 4. Extensive coronary occlusion is not infrequent in the hearts of 
 patients who during life have never suffered from angina. 
 
 5. Syphilitic aortitis is associated with angina in about 16% of 
 cases. Butin only a small minority of these do we find the coronaries 
 obstructed at their mouths. There must be some other connection 
 between syphilis and angina, perhaps that suggested by Sir T.- 
 Clifford Allbutt. 
 
560 FACTS ON THE HEART 
 
 6. Fibrous myocarditis and angina are often associated but there 
 is no evidence of a causal connection. The same is true of aortic 
 stenosis and angina. 
 
 7. Angina occasionally ceases with the advent of general passive 
 congestion. But in most cases of our series this was not true. 
 
 8. When a coronary is suddenly blocked by a clot death may 
 follow at once with or without pain. (See Cardiac Infarction, 
 Chapter. iV si) 
 
CHAPTER VII 
 
 ACUTE AND. SUBACUTE ENDOCARDITIS 
 
 DEFINITION AND TERMINOLOGY 
 
 The 180 cases studied here have in common this fundamental fact: 
 —on some portion of the endocardium, usually the heart valves, there 
 is situated a patch of soft inflammatory tissue composed largely of 
 blood platelets, fibrin and bacteria more or less firmly adherent to 
 the endocardium adjacent. These adherent masses are distinguished 
 from the dard fibrous or fibro-calcareous scars of chronic endocarditis, 
 which however may be present along with the acute soft vegetations. 
 
 The word “‘acute”’ refers primarily to the softness of the vege- 
 tations on the endocardium, that is, to the early stage of the inflamma- 
 tion. As will be seen below, some of the cases are /iterally acute in 
 the sense of lasting but a short time and leading rapidly to the death 
 of the patient. Other cases strictly deserve the term “‘subacute”’ 
 or even ‘“‘chronic”’ since they last for months or even for years. 
 But there is no justification for lumping all these cases under the 
 single termination “‘subacute”’ as has been done by some writers. 
 _ The term “‘subacute bacterial endocarditis,’’ much used at the pres- 
 ent time, seems intended to suggest that there are forms of endo- 
 carditis not due to bacteria, an assumption which seems insufficiently 
 grounded. I prefer therefore the general term “‘acute and subacute 
 endocarditis”? though admitting that it has to be stretched to cover 
 some cases lasting too long for the strict application of either term. 
 
 TYPES OF ACUTE AND SUBACUTE ENDOCARDITIS 
 
 The cases here studied fall into two main groups: (1) those which 
 apparently start in the heart and circulation and not in any septic 
 focus outside it; (2) those that apparently come to the heart, originating 
 either in a focus of sepsis or in a gravely weakened condition of the 
 whole organism due to cancer, nephritis, diabetes, or some other 
 debilitating disease. 
 
 Within the first group we may distinguish further (a) those which 
 
 manifest the first attack of disease in the heart, and (b) those which 
 36 561 
 
562 FACTS ON THE HEART 
 
 are recurrent or implanted upon a previously diseased endocardium. 
 Linking these two groups together I shall speak of them as ‘‘primary”’ 
 acute endocarditis.* In our 180 cases, 102 belonged to the primary 
 group. Of these, 36 cases represent first attacks and 66 recurrent or 
 implanted disease. 
 
 In contrast with these 102 cases there is a group of 78 in which 
 the endocarditis is relatively a secondary or minor feature while the 
 main cause of death is some such disease as general peritonitis or 
 cancer. Within this group one can distinguish two sub-groups, (1) 
 pyemic and (2) terminal. The pyemic group, comprising 44 cases, is 
 made up of those in which it seems clear, both from the post-mortem 
 examination and from the clinical history, that the disease has origi- 
 nated and done its most serious damage outside the heart. 25 of 
 the 44 cases belonging within this group showed only soft vegetations, 
 while in 19 these soft vegetations were implanted upon or associated 
 with a fibrous or fibrocalcareous base representing, I take it, a 
 previous attack of endocarditis. 
 
 Finally there is the terminal group of cases in which the endo- 
 carditis plays no part recognizable during life and is often so minute 
 as to be easily overlooked by the post-mortem examination. 34 cases 
 belong to this group. 
 
 TABLE 120 
 t.. (a) Prrtary acute endocarditis, 5... 2.5 0+. 02-45 ans ye oe OnCnaee 
 (b) PRIMARY acute endocarditis, recurrent ...............' 66 cases 
 2. (a) SECONDARY acute endocarditis, pyemic............... 44 cases (19 recurrent) 
 (b) SECONDARY acute endocarditis, terminal.............. 34 cases (17 recurrent) 
 180 cases 
 Total recurrent cases(66 + 19 + 17) = 102 
 Total non-recurrent cases = 78 
 180 
 
 Characteristics of the Main Subdivisions.—The distinguishing 
 marks of the primary group of cases, whether initial or recurrent, may 
 be set down here in the way of an introductory summary of the 
 pages to follow. The characteristic features of this type are as 
 follows: 
 
 * T realize fully the limitations of the word “primary” and the obvious fact that 
 endocarditis must in all cases be brought to the heart from outside it and not originate 
 there. The word primary is here used to mean that the bulk and most serious portion of 
 the lesions are situated in the heart itself rather than outside it. 
 
AGE AND SEX : 563 
 
 (a) The absence of any focus of infection or other important lethal 
 cause outside the heart. 
 
 (b) The presence post-mortem (in seven-eighths of the 
 cases), of relatively large shaggy masses or ulcerations on the 
 heart valves. . 
 
 (c) Embolism present in 60%. 
 
 (d) Nephritis present in one-third of the cases. 
 
 (e) Cardiac enlargement ante and post-mortem, associated in 
 most cases with dyspnea and often with edema. 
 
 (f) Constitutional evidences of sepsis, especially chills and stupor, 
 without any evidence of a septic focus outside the heart. 
 
 (g) The presence of murmurs other than the insignificant systolic 
 murmur. 
 
 (h) The presence in most prolonged cases of an increasing second- 
 ary anemia. 
 
 In contrast with these characteristics, the cases belonging in the 
 second group show: 
 
 (a) The presence of an important cause of death outside 
 the heart. 
 
 (b) Small lesions on the heart valves (in five-sixths of the 
 cases). 
 
 (c) Embolism almost never recognized before death and only in 
 one-third of the cases after death. 
 
 (d) Complicating nephritis relatively rare. 
 
 (e) Little or no recognizable enlargement of the heart. 
 
 (f) Murmurs, systolic or absent. 
 
 AGE AND SEX* 
 
 Uniting all groups we find 93 males and 87 females in this series. 
 The sex incidence is essentially the same in all the different sub- 
 groups above described. In the primary cases there were 57 males 
 to 45 females, in the secondary group 56 men to 42 women. The 
 predominance of males is in accordance with previous observations 
 on this subject, though it 1s not as extreme as is suggested by 
 Riesman.7 
 
 * In the whole 4000 necropsies among which these 180 cases occurred the males are 
 
 nearly twice as numerous as the females. 
 + Journal of the American Medical Association, May 21, 1921. 
 
564 . FACTS ON THE HEART 
 
 TABLE 121.—AGE AND SEX IN ACUTE AND SUBACUTE ENDOCARDITIS 
 
 Female 
 
 In Table 121 the distribution of the ages is shown in detail. Sum- 
 ming it up we may say that in the primary group the disease affects 
 especially young adults between the twentieth and fortieth year. 
 Fifty-six of the 102 cases fell within these limits. In the secondary 
 group the age and sex are those characteristic of the underlying 
 disease. In any form the disease ts rare in the first decade-and not 
 common before the twentieth or after the sixtieth year. 
 
 When we come to note the relation of age to sex we fad that 
 among the patients who died before the fortieth year females predomi- 
 nate in the relation of 60 to 51 males, while among those dying after 
 the fortieth year there are 42 males to 27 females. One may con- 
 jecture that this difference is due to the fact that in the first group 
 there fall a good many cases in which the disease is implanted upon a 
 previously existing chronic endocarditis of the mitral valve, a site of 
 infection commoner inwomen thaninmen. Onthe other hand, cases 
 falling in the second group have relatively few of the recurrent type 
 which is so prone to attack women. 
 
 72 of the 102 primary cases occurred before the fortieth year, and 
 only 30 in persons more than forty years of age. 
 
 In the whole 180 cases there were but 32 with a previous history 
 
 either of rheumatic fever or of chorea. Most of these fell into the 
 recurrent section of the primary group. 
 
 VALVE AFFECTED 
 
 The disease was confined to the mitral valve in 77 cases, to the 
 aortic valve in 36 cases, while both valves together were affected in 
 50. The further details as to the parts affected are shownin Table 122. 
 
 — 
 
VALVE AFFECTED 565 
 
 TABLE 122 
 
 Primary Secondary 
 
 Valve affected 
 I By: III IV 
 
 Initial Recurrent | Pyemic | Terminal 
 
 Mitral 
 
 Aortic 
 
 Mitral and Aortic 
 
 RS ST Ue oy d CO ee 
 
 MTECHISTME 8s cin 5 aos + ous. 
 
 Aortic and Tricuspid... 
 
 Pulmonary 
 
 Mitral and Tricuspid... 
 
 WaVOIVES®. «. 2+ 
 
 It is of interest here to notice the resemblance between the 
 cases of this series, the chronic non-deforming lesions and the com- 
 monest of the chronic deforming value lesions described in Chapter 
 II. The similarities, as will be seen in Table 123 are quite striking. 
 
 TABLE 123 
 
 Acute and sub- Chr. deform. Chr. non-deform- 
 
 Valve affected a Pap ‘ ef 
 acute endocarditis} endocarditis ing endocarditis 
 
 * All combinations other than the above. 
 
566 FACTS ON THE HEART 
 
 I do not wish to press this analogy too far but certainly it con- 
 tains at least a suggestion that the organism or organisms of acute 
 endocarditis are if not identical with at least closely similar to those 
 which produce chronic valvular heart disease. On the other hand 
 the dissimilarities of incidence obvious in chronic non-deforming 
 endocarditis argue a different etiology. 
 
 Another point of interest about these findings is the absence of 
 any notable tendency to favor the tricuspid valve. It has often been 
 said that acute endocarditis—the so-called malignant or ulcerative 
 forms—is especially prone to attack the tricuspid valve. But this 
 series shows that in only sixteen cases out of 180 was the tricuspid 
 valve attacked at all, and in only three was it attacked exclusively.* 
 
 A curious and interesting point is the relation of sex to the site 
 of the disease. Of 77 cases in which the mitral valve alone was 
 the seat of the acute endocarditis, 49 or nearly two-thirds were 
 women. On the other hand, in the 36 cases involving the aortic valve 
 alone, 23 or 24 were men. I have no idea how these figures are to 
 be explained. 
 
 One may also note that in the recurrent cases (grouped in the 
 second, third and fourth columns of Table 122) the preponderance of 
 cases confined to the mitral valve no longer exists. In the group of 
 recurrent cases the disease was confined to the mitral valve in only 38 
 or 38% and affected other valves in 64. The non-recurrent cases 
 show that the mitral valve was attacked exclusively in 39 or 50% 
 and the other valves also in 39. ‘The difference in the two groups is 
 considerable. 
 
 In 117 of the 180 or 64% the disease was confined to a single valve. 
 
 NATURE OF THE INFLAMMATORY PROCESS (TABLE 124) 
 
 There appear to be two main morphological types in the patho- 
 logical anatomy of acute endocarditis: (1) those in which the disease 
 is composed exclusively of soft thrombotic masses or vegetations, 
 and (2) those in which ulceration and destruction of the valve is 
 associated also with these vegetations. The latter or ‘‘ulcerative”’ 
 type is much the less common, occurring in only 34 of 180 cases. But 
 this predominance of the vegetative or polypous type of endocarditis 
 is less marked in the primary group of cases, where we find 29 ulcera- 
 
 * Gonorrheal endocarditis though carefully searched for was not found in the 4000 
 necropsies of this series. The proneness of this organism to attack the tricuspid and 
 pulmonic valves has been noticed by Thayer and others. 
 
 +In 19 cases within group III (Table 122) the sepsis was implanted upon an old 
 endocarditis so that these 19 cases are recurrent as well as pyemic, 
 
NATURE OF THE INFLAMMATORY PROCESS 567 
 
 tive cases out of 102, as compared with five ulcerative cases out of 78 
 in the pyemic and terminal varieties. 
 
 TABLE 124.—NATURE OF ENDOCARDITIS 
 
 ! I reer rer 
 
 ia . 
 Primary” : ? III I 
 | Primary | Septic + Mi 
 fete? Septic | Terminal 
 recurrent recurrent | recurrent 
 
 Bet PCADOLY DS. tens a. 20 24 
 
 Ulcers and polyps 
 
 Smale DOL PS. ss.<. a6 : 
 
 Pinhead sized polyps... . 
 
 Manite polypsis . 7%.) ss 
 
 Table 124 also shows that the lesions are much larger as a rule 
 in the primary than in the secondary cases. Nevertheless it is 
 notable that even in the latent terminal cases two showed large 
 polypoid masses. 
 
 Embolism.—86 out of 180 cases showed at necropsy evidences of 
 embolism (135 embolic lesions in all). The distribution of these 
 embolic lesions appears in Table 125. 
 
 TABLE 125.—DISTRIBUTION OF EmBoric LESIONS 
 
 I 
 LE III 
 c¢ . 
 i 4 : : 
 nee Primary | Septic + ae Total 135 
 non- Terminal ; 
 epee atnier recurrent | recurrent akan in 180 
 a6 76 1n 66 21 1n 44 
 
 Fextremities t.). <9. 0. 
 TET ase Oe Sees Sia ee i 
 SAT a, eee Ha To 7. 
 Coronary arteries 
 
 Bear Oi VIAN ke ts, ve: 
 Mesenteric vessels 
 
 Mae An ian oe ae 
 Paravertebral tissues... . 
 
 eC) OOO Pete O- O7N Cab 
 OS Ribs Ors © Sra) © VOnOmO aie 7 
 OR. Om O 205.07 0 £0 2 O7-O.. On On Ont 
 HH He HH HH HH DS HS HP HL LH 
 
 OR ORC Sis Ocs Ole (© She eh) 
 
 BONA artery. sa) lei. 
 
568 FACTS ON THE HEART 
 
 Embolic lesions are much commoner in the primary types of 
 acute endocarditis than in the secondary varieties. Thus 66% of 
 ‘the primary cases (Columns I and II above) showed some evidence 
 of embolism after death, while only 24 out of 78 or 32% of the second- 
 ary group showed such evidence. Emboli were commonest of all in 
 the recurrent-primary cases, occurring there in 43 out of 66 cases, or 
 65%; in the non-recurrent primary group, embolic lesions were found 
 in 19 out of 36 or 52%. In the other groups the percentage is pro- 
 gressively less, being only 26 in the terminal cases. Only a minority 
 of these embolic phenomena were recognized during life, 33 as against 
 86 post-mortem (see Tables 125 and 126). All but two of these 33 
 cases fall within the primary group. Aside from purpura which 
 some might hesitate to include as an embolic phenomenon, splenic 
 embolism was recognized most often, seven times in-all. Renal 
 embolism comes next with six diagnoses, then cerebral embolism with 
 
 TABLE 126.—EMBOLISM RECOGNIZED IN LIFE 
 
 Primary Secondary 
 
 Total 
 
 Dunes and spleeia.. ae se eae eee I 
 Brachial tite Ses ob eee ee 
 Radial ete ae trices ee eee 
 
 Kidney and spleene a an.ie ss |, 
 SUperiGrmmesenterios tare nr ate a" 
 PMNS sD. ak sa es ee ee tes ee a ne 3 
 PUrpuray syste eee rete see he 
 Splenic, renal, brain, subcutaneous 
 
 DET ela dey LDS ee tye eae eas 
 Kidneys, spleen, brain, lung...... 
 Brainsand kidneyes anc eure. 
 Brain, spleen and kidney......... 
 Brain and skin den st ee nee ") ie 
 Retinatand skins weet ete red ee a) I 
 
 Le 
 fot) 
 _ 
 =) 
 e+ + SS HS SS HS HS DH AS HS 
 e 
 
 mW FB Dh HW HF DN WH WH 4 HA 
 
 eS AS HH AH F&F 
 
 16 15 I I 33 cases in 172 
 
NATURE OF THE INFLAMMATORY PROCESS 569 
 
 five, and pulmonary embolism with four. There were three cases of 
 acute parotitis, very possibly metastatic or embolic in origin, though 
 the direct entry through the mouth is also possible. 
 
 The case of superior mesenteric embolism presented in life only 
 the evidences of acute intestinal obstruction with peritonitis. No 
 endocarditis was suspected, and the case was treated as a surgical 
 emergency. 
 
 The central artery of the retina was recognized as plugged in only 
 one case, although from the observations of others I should suppose 
 that some cases must have been overlooked in the present series. 
 
 The practical importance of emboli in the diagnosis of the disease 
 will be referred to later. But itis obvious that if we are to make the 
 diagnosis at all we must do so without recognizing emboli in the 
 great majority of cases. For though doubtless many were over- 
 looked in the present series, the fact that we were aware of their 
 presence in only 33 cases out of 180 in the whole series, and in only 31 
 cases out of 102 in the primary group, leads me to believe that even 
 with the best of clinical study we cannot as a rule recognize any 
 emboli in life. 
 
 Skin Hemorrhages.—Hemorrhages are recorded during life in 
 only 17 cases, ten of these belonging to the primary group and seven 
 consisting merely of purpuric spots. A generalized hemorrhagic erup- 
 tion such as is seen in other infectious diseases is seldom recorded in 
 our cases of acute endocarditis. 
 
 Tenderness of the Fingers and Toes.— Only in three cases of our 
 series was this noted, but I strongly suspect that with better observa- 
 tion we should have recognized this symptom in a larger number 
 of cases. I am convinced however that it is not common. 
 
 Nephritis.—Some type of nephritis occurred in 45 cases out of 180. 
 This is excluding suppurative infections of the kidney. Table 127 
 shows that nephritis was much commoner in the primary group of 
 cases than in the others. 33 out of 102, or practically one-third of 
 the cases in the first group showed some nephritis, while only 12 out 
 of 78 cases in the second group showed it. Among these cases of 
 nephritis 24 were of the acute glomerular variety, 10 were classified 
 as subacute glomerulonephritis, and the remaining as chronic 
 nephritis. In the primary group acute nephritis occurred 19 times, 
 subacute 7 times, chronic 7 times. In the secondary group acute 
 nephritis 5, subacute 3, chronic 4. It would appear therefore 
 that there is no single type of nephritis regularly associated with 
 acute endocarditis, as some writers have supposed. 
 
570 FACTS ON THE HEART 
 
 TABLE 127.—NEPHRITIS IN ACUTE OR SUBACUTE ENDOCARDITIS 
 
 Group I. 
 Initial 
 
 Primary 
 
 Group II. 
 Recurrent 
 
 Group III. | 
 Pyemic | Subacute 
 Secondary 
 
 Terminal 
 
 Group IV. 
 
 Meningitis.—In 11 cases of the first group, three of the recurrent 
 and eight of the non-recurrent types of endocarditis, acute lepto- 
 meningitis occurred as a complication. In the secondary type of 
 endocarditis none of these complications occurred. 
 
 Foci of Sepsis.—In the 78 cases of endocarditis believed to be 
 secondary to disease outside the heart, general peritonitis was most 
 often the source of infection and was believed to be the cause in 10 
 cases. Pneumonia comes next with’* seven cases, puerperal sepsis in 
 six cases, a septic extremity, arm or leg, in five cases, sepsis in the 
 urinary tract in five cases, empyema in three, lung abscess in two, 
 dermatitis in two, tonsillar sepsis, bed sore, appendicitis, osteomye- 
 litis, post-operative sepsis, once each. 
 
 Puerperal sepsis has long been recognized as prone to attack the 
 heart, but I do not think that general peritonitis has received suffi- 
 cient attention in this connection. The same is true of urinary 
 sepsis. On the other hand, I am surprised to find that osteomyelitis 
 and bed-sores have played so small a part. 
 
 By the classification adopted in this chapter no case has been 
 included in the primary group unless we were convinced, the patholo- 
 gist and I, that the sepsis manifesting itself as acute endocarditis had 
 originated within the circulatory system. Nevertheless there are 
 included within the 102 cases of this group five in which necropsy 
 showed suppurative lesions outside the heart, in our opinion second- 
 ary to the endocarditis or independent but not its cause. These 
 lesions were, in one case empyema, in another interlobar empyema 
 with tuberculosis, in a third lupus, in a fourth mastoiditis and 
 deep phlegmon of the neck, in a fifth meningitis, duodenal ulcer 
 
ae 
 
 NATURE OF THE INFLAMMATORY PROCESS 571 
 
 and pneumonia. We recognize that in any of these cases an inter- 
 pretation of the endocarditis as secondary is possible, and we men- 
 tion them here to make clear the consequent percentage of possible 
 error in our classification. 
 
 Underlying Disease in Terminal Cases of Endocarditis.—Neo- 
 plasms come first with ten cases, nephritis next with seven, the rest 
 of the causes, as shown in Table 128, are pretty well scattered. 
 
 TABLE 128.—ACTUAL SOURCES OF SEPSIS 
 
 General peritonitis 
 Pneumonia 
 Puerperal sepsis 
 Urinary sepsis 
 Septic leg (arm) 
 
 Se & H AH HH HH DY HWHB NL AN 
 
 TABLE 129.—UNDERLYING DISEASE 
 
 Neoplasm 
 Nephritis 
 Diabetes 
 Apoplexy 
 Pernicious anemia 
 Splenic anemia 
 
 Erysipelas 
 
 Leukemia 
 
 Pericarditis 
 
 Phthisis 
 
 Tabes dorsalis 
 Tuberculous peritonitis 
 
572 FACTS ON THE HEART 
 
 CLINICAL MANIFESTATIONS 
 
 1. Constitutional Sepsis.—Evidences of the influences of a general 
 infection upon the body (i.e. fever, leucocytosis, anorexia, loss of 
 weight), were present in only 79 of the 102 “‘primary” cases and in 4o 
 of the 78 “secondary” cases. But these were of value in calling 
 attention to the possibility of endocarditis only in the 102 cases of the 
 first group. In the others they would naturally be attributed to some 
 of the more obvious foci of sepsis present in the body. The type of 
 fever was continued in 17 cases and of the intermittent or picket-fence 
 type in 13 of 36 cases in Group J. Cv/ills were noted in only 27 cases 
 out of 172, 23 in the primary group and four in the others. They 
 were especially common in the non-recurrent primary cases, making 
 up 17 out of the total of 36 in this subdivision. It is only in this type 
 of case that chills are of any help in diagnosis. In a general way we 
 may say that when chills occur without any recognized cause such as 
 malaria or a known septic focus, there are three places to look for their 
 origin: (1) the biliary tract and gall-bladder, (2) the genito-urinary 
 tract, and (3) the heart. In our experience, however, chills even 
 when present as a symptom of acute endocarditis are rarely of diag- 
 nositic value as compared with more localizing and definite evidence 
 such as embolic phenomena or diastolic murmurs. 
 
 2. Mental State.—In the classical descriptions of acute endo- 
 carditis it has repeatedly been noticed that patients with this disease 
 do not feel sick, complain of nothing, want to get up and go about 
 their usual occupations, and sometimes actually do so. This state of 
 euphoria was distinctly noticeable in four of the 102 cases of primary 
 endocarditis here studied, and very possibly would have been noted 
 in others had it been more carefully looked for. In most of the cases 
 however it was certainly not present. One of the cases of striking 
 euphoria in this series occurred in a hospital orderly who up to one 
 week from the time of his death was actively at work carrying 
 patients and attending to the ordinary duties of his position. Ordi- 
 narily however either an overwhelming constitutional sepsis or the 
 discomfort attendant upon local foci of sepsis or sufferings from an 
 uncompensated chronic valve lesion prevented possibility from an 
 euphoria while the patients were under observation. 
 
 A ‘‘typhoidal state’? was noted in two cases of this group, and a 
 stuporous or comatose condition in eleven. One patient was notably 
 nervous and troubled with insomnia. | 
 
 3. Anemia.—In Table 130 are shown the blood counts of seven 
 patients in the non-recurrent subdivision of the primary group. 
 
CLINICAL MANIFESTATIONS 573 
 
 TABLE 130.—ANEMIA INGROUP I 
 
 Necropsy Age and Sex Red Cells Hemoglobin 
 
 2,248,000 48% 
 
 2,880, 000 45% 
 
 2,800,000 
 
 3,100,000 41% 
 70% 
 55% 
 60% 
 
 Leucocytes TEs tieand TI 
 
 Under 5000 
 
 5 ,OOO-10, 000. 
 
 10, 000-15, 000 
 
 15, 000-50, 000 
 
 50, 800-58, 000 
 
 “Leucocytosis’”’........ 
 
 SRETEOONT epee hs oo oe geal 
 
 The anemia here illustrated is of course of the secondary type 
 and is considerable though not extreme in degree. When it occurs, 
 however, it is of very great diagnostic value, supposing that hemor- 
 rhage and other obvious causes are absent; for chronic valve lesions 
 and the fevers most likely to be confused with that of acute endocar- 
 ditis rarely produce anemia. So that I think one may say that if a 
 case appears to be one of ordinary valvular heart disease but is 
 accompanied by fever and especially by anemia not obviously 
 accounted for otherwise, acute or subacute endocarditis is a very 
 probable diagnosis. 
 
 *These numbers (I, II, etc.) refer to the sub-groups of acute and subacute endo- 
 carditis explained above. ‘II + III”’ means a dominant septic focus outside the heart, 
 but also at necropsy an old chronic endocarditis underlying the fresh acute vegetations. 
 
574 FACTS ON THE HEART 
 
 4. Leucocytosis.—In Table 131 are shown the leucocyte counts in 
 103 cases of the present series. 71 of these fall into the class of 
 well-marked leucocytoses, most of them above 25,000 and under 
 50,000. In five cases the count ranged between 50,800 and 78,000. 
 There is, however, a small but important group of 14 cases with 
 leucocytes in normal numbers. In the absence of other causes for 
 leucocytosis, especially in the group here called primary, the presence 
 of a real leucocytosis is of considerable value, though it must be 
 remembered that intracardiac clots and peripheral infarcts are also 
 capable of producing fever and leucocytosis in the absence of any 
 septic foci inside or outside the heart. 
 
 Circulating Phagocytes—In one of the cases of this group the 
 progressive anemia and leucocytosis were associated with an extra- 
 ordinary number of circulating phagocytes which could be seen 
 actively ingesting both red and white corpuscles. This case has been 
 recorded in detail by Dr. Mary W. Rowley.* A similar case studied 
 by her also occurred in connection with a chronic endocarditis very 
 possibly overlaid by acute endocarditis but not proved to be such, 
 as there was no post-mortem examination. Another case similar to 
 these has been reported by Van Nuys.T 
 
 5. Arrhythmia.— Unfortunately our records upon this point are 
 worth very little. They suffice merely to show that in a majority of 
 these cases arrhythmia is either absent or so slight that it was not 
 noticed at all during the life of the individual. In 32 cases, 23 of 
 them falling within the primary group, some type of arrhythmia was 
 noticed. In a good many of the other cases the absence of any 
 arrhythmia was definitely stated. In others there is no record. 
 
 SYMPTOMS ON THE PART OF THE CIRCULATION 
 
 (a) In Table 132 it appears that in the primary group of cases 
 cardiac enlargement was usually recognized. ‘This is especially true 
 of the recurrent subdivision. In the cases of secondary and terminal 
 endocarditis, on the other hand, cardiac enlargement was recognized 
 only 16 times among 78 cases, as contrasted with 67 times in 102 cases 
 of the primary group. 
 
 (b) Very similar figures are seen as regards dyspnea in Table 133, 
 and as regards edema in Table 134. 
 
 * Occurrence of Atypical Phagocytic Cells in the Circulating Blood, New York 
 Medical Journal, 1907. Vol. 85; p. 674. 
 
 + F. Van Nuys: An Extraordinary Blood. Presence of Atypical Phagocytic Cells. 
 Boston Medical and Surgical Journal, 1907. Vol. 156, p. 390. 
 
“a 
 
 SYMPTOMS ON THE PART OF THE CIRCULATION 575 
 
 TABLE 132.—CARDIAC ENLARGEMENT IN LIFE 
 
 From a diagnostic point of view however it is obvious that cardiac 
 enlargement, dyspnea, and edema do not help us to recognize acute 
 endocarditis, but point rather towards a valvular or hypertensive 
 type of chronic heart trouble. Still when these manifestations of 
 impaired circulation are associated with those of constitutional sepsis 
 referred to above, we certainly have a basis for suspecting acute 
 endocarditis, a suspicion which cannot approach definite knowledge 
 unless we have bacterial findings from the blood stream or evidence 
 of embolism. This group presents itself ordinarily under the clinical 
 picture of chronic valve disease and is so diagnosed. 
 
 (c) Cardiac Murmurs—Murmurs of some sort were recorded in 
 118 out of 180 cases. In the cases of primary endocarditis they were 
 recorded in 79 out of 102. The definite absence of murmurs is 
 recorded in only to cases of this group; in the remaining 13 there is 
 no record. In the cases of secondary endocarditis, on the other hand, 
 murmurs were recorded in only 35 out of 78 and are definitely 
 recorded as absent in 34. Systolic murmurs alone—which of course 
 have no diagnostic significance—make up the whole record in 55 cases. 
 
 Turning to the more significant murmurs we find systolic and 
 diastolic murmurs together in 40 cases, systolic, diastolic, and pre- 
 systolic murmurs combined in 14 cases, systolic and presystolic mur- 
 murs in eleven. Obviously none of these murmurs or combinations 
 of murmurs has any peculiar diagnostic significance in relation to 
 acute endocarditis, though I believe it is entirely possible that an 
 acute endocarditis, quite unassociated with chronic deformity in 
 
576 FACTS ON THE HEART 
 
 the valve, can, through the presence of perforating ulcerations and 
 blocking polypous masses, produce either a stenosis or a regurgitation. 
 This, however, in my opinion, is rarely the case, the significant mur- 
 murs being due.in the great majority of cases to chronic underlying 
 lesions. The nature of the evidence on which this belief is based is 
 hard to present. With the heart in one’s hand, looking at the 
 vegetations and ulcerations and estimating their size, one arrives 
 at an impression that they are or are not capable of producing 
 stenosis or incompetency of the valve. When the vegetations 
 are so minute that it needs a hand lens to make sure of their presence, 
 it would be generally agreed, I take it, that they could not of them- 
 selves produce a leak or a blocking of the valve. On the other hand, 
 when the vegetations are as big as one’s thumb it is almost impossible 
 to avoid the conclusion that they have interfered seriously in the 
 
 function of the valve to which they are attached. Between these ~ 
 
 extremes there are of course doubtful cases where the presonal equa- 
 tion of the dbserver must enter in. 
 
 I do not believe that the quality or the exact locaticn of murmurs © 
 
 helps much if at all in interpreting them as evidence for or against 
 acute endocarditis. Much more important is a change in the posi- 
 tion or quality of the murmur within a few hours or days under the 
 observation of one person. Among the 36 cases of primary non- 
 recurrent acute endocarditis such a change occurred in seven cases out 
 of ten in which there is a definite record on the subject. But in the 
 majority of the cases both in this group and in the others, we have no 
 sufficient study or record upon this point. 
 
 (d) Thrills —Largely from the study of cases not included in this 
 group I have come to believe that a thrill is the most important of all 
 the features in the local examination of the heart as evidence of acute 
 endocarditis. Realizing of course that a thrill may be produced by a 
 chronic stenosing lesion at any of the valves as well as by congenital 
 defects and by aneurism, I believe nevertheless that the presence of 
 a thrill and especially the appearance or modification of such a thrill, 
 in a febrile case, is of considerable practical value in the diagnosis of 
 an acute lesion. In the present series, however, such thrills were 
 recorded in only 29 out of 180 cases, and 22 of these were in cases 
 associated with a chronic deforming lesion and may well have been 
 due to that rather than to acute endocarditis. My own belief, there- 
 fore, as to the significance of a thrill in this disease is not substantiated 
 
 in the figures here presented. I urge it nevertheless upon the atten- — 
 
 tion of others. 
 
SYMPTOMS ON THE PART OF THE CIRCULATION Swi 
 
 (e) Chronic passive congestion was found at necropsy in 86 out of 
 180 cases, 72 of these belonging to the primary group and 14 to the 
 secondary. It is notable that evidence of general stasis was present 
 in almost every one of the recurrent cases, in the first group, 59 out 
 of 66. Thisis only what one would expect from the association in this 
 group of a chronic valvular lesion. But it is notable that even in 
 the absence of any such chronic lesion, 13 oué of 36 non-recurrent 
 cases tm the primary group showed chronic passive congestion after 
 death. On the other hand, not a single case in the group of pure 
 sepsis with secondary involvement of the heart showed any passive 
 congestion after death, a fact which seems to suggest that sepsis 
 alone cannot weaken the heart in such a way as to produce chronic 
 passive congestion. About a quarter of the cases with sepsis and 
 secondary involvement of the heart valves implanted-upon a pre- 
 vious chronic endocarditis, showed passive congestion after death. 
 But where there was no chronic process on the valve, secondary sepsis 
 alone was never in this series associated with chronic passive 
 congestion. 
 
 TABLE 135.—HEART WEIGHTS AT NECROPSY 
 
 Pyemic; 
 
 mMormal.. >. 
 
 128-200 
 200-249 
 250-299 
 300-349 
 3509-399 
 400-~449 
 459-499 
 5909-549 
 559-599 
 600-700 
 700-800 
 
 “Enlarged” 
 
 850 
 II50 
 1273 
 
 37 
 
 Primary 
 acute 
 
 Primary 
 acute re- 
 current 
 
 tl 
 wW 
 
 Lan 
 
 I 
 I 
 1 
 I 
 r 
 2 
 I 
 1e) 
 2 
 2 
 12) 
 I 
 1e) 
 ce) 
 te) 
 
 = 
 COOH AW Ob Y 
 
 - 
 12) 
 
 H+ 4+ &# DS WH BR AO OO 
 
 Pyemic 
 
 (os oy Tey TaN eh Lon col akoy cee Fob Sy ES ee hes) 
 
 | 
 
 iS} 
 Wn 
 
 chronic 
 
 endo. as 
 well as 
 acute 
 
 Terminal 
 (IV) 
 
 OOO) Oe Het me et Go se Ca COO! -O 
 
 al 
 ve) 
 
 OF 050 A Boe eS NON Oo OF SB OO 
 
 roca 
 
578 FACTS ON THE HEART 
 
 WEIGHT OF HEART AT NECROPSY 
 
 In comment on the facts shown in Table 135, one may say that 
 in 111 out of 180 cases hypertrophy is slight or absent; 1.e. in 111 cases 
 the heart weighed 450 grams or less. In the 78 cases of secondary 
 acute endocarditis 38 or approximately one-half showed no hyper- 
 trophy whatever. On the other hand, in the 102 cases of the first 
 group there are many very large hearts and only 27 under 400 grams. 
 The largest hearts of this series were associated with chronic peri- 
 carditis as well as with acute endocarditis and valve lesions, so that 
 we have no reason to believe that the endocarditis played any 
 considerable partin theirsize. Ontheother handin thenon-recurrent 
 cases of the primary group there are eleven cases of hypertrophied 
 hearts the size of which is not explained by any chronic lesion or by 
 any hypertension evident during the period of observation in life, 
 so that it seems possible that acute endocarditis is of itself capable of 
 producing cardiac hypertrophy in some cases. Four cases of this 
 group occurred in persons less than thirty years of age and not the 
 subject of any nephritis or arteriosclerosis. ‘Three of these four were 
 women, one fourteen years of age, one twenty-one, and one twenty- 
 nine. It is hardly probable that hypertension should have produced 
 the cardiac hypertrophy in these cases, and there was nothing what- 
 ever in the heart, pericardium or kidneys to account for any such 
 enlargement as was found. Under these conditions we may reason- 
 ably believe that there has been no hypertension present to explain 
 the cardiac hypertrophy, and may therefore suppose that the ulcera- 
 tions and polypoid masses themselves produce enough disturbance of 
 cardiac function to account for the hypertrophy. 
 
 BACTERIOLOGY 
 
 So little perseverance was devoted to catching bacteria in the cir-_ 
 culation during the life of the cases here studied that I shall here 
 record only the results of post-mortem cultures. In 80 out of 180 © 
 cases (see Table 136) an organism very probably connected with the 
 endocarditis was cultivated from the blood at necropsy. 54 of these 
 positive cultures were in the first or primary group of cases, and only 
 26 in the secondary cases. 19 out of 36 of the primary non-recurrent 
 cases of acute endocarditis showed positive cultures. 35 out of 66 of 
 the recurrent cases, 1g out of 44 of the septic cases with secondary 
 endocarditis, gave positive cultures, while seven of the 34 terminal 
 cases were also positive. 
 
ASSOCIATED LESIONS 579 
 
 TABLE 136.—ORGANISM POST-MORTEM 
 
 Streptococcus 
 Staphylococcus aureus 
 Atypical streptococcus 
 
 Pneumococcus 
 
 Staphylococcus albus 
 Streptococcus and staphylococcus.. 
 Streptococcus and pneumococcus... 
 
 H | | 
 Ke) OO H30r SOs Onc. 
 i? 20 (O04. 0 MOEN 
 
 “I 
 
 The streptococcus was much the commonest organism, being 
 present either alone or in association with other organisms in 75%. 
 No careful study of the type of streptococcus was made in any 
 considerable number of these cases, so that I shall attempt no com- 
 parison with the results of others upon this very important point. 
 The staphylococcus aureus was found in nine cases all falling within 
 the sub-group of primary acute endocarditis, the pneumococcus in 
 nine cases, six of which fell in the first group and three in the second, 
 Staphylococcus albus not the result of skin contamination occurred 
 in one case. In two cases there was the association of streptococcus 
 and staphylococcus and in one case of streptococcus and pneumo- 
 coccus. Wo gonococct or “influenza bacilli” were found. 
 
 ASSOCIATED LESIONS 
 
 118 of these cases were associated with hypertrophy and dilata- 
 tion of the heart, and 62 were without any such association. Aside 
 from the question of cardiac enlargement, 54 cases showed no cardiac 
 lesion except the acute endocarditis. 69 were associated with 
 valve lesions and of these 69, 20 had also further pathology in the 
 circulatory system. 20 were associated with chronic non-deforming 
 endocarditis, seven of these being further complicated. There 
 were g cases of acute pericarditis and g of chronic pericarditis with 
 the acute valvular lesion. 13 of these pericardial cases were still 
 _. further complicated by other circulatory lesions. 17 cases were 
 associated with arteriosclerosis and 17 with chronic nephritis, nine 
 of these 34 cases having some further cardiac pathology as well. 
 One case is associated with goitre and one with myocarditis and other 
 lesions. The overlapping and duplication of these is obvious. 
 
580 FACTS ON THE HEART 
 
 If one looks for the gravest associated lesion in each case the results 
 are as in Table 137. 
 
 TABLE 137.—CHIEF* ASSOCIATED LESIONS IN 180 CASES OF ACUTE ENDOCARDITIS 
 
 Without With 
 
 Acute and subacute endocarditis 
 enlargementlienlargement 
 
 With nephritis 
 With goiter 
 With chronic pericarditis 
 
 With leukemia 
 
 With pernicious anemia 
 
 With acute pericarditis 
 
 With chronic non-deforming endocarditis 
 
 With arteriosclerotic degeneration of the kidney 
 With arteriosclerosis 
 
 With myocarditis 
 
 OR NHB OOH HON 
 
 Ov 
 iS) 
 
 * To avoid duplications the most important lesion associated with the endocarditis has in each 
 case been counted as the associated lesion. 
 
 TABLE 138.—PRIMARY ACUTE AND SUBACUTE ENDOCARDITIS 
 
 Nonrecurrent Recurrent 
 
 Duration 
 
 Less than 2 weeks 
 2— 3 weeks 
 4— 7 weeks 
 
 10-14 months 
 
 15-24 months 
 
 24 months 
 
 - 2— 3 years 
 4 years 
 
 Questionable 
 
 2 3 
 6 4 
 5 5 
 2 I 
 5 8 
 2 2 
 i (e) 
 I % 
 2 Z 
 
 2 
 
 toa 
 oO 
 
 fos 
 Ov 
 
DURATION 581 
 
 DURATION 
 
 We have no way of calculating the duration of cases in the group 
 of pyemic or terminal endocarditis since there the underlying illness, 
 septic, neoplastic or whatever, may always have produced the earliest 
 symptoms. In the group designated as primary we obtained the 
 figures shown in Table 138, from which I shall draw the following 
 conclusions. 
 
 The recurrent cases of primary endocarditis last usually for 
 months. 38 out of 50 with a known duration lasted two months or 
 more. On the other hand, the non-recurrent primary cases lasted as 
 a rule weeks rather than months, 23 out of 36 knowing nothing of 
 any illness until within two months from the day of death. Four 
 to seven weeks is the duration in nearly half of these cases, while 
 two to five months is the commonest duration in the recurrent cases, 
 tg of which fell within these limits. The majority of the notably long 
 cases, lasting ten months or more, are in the group of recurrent cases, 
 seven falling in this group to six in the non-recurrent group. 
 
 Among those in which the duration is stated as two or three years 
 (or four years as in one case), it is to be supposed that as in other 
 chronic infections, for example tuberculosis, there is a waxing and 
 waning of immunity against the disease, periods of latency or arrest 
 in the process followed by the periods of activity. That this was the 
 case in at least two of our cases was shown by the occurrence post- 
 mortem of clean-cut, smooth-edged holes in valves, easily distinguish- 
 able from congenital defects or fenestrations, and clearly the result of a 
 previously ulcerative process which had healed. 
 
 In one case the patient definitely stated that he had been through 
 exactly the same experience two years previously, had recovered 
 after some months of illness, and then had remained perfectly well 
 until a few weeks before the time when we saw him. 
 
 Especially in children and in adolescents I think there is reason 
 to believe that this alternation of periods of activity with periods 
 of quiescence in the inflammation upon the heart valves is not at all 
 uncommon. Many of the cases called “‘chronic”’ and listed along 
 with deforming valvular lesions had at certain periods leucocytosis 
 and fever unexplained by any known lesions outside the heart. Some 
 of these cases may well have suffered from a brief and relatively 
 mild attack of acute endocarditis, overcome, like the milder tuber- 
 culous infections, without ever subjecting the system to any 
 observable strain or producing any but the mildest evidences of a 
 constitutional reaction. 
 
582 FACTS ON THE HEART 
 
 In the primary non-recurrent group of cases the average stay in 
 the hospital up to the time of death was 17 days. Leaving out of 
 account four relatively long cases which were in the hospital between 
 37 and go days each, we have for the remaining cases an average of 
 ten days from the time when they were sick enough to be brought to 
 a hospital until the moment of death. 
 
 Diagnosis.—31 cases out of 102 of the primary group were 
 diagnosed in life. None of the secondary group was recognized 
 during life. 
 
 SUMMARY 
 
 1. Acute and subacute endocarditis can be divided into the “pri- 
 mary’”’ cases which appear to be confined to the circulatory system, 
 and the ‘“‘secondary” group which result from a septic focus outside 
 the heart (e.g. general peritonitis or a septic uterus) or from a chronic 
 debilitating disease (neoplasm, nephritis, etc.). In these secondary 
 cases the endocarditis is probably a terminal event. 
 
 2. In 56% of cases, acute or subacute endocarditis is a recurrent 
 process Implanted upon an old area of healed inflammation. This 
 percentage rises to sixty-four if we consider only the “‘primary”’ cases. 
 
 3. It occurs especially between the twentieth and the fortieth 
 year and affects the two sexes about equally. 
 
 4. The mitral valve is attacked in 76% of cases, and is the only 
 valve attacked in 43%. In general the frequency of occurrence of 
 the disease on the different valves is about the same as in chronic 
 deforming endocarditis. ‘There is no special tendency to attack the 
 tricuspid or pulmonary valves. 
 
 5. Embolism is shown post-mortem in nearly two-thirds of the 
 “primary” cases, but is recognized during life in only one-half of these, 
 or one-third of all “primary” cases. The skin, spleen, kidneys, brain, 
 and lungs are most often affected. In the ‘‘secondary”’ cases emboli 
 are but one-half as common as in the “‘primary.”’ 
 
 6. Nephritis occurs in 40% of all cases and in 33% of the 
 “primary” group. 
 
 7. Diagnosis is often, perhaps usually, impossible. Fever and 
 chills in a patient with a diastolic murmur and a palpable thrill 
 should always make us suspicious. If these are associated with an 
 unexplained secondary anemia and especially with evidences of 
 embolism (purpura, hematuria, enlarged spleen) we may expect 
 that assiduous search will demonstrate organisms (usually strepto- 
 cocci) by culture in the blood. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 583 
 
 In many cases the diagnosis is masked by the more striking 
 evidences of chronic valvular disease and general passive congestion. 
 
 8. Decided cardiac enlargement occurs in 37%. Most of these 
 cases can be accounted for by an associated valvular disease or by 
 hypertension. But in a few cases it seems probable that the acute 
 vegetations themselves disturb cardiac function enough to produce 
 hypertrophy. 
 
 9. The duration is usually weeks or months, occasionally years. 
 
 to. Recovery certainly occurs and in children is probably not 
 uncommon. 
 
 Points of Especial Interest to the Writer 
 
 1. The frequent occurrence of a palpable thrill. 
 
 2. The occasional occurrence of cardiac hypertrophy unexplained. 
 
 3. The absence of any evidence that the right side of the heart 
 suffers more often than in chronic valvular disease. 
 
 4. The proof of healed ulcerative lesions. 
 
 5. The absence of the gonococcus and the influenza bacillus. 
 
 6. The rarity of an association with acute pericarditis (only 9 cases 
 in 180). : 
 7. The absence of the sternal tenderness mentioned by Libman. 
 
 ILLUSTRATIVE CASES 
 Necropsy 2700 
 
 A housewife of twenty-nine entered August 20 with a diagnosis 
 of Banti’s disease made by an intelligent internist. She had always 
 considered herself healthy. She had had no rheumatic fever, pleu- 
 risy, or malaria. She had had two miscarriages and no subsequent 
 pregnancies. Her catamenia were usually profuse, regular and pain- 
 less; ceased the May before admission. During the present illness 
 she had urinated once or twice at night. Her bowels were always 
 costive. Her best weight was 99!4 pounds. 
 
 Eight months before admission she was curetted on account of 
 a miscarriage. Some time after this she began gradually to lose 
 strength, color and weight. In May she was in bed a week with 
 nausea, fever and pain in the right side (abdomen?). Two weeks 
 later she noticed peculiar numbness in the right arm; no paralysis; 
 but at this time she had difficulty in enunciation and next day com- 
 plete aphasia which lasted forty-eight hours but left her quickly. 
 
584 FACTS ON THE HEART 
 
 Two months before admission she had severe pain in the left 
 upper quadrant for four weeks. This kept her awake at night, was 
 not associated with any lump, and gradually passed away. Her 
 bowels were increasingly constipated, though there was no pain or 
 change in the stools so far as she knew. 
 
 The chief complaint was of increasing pallor and weakness, so 
 that for the two months before admission she kept to her bed. 
 There was no jaundice or bleeding from the gums. For the past 
 two months she had noticed crops of red spots on the legs. 
 
 Examination showed a fairly well developed, poorly nourished 
 woman with obvious loss of flesh. The skin was muddy, but not 
 really jaundiced. There were purpuric spots over both legs below 
 the knees. The apex impulse of the heart was in the fourth space, 7 
 cm. from the midsternal line. There was no right-sided enlargement. 
 A blowing systolic murmur was heard at the apex transmitted to the 
 axilla and back, also heard at the base. The sounds were of good 
 quality. The pulmonic second sound was not accentuated. The 
 lungs showed dullness, diminished voice and breath sounds at the 
 left base extending up about halfway to the angle of the scapula and 
 continuing around the chest to the front. There was a pleural rub at 
 the right base behind on deep inspiration. Over an area extending 
 from the umbilicus to the pubes and corresponding roughly with the 
 area which would be produced by a greatly distended bladder there 
 was distension, tympany, visible peristalsis and a succussion sound. 
 In the region of the spleen there was a hard mass with a definitely 
 nodular edge moving freely with respiration, on pressure not tender, 
 well felt from the flank. There was slight dullness in both flanks, 
 not shifting with change of position. There was some diastasis 
 of the recti. Vaginal examination showed nothing of importance. 
 The rectal examination was negative. The extremities and reflexes 
 were normal. 
 
 During more than seven weeks of observation in the hospital 
 the patient had waves of fever lasting a week or ten days each, 
 rarely reaching more than 103°. There were only three or four days 
 in this whole period when she was free from fever. As a rule 
 the daily swing was about 2°, but at times it was 4° or more. The 
 pulse was continuously elevated, usually between too and 120. The 
 respirations were 20 to 25 during most of the course. The output 
 of urine was 40 to 70 ounces, the specific gravity 1.002 to 1.005 at 
 five of seven examinations, 1.016 at the other two. ‘Traces of albu- 
 min were always present, sugar absent. The sediment usually 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 585 
 
 showed a few hyalin and granular casts; nothing else of importance. 
 At entrance the red cells were 2,500,000, the leucocytes 6,000, the 
 hemoglobin 38% (Sahli), the polynuclears 83%. The stained smear 
 showed moderate achromia, slight variation in size and shape, no 
 blasts. The blood plates counted by Dr. J. H. Pratt were 141,000. 
 August 29 the blood showed very little change. September 9g the 
 red cells were 2,280,000, September 13 2,056,000, September 17 
 2,000,000, September 24 1,900,000. There werenoimportant changes 
 in the look of the blood smear except that the achromia grew more and 
 more marked and polychromatophilia appeared. Blood cultures 
 August 22, 24, 25 and September 5 showed always a profuse growth 
 of atypical pneumococci. A urine culture August 25 and September 
 8 showed the same organism. September 19 a blood culture showed 
 a somewhat less definite organism, the surface growth showing diplo- 
 
 Fic. 104.—Rash following medication. 
 
 cocci while the water of condensation showed chains of streptococci. 
 A Wassermann August 24 was positive. August 26 20 minims of a 
 catheter specimen of urine were injected into a guinea-pig. Necropsy 
 on this animal October 3 was negative. 
 
 Further study of the mass in the left hypochondrium seemed to 
 show that it was a tender spleen. At entrance the patient was given 
 ten grains of potassium iodid three times a day. Forty-eight hours 
 later a very marked rash developed on the face and arms. (See 
 Figs. 104 and 105.) August 26 this rash was pustular, but cultures 
 taken from the pustules showed no growth. The mass in the region 
 of the bladder at first suggested the retention of urine. The patient 
 was catheterized with removal of thirty-six ounces of urine, but the 
 tumor still persisted. Apparently it was due to protrusion of intes- 
 
586 FACTS ON THE HEART 
 
 tines through the rectal diastasis. About August 25 she had several 
 sharp attacks of pain in the spleen with increase of its tenderness. 
 On the 26th a loud harsh systolic murmur was heard at the apex of 
 the heart apparently different from that heard at entrance. Dr. 
 K. Lawrence Oliver pronounced the cutaneous eruption to be due 
 to KI taken. 
 
 September 7 there was a slight colitis, which cleared up in a 
 few days. About this time the patient began to have constant 
 severe pain in the region of the spleen, and its lower edge was exqui- 
 sitely tender. At midnight on the eighth she suddenly developed 
 deep noisy breathing and when seen by the nurse was in a convulsion. 
 Next morning the reflexes of the right arm were increased and there 
 was right ankle clonus. The patient was drowsy and stupid all day, 
 the white count still, however, remaining low. At this time the 
 
 Fic. 105.—Rash following medication. 
 
 cardiac murmur replaced the first sound altogether. September 11 
 the left chest showed dullness to flatness from the angle of the 
 scapula to the base, with moist rales and absent breath sounds over 
 this area. The left clavicle was slightly tender. By September 19 
 the splenic tenderness had disappeared and the signs in the left chest 
 were gone. Her appetite was good, her spirits much improved, yet 
 the patient was steadily growing weaker. There was marked ankle 
 clonus, especially on the left. September 27 the liver was quite 
 tender. Toward the end of life she had to be kept under morphia 
 and became incontinent of urine and feces, so that a bedsore developed 
 over the sacrum. October g she died. 
 
 Clinical Diagnosis (from Hospital Record).—Subacute infectious 
 endocarditis. 
 
ie 
 
 ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 587 
 
 Multiple infarcts. 
 
 Septicemia. 
 
 Chronic passive congestion. 
 
 Dr. Richard C, Cabot’s Diagnosis.—Septicemia, streptococcus- 
 pnheumococcus. 
 
 Acute endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion of the lungs. 
 
 Infarcts of spleen, liver, lungs. 
 
 Perisplenitis. 
 
 Decubitus. 
 
 Anatomical Diagnosis.—Septicemia, atypical pneumococcus. 
 
 Acute and slight chronic endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Infarcts of the spleen and kidneys. 
 
 Slight chronic passive congestion, general. - 
 
 Hemorrhages of the liver. 
 
 Focal fibroid myocarditis. 
 
 Slight chronic pleuritis, right. 
 
 Decubitus. 
 
 Dr. RicHARDSON: The gastrointestinal tract showed nothing at 
 all except some reddening of the mucosa, the initial stages of passive 
 congestion. The abdominal wall was very thin, the muscles pale, 
 and while there was no distinct separation, yet the thinness of the 
 wall would easily permit the bulging forward of the intestines that 
 Dr. Cabot mentioned. 
 
 Dr. Casor: Do you think that just part of the general emaciation ? 
 
 Dr. RICHARDSON: Yes. 
 
 Dr. Casot: We said: ‘‘Why was there diastasis of the recti?”’ 
 The answer is, there was not any. The mystery is wiped out. The 
 patient was very thin everywhere, so thin that the intestines came 
 
 forward. 
 
 Dr. RicHarpson: The cultures showed the organism already 
 mentioned, an organism belonging to the streptococcus-pneumo- 
 coccus group and that particular one known as the viridans. That 
 was proved true in life, proved true in the heart blood and from the 
 spleen, establishing the streptococcus septicemia. 
 
 The heart showed only very slight hypertrophy and dilatation. 
 The right wall of the heart was 4 mm. thick, slightly thickened, the 
 left to mm., not thickened at all. The cavities were only slightly 
 enlarged. That is important, because there was only a slight amount 
 
588 FACTS ON THE HEART 
 
 of chronic passive congestion and not much dilatation. The aortic, 
 tricuspid and pulmonary valves were negative. On the mitral valve 
 in a few scattered places there were small polypoid vegetations, 
 taken together a very small mass. So that within the heart there was 
 no definite cause for hypertrophy and dilatation, and there was not 
 much. The aorta and its branches were negative. So that although 
 there was a polypoid mass of vegetations on the mitral valve, they 
 were so small that they produced but little decrease in the circum- 
 ference. She was a very small woman, and the valve would not ordi- 
 narily measure more than eight cm.; there was very little change. 
 That makes very little deformity of that valve. That is a point Dr. 
 Cabot has always insisted on. Where there is real stenosis of a valve 
 there is with it deformity or such change as can be called deformity. 
 There was nothing in the cavities, and no ball thrombus. 
 
 The spleen was very large as has been described. It weighed 465 
 grams; that is considerably enlarged. Scattered through it were 
 infarcts the outer surfaces of which showed acute splenitis resting 
 over these areas of infarction. The spleen tissue itself was a little 
 soft, as 1s apt to be the case in infections, although not always so. 
 
 The pleural cavities showed no fluid. The lungs showed a slight 
 amount of chronic passive congestion, and there was a slight amount 
 of chronic passive congestion in the liver, which is of course in har- 
 mony with the character of the heart. The liver weighed 1660 
 grams—a little large—and the interesting thing was that scattered 
 through it were some small areas of hemorrhage. Those were in 
 the nature of purpura, and probably are to be associated with the 
 infection present and also with the anemia. 
 
 Dr. Casot: Why do we have purpura in infections? 
 
 Dr. RicHARDSON: I don’t know. As the cases come here we find 
 it associated with infections and anemia. Those are the two com- 
 mon things, and then again we find it associated with nothing 
 that we can put our finger on. We do not know whether it is change 
 in the quality of the blood or in the character of the vessel walls 
 which produces purpura. 
 
 A PuysiciAN: How much purpura hemorrhagica do you see? 
 
 Dr. Cazsort: It is a very rare disease. We often go a full year in 
 this hospital without seeing any. 
 
 Dr. RICHARDSON: We get cases here of unexplained purpura, 
 something akin to hemorrhagic diathesis. One of the most marked 
 cases I have seen was in connection with tuberculosis. That of 
 course was infection. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 589 
 
 The microscopic examination confirmed the gross picture, showing 
 the vegetations on the heart valve laden with bacteria. Another 
 interesting point is that of the focal myocarditis of the left ventricle. 
 There was a small area of softening in the wall, and the vessel leading 
 to that area was occluded; it was definitely an area of infarction, a 
 focal myocarditis. 
 
 A PuysictANn: Is this case infection from the heart vegetation 
 itself? 
 
 Dr. Casot: I do not think anybody can answer the question 
 whether it starts in the blood and goes to the heart or starts in the 
 heart and goes to the blood. My own guess is that it starts in the 
 blood. 
 
 Necropsy 2910 
 
 A colored laborer of twenty-eight entered August 19. His past 
 history was negative except that he was kicked in the leg by a horse 
 a month and a halfago. For the past three weeks he had been drink- 
 ing two bottles of beer and one of gin daily. He formerly drank 
 much whiskey and beer. He smoked from two to six cigars a day. 
 He had “‘chancre”’ three weeks before admission. 
 
 A few days after the chancre appeared he began to have “‘rheu- 
 matism”’ in his ankles, calves, and left wrist, so painful that he had 
 difficulty in walking. For three weeks his appetite had been poor, 
 especially in the morning. August 12 examination in the Orthopedic 
 Room of the Out-Patient Department showed slight swelling of the 
 left wrist and right ankle. He was given aspirin. August 15 he is 
 reported that the pain was relieved, but that he now had pain in the 
 left lower quadrant. The leucocyte count was 16,000. August 19 
 the abdominal pain was still present. Physical examination showed 
 no tenderness. The constant dull ache in the left lower quadrant had 
 persisted. He had vomited a little white watery material during 
 the past two days, without relation to food. He thought he had had 
 slight edema of the legs. He urinated once or twice nearly every 
 night. 
 
 Examination showed a well-nourished negro. The right epi- 
 trochlear glands were the size of a pea; the left were not palpable. 
 The heart showed no enlargement to percussion. The sounds, 
 action, pulses and artery walls were normal. There was a soft 
 blowing systolic murmur at the apex, transmitted to the axilla. 
 The systolic blood pressure was 115. The lungs were clear. The 
 spleen seemed somewhat enlarged to percussion. The edge was not 
 
590 FACTS ON THE HEART 
 
 felt. There was a small indurated area on the corona of the 
 penis with a moist surface and slight discharge. No urethral 
 discharge was discovered. There was slight tenderness under the 
 outer malleolus of the left ankle. The left wrist was slightly painful 
 on extreme flexion or extension. The pupils were slightly irregular. 
 The right reacted sluggishly to strong light; the left reacted well. 
 The reflexes were normal. 
 
 The temperature was 101° to 105°, the pulse 84 to 160, the respira- 
 tion 28 to 80. The amount of urine was 25 to 81 ounces, the specific 
 gravity I.o12 to 1.020. There was the slightest possible trace to a 
 trace of albumin at all of five examinations, a few red blood corpuscles 
 at all, rare hyalin and granular casts at two, a large number of 
 granular casts, a few hyalin, and many casts with red and white 
 blood corpuscles attached at the last two. The hemoglobin was 
 100%. There were 25,000 to 52,000 leucocytes, 91% polynuclears. 
 A Wassermann was negative. Blood cultures August 19 and 23 
 showed streptococcus pyogenes. ‘The stools were dark red, showed 
 many red blood corpuscles, and gave a positive guaiac. A skin 
 consultant reported, “I think that the lesion of the penis is probably 
 a primary lesion. I do not believe his temperature is due tosyphilis, 
 and should think his present acute medical condition of more impor- 
 tance than his syphilis.” 
 
 August 25 the heart murmur had a muscial quality which dis- 
 appeared over night. Many fine crackles were heard at the lower 
 right axilla, and August 26 many crackles at the left base behind. 
 August 28 he had a chill. Although he gradually lost ground he felt 
 comfortable and ate his meals with evident relish. August 29 there 
 were many fine moist crackles at the right base in the axilla and in 
 front. September 4 the pulse and respirations rose. Autogenous 
 vaccines were given. The systolic murmur continued loud and harsh, 
 occasionally with a musical tone. Rales were heard at both bases. 
 September 7 he died. 
 
 Clinical Diagnosis (from Hospital Record).—Streptococcus 
 septicemia. 
 
 Syphilis. 
 
 Dr. William H. Smith’s Diagnosis Streptococcus septicemia. 
 
 Ulcerative endocarditis of the mitral valve. 
 
 Possibly multiple foci of bronchopneumonia. 
 
 Passive congestion? 
 
 Infarction of the lungs? of the spleen? of the left kidney? 
 
 Anatomical Diagnosis.—Septicemia, streptococcus. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 591 
 
 Acute endocarditis of the mitral valve with occlusion of the valve 
 orifice. 
 
 Extensive infarcts of the spleen and kidney with purulent soften- 
 ing of a large splenic infarct. 
 
 Thrombosis of the right common iliac artery, the splenic artery, 
 the branch of the left renal artery. ; 
 
 Hypertrophy and dilatation of the heart. 
 
 Fic. 106.—Acute polypous endocarditis of the mitral valve with a huge mass occluding 
 the mitral orifice. (Photograph by Lewis S. Brown. Dr. Oscar Richardson.) 
 
 Chronic passive congestion, general. 
 
 Acute glomerulo-nephritis. 
 
 Slight chronic pleuritis, left. 
 
 Dr. RicHarpson: The illustration (Fig. 106) shows the mitral 
 valve with the huge mass on it. When all its edges are brought 
 together there is little space for the circulating fluid to go through. 
 
592 FACTS ON THE HEART 
 
 It was gradually closing down. This was a case of streptococcus 
 septicemia with which was associated the large polypoid mass of 
 vegetation on the mitral valve and the acute glomerulo-nephritis, 
 By the latter I mean a condition in which there is proliferation of the 
 endothelial cells of the capillaries of the glomeruli with the occlusion 
 of the glomeruli. At this time we associate the condition with 
 organisms of the streptococcus-pneumococcus group. From the 
 picture of the mitral valve it is plain to see how small particles could 
 be washed off and carried into the various vessels. We do not 
 always find the plugs in the vessels as we did in this case, where we 
 found them in three places. That picture is rather uncommon. 
 The question arises in these cases of infection with this group of 
 organisms as to whether it may not be an arteritis of the vessels and 
 the thrombi erected at that point. We had a case the other day 
 which supports this hypothesis well. In this particular place 
 we do have a definite source for the thrombi, that is, the thrombi are 
 embolic. The emboli come down, get plugged there, and become 
 adherent to the wall. In the other case the valves were perfectly 
 smooth and free, and there was marked infarction of the kidneys 
 and the thrombus in the renal artery. 
 
 The heart weighed 363 grams and was moderately dilated. 
 With the exception of the mass on the mitral valve it showed nothing 
 remarkable. 
 
 We made a careful examination for gonococci and spirochetes, 
 not only by the cover glass method but also by staining sections 
 according to Levaditi’s method. There was no evidence of syphilis 
 or gonorrhea. 
 
 The lungs showed chronic passive congestion. 
 
 The liver and the gastro-intestinal and the genito-urinary tracts 
 were negative with the exception of the kidneys. They weighed 404 
 grams, rather large. (Normally 200-400.) They showed the infarcts 
 mentioned in the anatomical diagnosis and a rather wide cortex, 6-7 
 mm. The glomeruli were visible at points. 
 
 Although this man was a negro, in whose race the prevalence of 
 tuberculosis 1s well-known, there is no tuberculosis recorded; even 
 the lymphatic glands were negative. 
 
 Necropsy 3030 
 
 An Irish laborer of thirty entered January 8. His past history 
 was negative except for “‘fever’* for a few days asa child. He drank 
 six glasses of whiskey and eight of beer a day, sometimes more. 
 
ACUTE ENDOCARDITIS—-ILLUSTRATIVE CASES 593 
 
 For a year he had had ulcers on his legs. Three months before 
 admission they practically healed, but soon broke down and since this 
 had not healed. He had never noticed any varicosities, and denied 
 all symptoms of syphilis. 
 
 For six weeks he had had a troublesome cough with a moderate 
 amount of sputum. He had been increasingly dyspneic, especially 
 at night. His feet and ankles had been swollen at times. He uri- 
 nated three or four times at night. He slept poorly, especially after 
 drinking heavily. He had anorexia and was constipated. 
 
 Examination showed a well-nourished man tossing restlessly 
 about, with occasional unproductive cough. The mucous mem- 
 branes were slightly dusky. The apex impulse of the heart was in 
 the fifth space. The borders of dullness were 14.5 cm. to the left, 
 4 cm. to the right, the substernal dullness 6 cm. The action was 
 rapid and slightly irregular. The sounds were of fair quality, heard 
 with difficulty on account of noises in the bronchi and lungs. There 
 was a loud blowing systolic murmur at the apex transmitted to the 
 axilla, a to-and-fro murmur at the second right rib transmitted to the 
 neck. The aortic second sound was accentuated. The pulses were 
 irregular. The blood pressure was 150/80 to 120/70; the systolic 
 later fell to 100. The lungs showed poor expansion. Expiration 
 was somewhat prolonged, especially on the right. There were many 
 coarse crackles and groans. There was moderate dullness through- 
 out the right side of the abdomen, not shifting. The liver dullness 
 extended from the fifth space to 3 cm. below the costal margin. 
 The edge was not felt. The genitals were normal. ‘There was con- 
 siderable pitting edema of the lower legs and ankles. On the lower 
 legs were two ulcers, discrete, with well defined edges and granulating 
 centers, and a small healed scar surrounded by an area of scaly 
 brownish skin. The pupils and reflexes were normal. 
 
 The temperature was 95.7 to ror.8°, the pulse 65 to 116. The 
 respirations were 17 to 36, after February 1 not remarkable. The 
 amount of urine was 17 to 75 ounces, the specific gravity 1.030 to 
 1.012. There was albumin ’in large amounts in twenty-four of 
 twenty-eight examinations, a slight trace at the other four. Hyalin 
 and granular casts were seen at all examinations, in large numbers 
 at the first three, red blood corpuscles at all, leucocytes at nine. 
 A culture from the urine showed a few bacilli. The hemoglobin was 
 80 to 60%. There were 7,200 to 12,600 leucocytes, 75% polynuclears. 
 
 The smear at entrance was not remarkable; March 18 the reds were 
 38 
 
594 FACTS ON THE HEART 
 
 2,648,000. Four Wassermanns were negative. The fundi at admis- 
 sion and February 13 were normal. 
 
 The patient was very uncomfortable at entrance. January 13 
 he was resting better at night, the edema was clearing, and the 
 heart borders coming in. He continued to improve slowly. Janu- 
 ary 21 the left border of dullness was 16 cm., the substernal dullness 
 8 cm., the apex impulse diffuse in the 5th and 6th spaces. There 
 was a short rough musical systolic over the left precordia, a short 
 rough systolic of different quality in the aortic area, a soft diastolic 
 
 Fic. 107.—The heart is greatly enlarged to the left. There is a shadow at the right 
 of the sternum probably due to peribronchial thickening. The aortic arch is not 
 enlarged. General peribronchial thickening and glandular enlargement. By fluro- 
 scope no abnormal pulsation was made out. 
 
 in the aortic area and along the right sternal margin. ‘There were 
 a few rales at the bases of the lungs. The ulcers of the legs were 
 improving rapidly with corrosive dressings. X-ray January 24 
 showed the chest as in Fig. 107. He was put upon mercury salicylate 
 and potassium iodid. Because of marked coryza and lachrimation 
 the potassium iodid was omitted next day, and because of saliva- 
 tion the mercury was omitted January 31. February 4 the systolic in 
 the aortic area was barely audible. He was running a slight irregular 
 
 temperature without obvious cause. Blood cultures were negative - 
 
 February 4 and 21 and March 2. March 5 the temperature was no 
 longer elevated. He was allowed to sit on the porch. He was given 
 
 q 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 595 
 
 two carbon dioxid baths and felt better after them. There was a 
 slight amount of fluid in the abdomen. 
 
 March 14 the right ear and mastoid region were painful, the mas- 
 toid tender on pressure. This drum was incised by an ear consultant, 
 with a free discharge of pus, which continued. March 21 there was 
 a butterfly patch of dull red over the nose, slightly tender and 
 indurated. The patient had a slight chill. Two days later the 
 patch had disappeared, but the mastoid tenderness was exquisite. 
 The patient was dull, often irrational, complaining of no pain. The 
 aural consultant advised postponing operation on account of the 
 general condition. There was considerable edema of the legs, later 
 of the hands, and marked edema and tenderness down under the 
 right jaw. March 30 the eyes were turned to the right; there was 
 slight nystagmus. The knee-jerks were feeble. The patient was 
 noisily delirious, and died that day. 
 
 Clinical Diagnosis (from Hospital Record).—Chronic glomerulo- 
 nephritis. 
 
 Chronic endocarditis. 
 
 Aortitis? 
 
 Chronic middle ear. 
 
 Chronic mastoid. 
 
 Dr. Richard C. Caboi’s Diagnosis —Chronic endocarditis of the 
 aortic and mitral valves, with stenosis of each. 
 
 Hypertrophy and dilatation of the heart. 
 
 Subacute glomerulo-nephritis. ) 
 
 Secondary anemia. 
 
 Terminal streptococcus infection. 
 
 Chronic passive congestion. 
 
 Anatomical Diagnosis.—Acute vegetative endocarditis of the 
 aortic valve. 
 
 Chronic ulcerative endocarditis of the aortic valve. 
 
 Subacute glomerulo-nephritis. 
 
 Septicemia, pneumococcus streptococcus. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Hydropericardium. 
 
 Hydrothorax. 
 
 Ascites. 
 
 Anasarca. 
 
 Scar in the region of the right mastoid with sinus formation. 
 
 Phlegmon of the deep tissues of the right side of the neck. 
 
596 FACTS ON THE HEART 
 
 The heart weighed 584 grams (normally 200-300). The cavities 
 were considerably enlarged. The mitral valve was 12 cm. in cir- 
 cumference (normally 1ocm.). The valve was not otherwise remark- 
 able. The circumference of the aortic valve laid open was 8 cm.; 
 but there was a large fibrocalcareous mass 3 cm. X 2 cm. which fused 
 two of the cusps together and pushed up into the orifice of the valve, 
 thereby considerably decreasing its actual circumference. The 
 circumference of the tricuspid valve was 14 cm. (normally 12-13). 
 Except for enlargement the valve was not remarkable. The pul- 
 monic valve measured 9.75 cm. (normally 8-9 cm.), not remarkable. 
 
 Note by Dr. G. W. Holmes.—In reviewing the X-ray plates in 
 the light of the outcome it may be noted that the general shape of 
 the heart, roughly triangular, suggests fluid in the pericardium. 
 
 Necropsy 4577 
 
 An Italian clerk of twenty-three entered August 4, 1923, for 
 relief of general weakness, malaise, dyspnea, slight cough, palpita- 
 tion, and slight aching in the joints. His general health had always 
 been good. He had the usual diseases of childhood and possibly 
 scarlet fever. He had occasional head colds and slight headaches. 
 Since tonsillectomy at seven he had had occasional sore throats. 
 Several years before admission his nose was injured. 
 
 Four and a half years before admission, after a mild attack a week 
 and a half in duration of influenza and tonsillitis associated with 
 general malaise, slight fever and some chilliness, he had his first 
 attack of painful and swollen joints. He was confined to bed for 
 nine weeks. On returning to work he developed sore throat, soon 
 followed by mild general constitutional symptoms. One morning on 
 waking he had considerable swelling of all the joints, and pain which 
 increased in severity until it was almost impossible to bear the 
 weight of the bed clothes. There was local heat but no redness. 
 He felt slightly feverish and at times chilly, but had no actual 
 chill. At the initial attack all the joints became involved simul- 
 taneously. Active or passive motion aggravated the pain consider- 
 ably. In addition to it there was swelling of the precordia. The 
 acute condition did not last very long. Most of the nine weeks of his 
 illness was a gradual recovery. In addition he spent a few months 
 in recuperation. From that time he was free from symptoms until 
 two months before admission, when he had a second attack of painful 
 and swollen joints. A month later cardiac signs were discovered. 
 During the past two weeks cardiac symptoms had developed. He 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 597 
 
 attributed the present attack of debility to worry about his mother’s 
 condition. A short time before the joint symptoms developed he had 
 slight malaise and weakness. ‘Then followed pain and stiffness in 
 the left calf muscle, and soon afterwards pain and swelling in the right 
 ankle, with rapid involvement of the left ankle. He gave up work. 
 A few days after the ankles had been involved, when the inflammation 
 was subsiding, the knee-joints became involved, and soon after this 
 the ankle-joints again, with the left shoulder joint. Until a few weeks 
 ago he was up and about the house. For three weeks his joints had 
 given him no trouble, but he had developed at first a “‘full feeling”’ in 
 the epigastrium, with gradual development of slight dyspnea, which 
 in the past week had increased so that he slept in a more or less semi- 
 recumbent position. His sleep was still considerably disturbed, 
 especially in the past few days. The ‘‘fullness in the stomach” 
 had increased until it had several times caused him to vomit. In the 
 past few days he had had palpitation and slight precordial pain. 
 Recently he had had slight unproductive cough and had urinated 
 once or twice at night. 
 
 3-5 Ee 
 
 Fic. 108.—Measurements by percussion. 
 
 Examination showed a poorly nourished, rather pale man. The 
 lungs were clear. The apex impulse of the heart was felt in the fifth 
 space, diffuse. The heart was enlarged to the right and left. The 
 percussion measurements were asshownin Fig.108. There was force- 
 ful bounding pulsation, best seen and felt in the fifth space one cm. 
 outside the nipple line, faintly felt in the sixth space. The whole pre- 
 cordia lifted with the apex. There was an apical thrill. A systolic 
 murmur replaced the first sound at the apex and the base. A short 
 diastolic was heard at the aortic area and the apex. The blood pres- 
 sure was 130/50-0. ‘The abdomen was dull, perhaps because of feces. 
 The liver and spleen were palpable. ‘The liver edge was felt. The 
 fingers weresome whatclubbed. ‘Thepupilsand reflexes were normal. 
 
 The temperature was 98° to 103.1°, the pulse gt to 120, the respi- 
 ration 18 to 36. The output of urine was 42 to 83 ounces, the specific 
 gravity 1.010 to 1.018. ‘There was a very slight trace to a trace of 
 albumin at all of five examinations. Red and white blood corpuscles 
 were present at all but one, twice in large numbers, granular casts 
 
598 FACTS ON THE HEART 
 
 at three. The renal function was 50%. The hemoglobin was 65%. 
 There were 13,600 to 34,500 leucocytes, 3,580,000 to 4,160,000 to 
 3,100,000 reds, moderate achromia, only slight variation in shape, 
 with an occasional tendency toward tailed forms. One blood culture 
 was negative, one showed streptococcus. One Wassermann was 
 
 4 
 | 
 Fic. 109.—Chest 25.5 cm. Marked enlargement of the heart shadow. Increase 
 apparently marked across the base in the region of the auricles. No change in the 
 supracardiac dullness. Marked increase in the hilus shadows on both sides, with 
 thickened prominent lung markings extending well out toward the periphery of the 
 chest, and a large amount of mottling between the larger lung markings. These changes 
 apparently do not reach the periphery or apices, and may be cardiac in origin. 
 
 weakly positive, one negative. The X-ray findings August 17 are 
 shown in Fig. ro9. 
 
 August 16 transfusion of 510 c.c. was followed by a chill for 
 a short time. The red count was not markedly changed. August 21 
 the patient was discharged with instructions for rest and hygiene. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 599 
 
 September 18, 1923, he reentered. During the greater part of the 
 interval since his discharge he had been in bed, in the afternoon 
 walking about for a short time. His condition had remained in 
 general about the same, perhaps growing somewhat worse, definitely 
 so for the past few days. After he had been home a short time he 
 began having bloating and a full feeling in the epigastrium, so that it 
 embarrassed his breathing a good deal toward the evening and usually 
 after eating. With the bloating he usually had cough with watery 
 mucoid sputum, and frequently vomited withrelief. After the vomit- 
 ing he frequently had palpitation and precordial pain which at 
 times radiated to the right side. A few days before reentry he 
 noticed for the first time toward evening pitting edema of the ankles. 
 He was dyspneic when at rest, especially when bloated. He had had 
 
 IN 
 SPL 
 ) | 
 LA / 
 WD, 
 6A 
 
 Dull. Distant 
 
 Smooth breath and 
 tender voice sounds, 
 liver A few rales, 
 
 Fic. 110.—Chest sign in Case 4577. 
 
 no joint symptoms except some pain and stiffness in the right calf 
 a few weeks ago. He thought he had some evening rise of 
 temperature. 
 
 Upon examination he was very emaciated, with slight mucoid 
 cough. The lung signs were as shown in Fig. 110. The heart was 
 very large, with diffuse heaving precordial impulse and thrill. There 
 was a systolic blowing murmur over the precordia, best heard at 
 the pulmonic area, and a crisp short diastolic. The heart was 
 heard throughout the chest. The blood pressure was 105/50. The 
 spleen was not felt because of abdominal distension. The liver 
 was as shown in the diagram. There was great edema of the feet 
 and ankles. Over the shins were red petechiae. 
 
 The temperature was 99° steadily falling to 94°, the pulse 130 
 falling to 86, the respiration 34 to 16. The output of urine was 20 
 
600 FACTS ON THE HEART 
 
 to 33 ounces, the specific gravity 1.018. There were occasional 
 leucocytes, no albumin. The hemoglobin was 50 to 55%. There ~ 
 were 32,800 to 33,200 leucocytes, 2,980,000 reds, 89% polynuclears. 
 The mononuclears showed large vacuoles in cytoplasm. The red 
 blood corpuscles showed considerable variation in size, typical 
 macrocytes, a few microcytes. Most of the fields showed red cells 
 well filled with hemoglobin; others showed slight achromia. There 
 were a few tailed forms and oblong cells. The platelets were 
 strikingly decreased and small. A Wassermann was moderately 
 positive. The non-protein nitrogen was 95 mgm. X-ray showed 
 the general appearance of the heart practically the same as at the 
 previous note, possibly slightly more enlarged. The right antrum 
 was dull. The right superior bicuspid tooth supporting a bridge 
 showed evidence of a small area of 
 absorption at its apex. 
 
 The patient vomited almost 
 everything taken. There was con- 
 siderable abdominal pain from liver 
 distension. 
 
 September 18 transfusion of 500 
 c.c. was followed by a moderately 
 severe chill and prostration. The 
 patient had been growing pro- 
 
 op gressively worse since admission. 
 Takiae neatenieoetee The evening of September 18 he 
 Fic. 111.—Measurements by X-ray became weaker, andthe pulse failed 
 apes ee decidedly, though it improved with 
 caffein. Early the next morning he quietly died. 
 
 Clinical Diagnosis (from Hos pital Record) —Bacterial endocarditis. 
 
 Streptococcus infection of blood. 
 
 Dr. Richard C. Cabot’s Diagnosis —Acute and chronic endocardi- 
 tis of the aortic and mitral valves. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion. 
 
 Acute nephritis (?). 
 
 Chronic pericarditis (?). 
 
 Anatomical Diagnosis—Vegetative endocarditis of the mitral 
 and aortic valves. 
 
 Vegetative endocarditis of the endocardium of the right auricle. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Total heart diameter. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 601 
 
 Infarcts of lungs, spleen and kidneys. 
 Chronic glomerulo-nephritis, capsular. 
 Ascites. 
 
 Edema of the ankles. 
 
 we Se 
 
 Fic. 112.—Case 4577. Streptococcus viridans endocarditis. Section of valve A, B, 
 bacterial fringe. (X 1000). (Photomicrograph by Dr. Albert E. Steele. Dr. William 
 H. Smith.) 
 
 Fic. 113.—Case 4577. Streptococcus viridans endocarditis. High magnification 
 of the area at A in Fig. 112. (X 1500.) (Photomicrograph by Dr. Albert E. Steele. 
 Dr. William H. Smith.) 
 
 Dr. RicHarpson: We were not permitted to examine the head. 
 
 _ There was edema of the legs. There were red spots scattered 
 over the feet and the anterior aspect of the right arm. 
 
 There was considerable thin clear fluid in the peritoneal cavity,— 
 
 ascites. The liver was seven cm. below the costal border. The dia- 
 
602 FACTS ON THE HEART 
 
 phragm was at the fifth rib on the right, at the fifth interspace on the 
 left. 
 
 In the pleural cavities there were fifty c.c. of fluid on the right 
 and forty c.c. on the left, with a few adhesions on each side. The 
 lungs were rather voluminous, but showed nothing for note except 
 for a few small dark red areas scattered in the lung tissue. 
 
 9 
 
 - 
 a 
 
 There was fifty c.c. of clear fluid in the pericardium, the begin- — 
 
 nings of hydropericardium. The heart weighed 670 grams,—a very 
 large heart for the lesions mentioned. The myocardium was three 
 to four mm. on the right, eight to nine on the left. The cavities 
 showed some dilatation and were filled with blood clot. The valve 
 measurements were as follows: mitral 12 cm., aortic 7.5 cm., tricuspid 
 14 cm., pulmonic 9.5 cm. That is an increase in the circumference 
 of the mitral, with the others about as usual, except that the tricuspid 
 is a little large. The tricuspid and pulmonary valves showed no 
 lesions. But on the mitral, extending over practically the whole 
 length of the free margin of the curtain, there were numerous smaller 
 and larger frank vegetations. These vegetations extended up high 
 on the wall of the auricle. The aortic cusps showed a number of 
 vegetations, not so large though as those on the mitral. 
 
 Dr. Cazort: Was there anything chronic on those valves? 
 
 Dr. RicHARDSON: I did not see any; and a mitral valve of twelve 
 cm. of course indicates that the amount of chronicity, if there was 
 any, was very slight. The extension of the vegetative patches upon 
 the auricle is rather characteristic in these viridans infections. 
 
 The spleen weighed 395 grams and was moderately enlarged. 
 We must remember that this man was an Italian. There were a 
 few infarcts in it. 
 
 The kidneys weighed 582 grams. This means they were enlarged. 
 The microscopical examination showed capsular glomerulonephritis 
 and infarcts. | 
 
 The culture from the heart blood showed a streptococcus of the 
 viridans type. 
 
 Dr. Casot: There was no pericarditis? 
 
 Dr. RICHARDSON: None. 
 
 Dr. Younc: Would you get as much nitrogen retention as this 
 in the terminal hours of any other condition than one causing passive 
 congestion? This was done the day of death. 
 
 Dr. Casot: I remember 125 in a case of typhoid fever; we 
 scratched our heads over that a lot. Of course there is passive con- 
 gestion. So that I should not be able to say I had seen it in cases 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 603 4 
 
 without passive congestion. But I do think it is important not to 
 make a diagnosis of nephritis on a high blood retention unless we 
 have other evidence. 
 
 A PuysiciAn: May I ask Dr. Richardson if the lungs showed any 
 changes? 
 
 Dr. RicHARpDSON: Nothing but chronic passive congestion. 
 
 Dr. Casot: The X-ray did not lead us to expect anything more 
 than passive congestion. 
 
 A PuysicrAn: I have been interested in the changes in the lungs 
 in passive congestion. I wondered whether that mottling was wholly 
 due to passive congestion or whether there was a true fibroid condi- 
 tion there. 
 
 Dr. Casot: But our general impression is that we can get just as 
 much mottling from passive congestion alone, that we must not 
 conclude that we have an organic condition in the lungs if we have 
 something else like passive congestion to account for the mottling. 
 
 A PuysiciAN: How do you explain the weakly positive 
 Wassermanns? 
 
 Dr. Casot: I do not explain them. We have a great many here, 
 although the test is done as carefully as possible. Our rule in all 
 departments of this hospital, including the syphilis department, is 
 never to make a diagnosis of syphilis on a weakly or a strongly positive 
 Wassermann without any other evidence of syphilis. 
 
 A Puysictan: What is the antigen used? 
 
 Dr. Casot: I don’t know what antigen we are using now. But I 
 think it is a generally accepted observation that one should never 
 make a diagnosis of syphilis on a Wassermann reaction no matter 
 who made it or what kind of antigen was used, unless there is other 
 evidence in the patient’s history or body to support it. I think a 
 great deal of harm is done by concluding from a weakly or moderately 
 or strongly positive Wassermann that a patient has syphilis. 
 
 Necropsy 4081 
 
 An English housewife of thirty-two entered May 3. From the 
 age of twelve she had attacks of dull frontal headache lasting a 
 few hours, usually relieved by vomiting, at first very frequent 
 and severe, later occurring once in three or four weeks. She had 
 had none for ten years. She had always been near-sighted, and for 
 twenty years had worn glasses. At fifteen she was in bed ten weeks 
 with chorea, and ever since that time had had palpitation, slight 
 
604 FACTS ON THE HEART 
 
 dyspnea and rapid pulse after exertion. At twenty-seven she was 
 ill two weeks with mumps. She had had four or five attacks of 
 severe bleeding from both nostrils lasting two to six hours, relieved - 
 by packing. The last attack was four years ago. She had one or 
 two ‘‘colds”’ each winter. At twenty-two she weighed 135 pounds, 
 her best weight. A year before admission she weighed her usual 
 weight, 128 pounds. 
 
 Five months ago she gave birth to her first child. She was in 
 labor for more than ten hours and finally was delivered with forceps 
 under ether. She stayed in bed for two weeks and felt well. She 
 had slight bloody discharge for eight or nine days. She was said 
 to have a normal puerperium. The baby was breast fed for four 
 weeks, then put upon artificial feeding because it was not getting 
 enough. Meanwhile the mother felt sick and tired easily. ° There 
 was a gradual onset of slight irritating cough with or without being 
 preceded by a tickling sensation of the throat. The cough was 
 unproductive and was more frequent towards the evening then the 
 rest of the day. She felt alternate cold and warm sensations over 
 her body. There was insidious onset of-night sweating. She hada 
 feverish sensation, usually worse in the afternoon, and at times 
 her temperature rose to ror®° or more. She had taken many kinds 
 of tablets and syrup for the cough without any relief. Her weakness 
 and cough became more marked and she had been compelled to stay 
 in bed for the past three and a half months. For three or four weeks 
 the temperature rose as high as 104° in the evening on several occa- 
 sions. The night sweats became much worse. Her appetite became 
 very poor and her sleep much disturbed. Her bowels were moved 
 once In one or two days by salts or enema. 
 
 Examination showed a poorly developed and nourished woman 
 with some mental confusion simulating partial aphasia. Over the 
 chest and abdomen were numerous scattered pin-point purpuric spots. 
 The scalp was yellow, scaly, the hair thin. The mucosae were slightly 
 pale. There was slight pyorrhea. The tongue was protruded in 
 midline with coarse tremor. The chest expansion was slightly 
 greater on the right than on the left. The lungs showed slight dull- 
 ness over the left top in front and harsh breath sounds throughout, 
 with high-pitched inspiration. The heart sounds were transmitted 
 throughout both backs. There were a few scattered medium moist 
 rales at both bases posteriorly. The apex impulse of the heart was 
 seen and felt in the fifth space 10 cm. to the left. There was a 
 systolic thrill. The action was very rapid (140). The pulmonic 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 605 
 
 second sound was markedly accentuated. At the apex was a short 
 presystolic roll. A snapping first sound and a loud blowing systolic 
 murmur were heard over the precordia. The pulses were of small 
 volume and tension. The blood pressure was 150/70 to go/so. 
 The liver dullness extended from the fifth rib to two centimeters 
 below the costal margin. The edge was not felt. There was a firm 
 smooth mass in the left upper quadrant extending 6 cm. below the 
 costal margin to the midline, probably spleen. The rectal examina- 
 tion showed nothing of importance. There was slight cystocele 
 and rectocele. Pelvic examination showed a lacerated perineum. 
 The anterior lip of the cervix was cystic. There was slight edema 
 of the feet, more on the nght. The fingers showed slight tremor. 
 The right pupil was greater than the left. Both were slightly 
 irregular, with poor reactions to light and distance. The reflexes 
 were normal except for poor position sense in the toes on the left. 
 
 The temperature was 98° to 103.2°, the pulse 108 to 147, the 
 respiration 20 to 38. The output of urine was 11 to 42 ounces, the 
 specific gravity 1.014 to 1.030. The urine was cloudy at all of five 
 examinations and showed a very slight trace to a trace of albumin at 
 all, leucocytes at all, red cells at three, granular casts at two. The 
 hemoglobin was Tallqvist 70%, Sahli 72%. There were 4800 to 
 8600 leucocytes, 78% to 90% polynuclears, 4,012,000 to 3,136,000 
 reds, showing slight achromia. The platelets were slightly increased 
 at one examination, the reds and platelets normal at another. No 
 endothelial leucocytes were seen in sixteen smears. A Wassermann 
 was negative. May 3 a blood culture showed streptococcus and 
 Gram-positive bacilli in one flask, staphylococcus and Gram-positive 
 bacilli in another. May 7 there was streptococcus viridans in both 
 flasks. May 11 streptococcus in both and staphylococcus albus 
 in one. 
 
 The patient lost ground and was very confused at times. The 
 pulse rate was 130. New purpuric lesions appeared on the neck and 
 feet. The presystolic murmur was variable. May 11 there was 
 marked hallucinosis and her fingers were very cyanotic. May 13 she 
 was failing rapidly. The pulse rate varied from 80 to 135 from minute 
 to minute, and was very poor in quality. There was slight edema 
 over the upper lumbar region. ‘There were frequent new crops of 
 ecchymoses, or rather purpuric spots, on the chest, abdomen, back 
 and mostly on the neck, occasionally on the finger tips and toes. 
 There was no change in the heart sounds except occasional extra- 
 systoles. May 20 for a few minutes she had twitching of the right 
 
‘ 
 ‘ 
 
 606 FACTS ON THE HEART ‘. 
 
 hand and leg. May 22 she was more or less stuporous, with a fixed 
 stare. Cyanosis of the hands was marked at times. The anemia 
 was progressive. The temperature was normal, but the condition 
 was poor. Early in the morning of the 23rd she suddenly cried out, 
 and at once went into a series of violent convulsive movements of the 
 whole body, slightly more marked on the left side. Her eyes were 
 turned to the left and her legs drawn up. The respirations became 
 weaker, and she died. 
 
 Clinical Diagnosis (from Hospital Record) Malignant endo- 
 carditis. 
 
 Mitral stenosis. 
 
 Secondary anemia. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic and acute endocarditis 
 of the mitral valve. 
 
 Mital stenosis. 
 
 Septicemia, streptococcus. 
 
 Infarcts of the spleen. 
 
 Cerebral embolus. 
 
 Secondary anemia. 
 
 Anatomical Diagnosis —Septicemia, streptococcus viridans. 
 
 Malignant endocarditis, mitral valve. 
 
 Small vegetation on one of the cusps, aortic valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Slight hydropericardium. . 
 
 Hydrothorax and ascites; slight anasarca. 
 
 Slight chronic passive congestion, general. 
 
 Infarcts of the spleen and kidneys. 
 
 Cholelithiasis. 
 
 Obsolete tuberculosis of a bronchial gland. 
 
 Dr. RicHAarpDson: This case showed a streptococcus viridans 
 septicemia, established during life and from the heart blood at 
 necropsy. 
 
 The heart weighed 350 grams; considerable enlargement and 
 moderate dilatation. Except for a small vegetation on one of 
 the aortic cusps the aortic valve was negative and the tricuspid and 
 pulmonary negative. The mitral valve showed a very extensive area 
 of vegetations forming a thick mat extending along the free margin 
 and from the posterior cusp extending up along the auricular wall. 
 This mass taken all together when the valve was closed produced 
 considerable obstruction to the valve. But so far as any extensive 
 chronic process goes, that was not found. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 607 
 
 The kidneys were negative for glomerulo-nephritis, but showed- 
 extensive infarcts. The spleen was markedly enlarged and showed 
 numerous infarcts. The circulatory apparatus elsewhere was nega- 
 tive and the uterus and adnexa negative. The gall-bladder was 
 negative save for about eight stones of pretty good size. 
 
 (Specimens of heart and spleen.) The spleen weighed 850 
 grams. We can plainly see the infarcts showing here and there. 
 Some pleces were cut from the valve, but the marginal process is 
 evident. If we supply the gaps with material like that extending all 
 along the free margin of the valve and note the process on the 
 auricular wall and where it extends down on the chordea tendineae, 
 we have a typical picture of malignant endocarditis. The appendices 
 in this heart were free. Small masses broke off from what we see 
 here and passing into the vessels plugged them up, with the produc- 
 tion of infarcts. 
 
 Necropsy 3945 
 A divorced Irish-American woman of twenty-nine, unoccupied, 
 
 entered September 21 for relief of weakness. She had always been 
 “nervous.” She had measles, pertussis, chicken-pox and scarlet 
 fever before she was seven. At eight and at twelve she had chorea, 
 and about the same time two attacks of inflammatory rheumatism. 
 Since childhood she had sweat so heavily that her clothes were very 
 wet most of the time. She had hysterical attacks about once a 
 month, at the time of catamenia. At twenty-one she was anemic 
 and did not menstruate for two months. At twenty-seven she was 
 divorced from her husband, a drunkard and drug addict of sixty-one. 
 She had one miscarriage. She had dysmenorrhea, and for a year 
 had had leucorrhea. Once or twice a month she had cramps in the 
 legs, often awakening her from sleep. Her best weight was 130 
 pounds, her present weight 116. 
 
 3 1.5 4.5 
 Fic. 114.—Heart measurements by percussion. 
 
 For thirteen years she had had palpitation. For five years she 
 had had “gas pains” and epigastric distress once or twice a week 
 either shortly after meals or when she was nervous, relieved by 
 belching, by induced vomiting, and by indigestion pills. She was 
 afraid to eat because of gaspains. For two years she had had chills, 
 especially in damp weather, one to three in a fortnight, lasting two 
 
608 FACTS ON THE HEART 
 
 ‘minutes, relieved by hot drinks. For two months she had been 
 growing more nervous and had had increasing weakness, especially 
 in the legs. She had a horror of being alone, and when left so had 
 palpitation. Her hysterical attacks 
 caused more weakness than formerly. 
 For four to five weeks she had had 
 swaying sensations in the head brought 
 on usually by worry or excitement. 
 The day before admission for the first. 
 time she had sharp gnawing pains in 
 the abdomen for five minutes. 
 Examination showed a well-nour- 
 ished woman with marked pulsation 
 sat tkek te iva feat by Of the vessels of the neck. The throat 
 X-ray. was reddened. The apex impulse of 
 the heart was in the fifth space, 12 cm. 
 to the left of the midsternum. The measurements by percussion and 
 X-ray are shown in Figs. 114 and 115. Short high-pitched systolic 
 
 6 cm. 
 
 sternal 
 
 Mi 
 
 Fic. 116.—September 29. Enlarged and calcified glands at the lung roots. 
 Increased density of the lung markings, noticeable in the ascending trunks. The signs 
 are more marked on the right. The heart shadow is symmetrically enlarged. 
 
 and diastolic murmurs were heard at the apex and in the left axilla, 
 a rough loud systolic at the base transmitted upward, and a long 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 609 
 
 rough blowing diastolic transmitted downward along the left sternal 
 border. The pulses were synchronous, of good volume, high ten- 
 sion, Corrigan in type. Pistol shot was well heard over all the large 
 vessels. The fingers showed capillary pulse. The systolic blood 
 pressure was 160 to 170, the diastolic 50. The artery walls were pal- 
 pable. The abdomen was normal except for a dynamic aorta. The 
 extremities, pupils and reflexes were normal. 
 
 The temperature was 96.7° to 99°, the pulse 71 to 128, the respira- 
 tions normal except for one rise to thirty-one the day before discharge. 
 The output of urine was 17 to 63 ounces, the specific gravity 1.010 
 to 1.020. The urine was cloudy at three of four examinations. 
 There was no albumin. The sediment was full of pus at the first 
 examination and showed many to occasional leucocytes at two others. 
 Two more specimens, taken by catheter, showed very rare leucocytes. 
 A urine culture showed a slight growth of staphylococci. The renal 
 function was 30% in the first hour; no urine the second hour. The 
 hemoglobin was 80%. There were 6200 to 22,000 leucocytes, 61% 
 to 74% polynuclears. A Wassermann was negative. The blood 
 nitrogen was 42 mgm. per 100 c.c. of blood. A stool was negative to 
 guaiac. A vaginal smear showed no gonococci. The fundi were nor- 
 mal. X-ray September 22 showed evidence of a small amount of 
 fluid at the left base. September 29 (see illustration) there were 
 enlarged and calcified glands at the lung roots, increased density of 
 the lung markings, noticeable in the ascending trunks. The signs 
 were the most marked on the right. The heart shadow was symme- 
 trically enlarged. The kidney outlines were obscured by gas. There 
 was no evidence of stone. 
 
 The condition changed very little. She complained of pains in 
 the right lower quadrant. After September 29 the leucocyte count 
 ranged from 16,200 to 22,000. ‘There was a considerable neurotic 
 element in the case. The patient had many pains and complaints 
 for which no cause could be found. October 2 the digitalis was 
 omitted, and October 5 KI gr. x t.i.d. was ordered. October g she 
 was discharged relieved. 
 
 March 21, two years and a half later, she reentered. She had 
 worked steadily as cashier or as maid in a club. All the summer 
 before readmission she had felt tired. In January she began to have 
 dyspnea, then edema of the legs and some cough. Four weeks 
 before readmission she gave up work because of edema, increasing 
 dyspnea and some orthopnea. For three weeks her abdomen had 
 
 been swelling. For two weeks she had been in bed. 
 39 
 
610 FACTS ON THE HEART 
 
 Examination was as before except for the points noted. She 
 was fairly well nourished, very dyspneic, with jumping carotids— 
 the chest shook with every heart beat. The mucosae were cyanotic. 
 There were moist rales in both lungs behind below the angles of the 
 scapulae. The apex impulse of the heart was seen and felt all 
 over the chest and in the seventh space in midaxilla, with systolic 
 retraction at the apex. The left border of dullness was in the 
 midaxillary line. The other borders were as before. The action 
 was regular and rapid (124), the sounds of good quality, the pulmonic 
 second sound accentuated. Murmurs replaced all the _ heart 
 sounds. At the apex the first sound was sharp and replaced (sic) 
 by a loud blowing systolic transmitted to the axilla and back; also 
 a loud blowing diastolic. At the base both a systolic and a diastolic 
 were heard. The aortic second sound was gone. All the murmurs 
 were heard over the back. There was pistol shot in the groin. A 
 presystolic thrill was felt at the apex. The pulses were of poor 
 tension, the artery walls not palpable. The systolic blood pressure 
 was 180 to 145, the diastolic 50 to 60. The liver edge was 6 cm. 
 below the costal margin, tender and pulsating. The extremities 
 showed marked tremor. There was edema of the legs and lower 
 back. The shins were smooth. The knee-jerks and ankle-jerks 
 were sluggish. 
 
 The temperature was 95° to 99.2°, the pulse 82 to 142, the respira- 
 tion 21 to 48. The output of urine was g to 32 ounces, the specific 
 gravity 1.018 to 1.032. The urine was muddy or cloudy at four of 
 five examinations and showed a very large to slight traces of albumin 
 at all, diacetic acid at two. The sediment was red at one examina- 
 tion and showed red blood corpuscles at three, leucocytes at four, 
 a few hyalin casts at two. The hemoglobin was 95%. There were 
 11,600 to 24,000 leucocytes, 71% polynuclears. A Wassermann was 
 negative. The non-protein nitrogen was 19 mgm. per 100 gm. of 
 blood. 
 
 The day after admission the chief of service found a suggestion 
 of presystolic thrill at the apex and of systolic thrill at the base. 
 March 23 the heart started fibrillating. There was marked orthop- 
 nea. March 29 there was some distension, relieved by enema. 
 March 30 the patient was fairly comfortable, slept most of the time, 
 and had the slowest pulse since admission, 84, with no pulse deficit; 
 still absolutely irregular. April 2 she became very dyspneic and 
 cyanotic and complained of a sense of great oppression in the chest. 
 The heart was rapid, weak, and absolutely irregular. Caffein gr. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 611 
 
 iii s.c. gave relief. There was a return of distension. The patient 
 became very orthopneic, and complained of pain in the right scapular 
 region. There was pulse deficit 5-10. When asleep she had Cheyne- 
 Stokes breathing. She grew steadily worse. The edema increased. 
 April 15 there was ptosis, external strabismus and dilatation of the 
 pupil of the left eye, and some difficulty in talking. Soon after 
 this she was comatose for a while, with rapid contraction and dilata- 
 tion ‘of the pupils, and was afterwards unable to articulate clearly. 
 April 17 she died. 
 
 Clinical Diagnosis (from Hospital Record).—Cardiac decompensa- 
 tion. 3 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis of aortic 
 and mitral valves with stenosis and regurgitation of each. 
 
 Hypertrophy and dilatation of the heart. 
 
 Cardiac thrombosis or acute endocarditis. 
 
 Chronic passive congestion, general. 
 
 Infarcts of spleen and kidneys. 
 
 Anatomical Diagnosis —Chronic endocarditis of the mitral, aortic 
 and tricuspid valves; stenosis. 
 
 Acute endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Infarcts of the right lung. 
 
 Hydrothorax, double. 
 
 Hydropericardium. 
 
 Slight ascites. 
 
 Anasarca. 
 
 Slight arteriosclerosis. 
 
 Dr. RIcHARDSON: The heart in this case weighed 772 grams (nor- 
 mally 200-300). It was greatly hypertrophied. It was dilated 
 markedly on the left, slightly on the right. The mitral circumference 
 was reduced to 7 cm. (normally ro), the tricuspid to 5.5 (normally 
 12-13). The aortic was 7 cm. (normal), but the cusps were greatly 
 shortened by the fibrosis. 
 
 Dr. Casot: Were there no infarcts? 
 
 Dr. RicHARDSON: None except one in the lung. 
 
 Dr. Cazort: And no thrombi in the heart? 
 
 Dr. R1icHARDSON: There was an acute endocarditis on the mitral 
 which was a thrombus mass on the valve. This of course could be 
 a source for emboli. 
 
 The kidneys were negative. 
 
612 FACTS ON THE HEART 
 
 Necropsy 3542 
 
 An Irish-American painter of forty-five entered October 11, 1915, 
 for relief of edema and dyspnea. He had ‘‘typhoid-pneumonia” 
 at ten years. For eighteen years he had been a carriage and auto- 
 mobile painter, and until 1910 used much lead paint. In 1900 he had 
 lead poisoning. Since that time he had been careful about washing, 
 etc. For five years he had used no lead. For ten years he had had a 
 sharp stabbing pain in the left axilla, worse when he had a cold or 
 cough. Until t910 he used to have slight attacks of dizziness. 
 From rgro until six weeks before admission he had daily dull frontal 
 headaches coming at any hour, sometimes at night. For over a year 
 he had had dull epigastric pain half an hour after eating, associated 
 with an ‘‘awful feeling like a bunch in the epigastrium” with nausea 
 and vomiting. Vomiting, and nothing else, gave relief. There was 
 some pyrosis. For a year he had had one loose movement a day and 
 had urinated six or seven times by day, five or six at night. His 
 best and usual weight was 142 pounds, his weight a year before 
 admission and at present 118. 
 
 In rgrt he had a pain over his heart on exertion travelling to the 
 axilla and back, sharp for twenty-four hours, then growing dull. 
 With it was dyspnea. Every two or three nights he had attacks of 
 nocturnal dyspnea. He had occasional edema of the legs and ankles 
 in the evening. His appetite began to be poor. For two years he 
 had had a real chill every morning and afternoon, followed by fever. 
 For six months he had had swelling of the abdomen. He stopped 
 work because it was slack and in order to rest. His dyspnea, edema 
 and precordial pain grew worse, so that two months ago he could 
 hardly walk upstairs. He slept on three pillows. He now had 
 constant “‘dragging”’ precordial pain radiating to the back and the 
 epigastrium. Six weeks before admission his knees, ankles, and 
 great toe were red, hot, swollen, stiff, and so painful he could not 
 stand up, but remained in bed. For five days he had had a short, 
 dry cough with very little sputum. 
 
 Examination showed a fairly well developed and nourished man, 
 slightly dyspneic. The skin had a slightly yellowish pallor. The 
 mucous membranes were pale. There was much pyorrhea; no lead 
 line. The chest expansion was greater on the right than on the 
 left. The apex of the heart was in the fifth space, 12 cm. to the left of 
 midsternum, 14 cm. outside the nipple line. The left border of 
 percussion dullness was 13.5 cm. outside the nipple line, the right 
 border 3 cm. to the right of midsternum, the substernal dullness 7 cm. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 613 
 
 The sounds were of fair quality. ‘There was an occasional dropped 
 beat and extrasystole with compensatory pause. The aortic 
 second sound was accentuated. At the base the sounds were faint 
 and there was a faint systolic murmur. At the apex there was a 
 rough systolic murmur loudest just inside the nipple line, following 
 a rough first sound. The second sound was reduplicated. The 
 rhythm and sounds changed from minute to minute. The pulses 
 were of fair volume and low tension, with an occasional dropped beat. 
 The artery walls were felt. The lung signs are shown in Fig. 117. 
 The abdomen bulged, and showed tenderness under the left costal 
 margin. ‘The liver dullness extended from the sixth rib to two centi- 
 meters above the costal margin. ‘The genitals were negative. The 
 
 i few medium moist rales. i 
 Vocal fremitus increased. oe 
 a 
 Whispered aN 
 voice and BV SS 
 tactile 
 fremitus 
 increased, eS 
 Increased eZ 
 
 roughened inspiration.| 
 Bronchovesicular 
 breathing. Rough, 
 coarse dry rales. 
 
 Hyperresonant throughout, 
 with distant breathing. 
 
 Fic. 117.—Physical signs in Case 3542. 
 
 “voice 
 
 fyeteo 
 increased, 
 
 extremities showed no edema. The pupils were slightly irregular, 
 reacted to light and distance through a small arc; the right was 
 greater than the left. The reflexes were slightly exaggerated. The 
 fundi were normal except for arteriosclerosis. 
 
 Until November 1 the temperature was usually 98° to 100°; 
 the later chart is shown (Fig. 118). The pulse was 68 to 140, the 
 respiration 19 to 37. The blood pressure was 200/100 to 105/70. 
 The output of urine was to to 72 ounces, usually 15 to 40 ounces, 
 the specific gravity 1.006 to 1.012 at seventeen tests. There were 
 small amounts of albumin at all, granular casts at 12, hyalin at 9, 
 fatty at 3, cellular at one, leucocytes at 3. The renal function at 
 three tests was 10%, at one test 15%. The hemoglobin was 65 to 
 45%. The leucocytes were 10,100 to 24,600, the polynuclears 82 to 
 66 to 87 %, the reds 4,600,000 to 1,840,000, with slight achromia and 
 variation in size, very slight poikilocytosis at two of six examinations, 
 slight polychromatophilia. The non-protein nitrogen was 66 mgm. 
 per 100 gm. of blood. A Wassermann was negative. The stools 
 
614 FACTS ON THE HEART 
 
 gave a negative gualac at three tests. A Mallein skin test was nega- 
 tive. In an X-ray of the kidneys the outline was fairly well seen. 
 There was no evidence of stones. Plates of the teeth showed multiple 
 tooth roots and pus pockets. The sinuses were negative. 
 
 October 16 the knees and great toe joints were stiff and painful, 
 the left knee hot, tender, and slightly fluctuant. Next day there 
 was a loud roughened systolic at the apex, faintly heard in the axilla 
 and at the base, and the aortic second sound was more accentuated. 
 The left knee was more painful October 22. The heart action was 
 regular, the second sound accentuated, the murmur heard in the neck. 
 
 O obey No 
 
 Li 
 rence | | LT Fe EA EE 
 
 iscase 
 : aioe ee 
 
 BMBMe ac 
 fed ER GT 
 fe a TN 
 ee LL 
 SI TNLURTARARIGITEREEITAR PRM MRRRGe 
 STOTT oa ear 
 Po A et oa ec el a onl ook ers doe a ce Seed 
 es A De 
 Soil he ie ee a re a Ee 
 
 cs SEE EES eee eee 
 
 see tt EEE EEEEEHEE EEA 
 Hot | 1 da tT ALN A 
 SACO 
 HE oo all EP Seeee0500 
 
 ata |e pat ag BRR MMMEM Man 
 eet Te aa 
 NE 
 
 Fic. 118.—Temperature and pulse in Case 3542. 
 
 The apex impulse was 9.5 cm. from midsternum, 1.5 cm. inside the 
 nipple line, the right border 4.5 cm. to the right, the supracardiac 
 dullness 6cm. October 25 the knees were better but the ankles were 
 stiff and painful. A throat consultant found no evidence of a focus 
 of infection in the tonsils or sinuses but was in doubt about the teeth. 
 October 27 several teeth were extracted for drainage of pus pockets. 
 Two days later the joint condition had subsided and the right cardiac 
 border had come in to 3.5. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 615. 
 
 November 2 the temperature began to run from 100° to 103.4° 
 and the pulse from 80 to 125 with no discoverable cause. The 
 joints were not troubling. ‘The murmurs and the aortic second sound 
 were as at entrance. The urinary output was up and down. By 
 December 2 the temperature was down, the appetite better. Decem- 
 
 Slightly dull. 
 Bronchial 
 breathing. 
 
 Slight bronchial | 
 whisper, 
 
 No rales, 
 
 | 
 i 
 
 Fic. 120.—Heart shadow normal. Prominent aortic knob. Mottled opacity, left 
 lung, from the apex of the fourth rib. 
 
 ber 13 he was coughing less. December 15 the lung signs were 
 asin Fig. 119. The breath was very foul, especially at night, and the 
 patient was spitting up about an ounce of mucopurulent material 
 daily. X-ray of the left chest (see Fig. 120) showed a rather mottled 
 
616 FACTS ON THE HEART 
 
 opacity extending from the apex to the fourth rib in front. The 
 heart shadow was not displaced. ‘The left chest expanded less than 
 the right. The right lung appeared normal. Electrocardiogram 
 showed normal rhythm. 
 
 December 24 the left upper back was dull, with increased breath- 
 ing and whisper. December 28 the lung signs were as shown in Fig. 
 121. January 3 he was coughing more, with still increasing amounts 
 
 Bronchial breathing 
 
 Slightly dull. | 
 slightly increased. 
 
 Increased breathing 
 and vocal and tacte 
 ile fremitus, 
 Occasional fine 
 non=c onsonating 
 rales. 
 
 Bronchial 
 breathing, 
 
 Fic. 121.—Physical signs Dec. 28. 
 
 of sputum. January 6 the lung signs were as in Fig. 122. He grew 
 weaker. The signs became most marked in the left upper back. 
 January 24 he died. | 
 
 Inter pretation of X-ray, December 16.—Pneumonic process in the 
 left upper lobe. 
 
 Abscess. 
 
 ESL 
 
 Dull. Vodice unchanged. 
 Whisper negative, Many 
 
 hy \ 
 < 
 
 Slightly dull. 
 Bronchial breathing. 
 
 consonating rales: BSH Bronchial whisper. 
 throughout the dull ES v= Tectile fremitus 
 
 NY 
 
 area and below. the same, 
 
 No rales. 
 Bronchial breathing 
 
 No amphoric respiration or other signs of cavity. 
 Breath very foul. 
 
 Fic. 122.——Physical signs Jan. 6. 
 
 Clinical Diagnosis (from Hospital Record)—Chronic nephritis. 
 Lung abscess. 
 
 Arteriosclerosis. 
 
 Secondary anemia. 
 
 Bronchopneumonia. 
 
 Extraction of teeth. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Arteriosclerosis. 
 Arteriosclerotic kidney. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 617 
 
 Hypertrophy and dilatation of the heart. 
 
 Abscesses of the left lung. 
 
 Terminal pneumonia of the right lung? 
 
 Secondary anemia. 
 
 Acute endocarditis? 
 
 Anatomical Diagnosis.—Arteriosclerosis. 
 
 Arteriosclerotic nephritis. 
 
 Hypernephroma of the kidney. 
 
 Acute endocarditis of the aortic valve. 
 
 Chronic endocarditis of the aortic valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Abscess of the left lung. 
 
 Infarct of the spleen. 
 
 Anemia. 
 
 Chronic pleuritis. 
 
 The heart weighed 282 gm. The organ was slightly enlarged. 
 The right ventricle wall measured 3 mm., the left ventricle wall 
 12 mm. The cavities on the right were moderately increased, on 
 the left slightly increased. The mitral valve measured 10.5 cm., the 
 aortic in the region of the aortic ring 6.5 cm., with 4.5 cm. for 
 the circumference of the cusp margins. The tricuspid measured 13 
 cm., the pulmonary 7 cm. ‘The mitral and tricuspid valves showed 
 a slight amount of fibrosis. The pulmonary valve was negative. 
 In the region of the junction of the anterior and the posterior cusps 
 of the aortic valve there was a small irregular fibrocalcareous mass 
 of material about 1 cm. in greatest dimension. Adherent and erected 
 upon this was a cauliflower-like mass 1.5 by 1 cm. by 6 mm. consist- 
 ing of pale grayish granular rather friable material mottled with spots 
 and flecks of adhering blood-like material. The mass rested upon 
 the ventricular aspect of the cusp. On the right posterior cusp, 
 ventricular aspect, and in the region of the corpus Aurantii there was a 
 group of small, rather flat vegetations, otherwise similar to the vegeta- 
 tions already described. The cusps elsewhere showed a slight 
 amount of fibrosis. In the endocardium beneath the cusps there 
 were a few small fibrous areas. 
 
 Necropsy 4522 
 
 An American student of twenty-one came to the Emergency Ward 
 May 3, 1923. At twelve he had rheumatic fever. Since that time 
 he had been active except that he had not taken part in strenuous 
 games. 
 
618 FACTS ON THE HEART 
 
 April 21 he came down with influenza. After three days in bed he 
 returned to school. April 28 he was obliged to go to bed again, and 
 had remained there, with a fluctuating temperature up to 102°. 
 He was feeling better until four o’clock the day of admission, when 
 he was seized with a sudden left-sided hemiplegia with spasticity. 
 At admission he was unable to talk. | 
 
 Examination showed a well nourished, semistuporous boy with 
 left-sided paralysis, the left arm and the fingers of the left hand rigidly 
 flexed and the left leg fixed in one position. He restlessly moved his 
 right arm and leg. He was incontinent of urine. He made a feeble 
 attempt to put out his tongue and open his mouth; it was not possible 
 to determine whether there was paralysis here or not. The cranial 
 nerves were not tested. ‘There was slight tremor of the tongue on 
 extension. The neck was possibly slightly stiff. There was no neck 
 sign. The heart was slightly enlarged to the left. The percussion 
 measurements were not recorded. The point of maximum intensity 
 of the beat was outside the nipple line. There were thrill and systolic 
 and diastolic murmurs at the base. The blood pressure was 130/68. 
 The lungs, abdomen, genitals and pupils were normal. The reflexes 
 were increased on both sides, more on the left. There was clonus 
 of the left ankle. Babinski and Kernig were positive. The knee- 
 jerks were active, especially the left. 
 
 The temperature was 100°, the pulse gt to 108, the respiration 
 20 to 36. The amount and specific gravity of the urine were not 
 recorded. There was the very slightest possible trace of albumin 
 at the single examination, many hyalin and cellular casts, thirty to 
 forty red blood corpuscles and eight to ten leucocytes per high power 
 field. The hemoglobin was 80%, the leucocytes 17,000, the poly- 
 nuclears 83%, the reds and platelets normal. The Wassermann is 
 not recorded. A pharyngeal culture showed pneumococci and strep- 
 tococcl. Lumbar puncture gave to c.c. of slightly cloudy pearly 
 whitish fluid. The specific gravity is not recorded. The initial 
 pressure was 170, the pressure after withdrawal of 5 c.c. 140, after 
 withdrawal of 5 c.c. more 120. The pulse, respiration and jugular 
 compression were normal. There were 860 cells, 70% poly- 
 nuclears, 30% lymphocytes; no organisms. A Wassermann was 
 negative, alcohol a trace above normal, goldsol 0011100000, total pro- 
 tein 68, sugar .714%. Neurological examination showed bilateral 
 spasticity, more on the right, a very spastic flexed left arm, some spas- 
 ticity of the right, with some voluntary motion. ‘The knee-jerks were 
 very greatly increased, the right more than the left. There was 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 619 
 
 bilateral Oppenheim and Gordon. ‘The fundi showed clear discs, the 
 margins normal, the vessels full; not so well seen on the left. Aneye 
 consultant reported early choked discs, both eyes, the left more than 
 the right. 
 
 The morning of May 4 the patient was more stuporous, the 
 breathing was Cheyne-Stokes in type, and the reflexes were more 
 active than the night before and slightly more active on the right 
 side than at the previous examination. He was not able to respond 
 at all to.questions, and made no attempt to comply with commands 
 to put out his tongue, etc. The cardiac condition, temperature 
 and blood pressure remained unchanged. It was hard to be certain 
 whether Kernig was present or whether the limitation of motion was 
 due to spasm. Both sides reacted in about the same way, but the 
 left Kernig seemed slightly more pronounced than the right. 
 
 In the afternoon he was still more stuporous and there were many 
 loose moist coarse tracheal rales. He made no attempt to move. 
 The neck was still stiff. The pupils reacted sluggishly, and there 
 were slight slow lateral movements. That evening he quietly 
 ceased breathing. The heart continued to beat for five minutes 
 after the respirations stopped. At first the beat was regular, then 
 coupled, then in triads. 
 
 Clinical Diagnosis (from Hospital Record)—Rheumatic heart 
 disease (mitral stenosis). 
 
 Left hemiplegia (embolus). 
 
 Meningitis. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic endocarditis, aortic 
 (and mitral?) ; aortic stenosis and regurgitation. 
 
 Acute endocarditis, aortic. 
 
 Hypertrophy and dilatation of the heart. 
 
 Cerebral embolism and abscess. 
 
 Acute meningitis. 
 
 Anatomical Diagnosis.—Chronic and acute endocarditis of the 
 mitral valve. 
 
 Embolic occlusion of middle cerebral arteries with large areas of 
 infarction of the brain. 
 
 Hypertrophy and dilatation of heart. 
 
 Slight chronic passive congestion. 
 
 Infarcts of spleen. 
 
 Soft hyperplastic spleen. 
 
 Dr. RicHarpson: There was much pale froth running from the 
 nostrils. Opening the skull we found considerable edema of the pia 
 
620 FACTS ON THE HEART 
 
 but no definite meningitis. The left cerebral artery was solidly 
 plugged, and the anterior half of the brain, especially on the right 
 side, showed marked softening and disintegration. The sinuses and 
 middle ears were negative, the pituitary and pineal glands negative. 
 In other words there was an embolus plugging the middle cerebral 
 artery, with softening of the brain. It is fair to say that the speci- 
 men was kept intact because it is not so very usual to find such a 
 typical picture of embolus plugging the middle cerebral. It is 
 possible that the original embolus was infected, coming from 
 the vegetations on the valve. But there was no definite meningitis, 
 and if there was any infection present it was probably in the disinte- 
 grated tissue. 
 
 There was nothing in the peritoneal cavity. An appendix was 
 recorded only two cm. in length. That is very small, but otherwise 
 there was nothing the matter with it. 
 
 The gastro-intestinal tract showed streaks and areas of reddening 
 of the mucosa,—beginning chronic passive congestion, not very 
 extensive. The diaphragm on the right was at the fourth rib, on the 
 left at the fifth rib. 
 
 The pleural cavities showed no fluid and no adhesions. The 
 trachea and bronchi contained much reddish frothy fluid. The lung 
 tissue was leathery, brownish-red, yielding considerable frothy 
 fluid,—beginning chronic passive congestion, not very marked 
 as yet except for considerable edema. ‘There was no hydrothorax, no 
 hydropericardium, but the fluid was beginning to infiltrate into the 
 lungs. 
 
 The heart weighed 329 grams, not much enlarged. The myo- 
 cardium was good, the right ventricular wall four mm., a little thick, 
 the left twelve mm., about what it should be. On the left the 
 cavities showed slight dilatation. That goes very well with the 
 picture we have already mentioned. The mitral valve was seven 
 cm. in circumference,—a little decrease. In places it showed fibrous 
 thickening, and for a length of about three cm. there was a thick 
 fibrous base on which was erected a mass of thrombotic material, a 
 little firm at the base, but as we came to the surface soft spongy 
 acute endocarditis. From that of course the bit was washed off that 
 went up into the brain. 
 
 In the spleen, which was definitely enlarged at one pole, a definite 
 infarct. ‘The kidneys were free from infarcts. 
 
 The aortic valve was six cm. in circumference, the tricuspid 
 twelve, the pulmonary seven, and those valves were frankly negative. 
 
 Cd 
 x 
 
 br eS we tt 
 
 are i IE 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 621 
 
 The intima of the aorta and great branches was smooth, showed no 
 evidence of sclerosis. The pulmonary artery, veins, and vena cava 
 were negative. 
 
 The liver showed beginning chronic passive congestion. The gall- 
 bladder and bile-ducts were negative. The kidneys weighed 245 
 grams, and macroscopically and microscopically showed nothing 
 except a little bit of congestion. The pelves, ureters, bladder, 
 prostate, seminal vesicles, and testes were negative. 
 
 Culture from the blood at the time of necropsy gave no growth. 
 But in these cases of infection with an organism of the viridans 
 group, as this one is, it is not infrequent to get negative cultures. 
 
 Dr. Casot: Is there any way in which that soft area of the brain 
 could have communicated with the spinal canal so that the lumbar 
 puncture findings might be explained? 
 
 Dr. RICHARDSON: It was pretty well disintegrated. The whole 
 artery was shut off. 
 
 Dr. Casot: We want to account, if we can, for this very queer 
 lumbar fluid. 
 
 Dr. RicHARDSON: That is the only way,—1.e., by the softening. 
 But there was no definite abscess so far as we dissected, and it would 
 be just the same as sometimes happens in an infarct of the spleen, 
 where I have in some cases recovered the organism from the infarct 
 and not from the blood. That of course immediately points the 
 finger at me. It would have been a good idea if we had taken a 
 culture from the infarcted area of the brain. It is a possibility. 
 
 Dr. Casort: It seems possible for us if we want to be obstinate 
 to say that this was an abscess of the brain which communicated 
 with the spinal cord and so gave us this fluid as we supposed. We 
 have no culture. I do not feel at all sure that it is so. But in the 
 absence of culture it is very hard to say that it is not. Unless we 
 say something of that kind it is very hard to account for the spinal 
 fluid. : 
 
 Dr. RicHARDSON: Did they describe the macroscopic appearance 
 of that fluid? 
 
 Dr. Casor: It was “pearly white,’’—that is, not clear. 
 
 Dr. RicHarpson: I should not expect to find many leucocytes 
 in a peerly fluid. 
 
 Dr. Foster: A very interesting thing about this case is that the 
 only history of any possible heart incapacity was at school. The 
 doctor there had told him he should not take part in any strenuous 
 athletics. At the beginning of his iilness a local doctor examined his 
 
622 FACTS ON THE HEART 
 
 heart and said there were no murmurs. He was here at the necropsy 
 and was about ready to give up medicine. JI was wondering whether 
 or not this murmur could have developed as rapidly as that. 
 
 Dr. Casor: Of course the murmurs of mitral stenosis in a well- 
 compensated case are just the kind that most physicians of this 
 country do not hear. A presystolic roll with very little else most 
 people miss. But if there was as little as you got it might depend 
 perfectly well on the acute endocarditis. 
 
 A Purysician: In a leucocytosis of the blood ordinarily you would 
 not get such a spinal fluid ? 
 
 Dr. Casot: Nothing like that at all. 
 
 Necropsy 2439 
 
 An Trish stone cutter of fifty-eight entered September 2 for relief 
 of difficulty in urination of two or three years’ duration. He had 
 always had the best of health though he had lost considerable weight, 
 he did not know how much. He denied venereal disease. Five 
 days before admission he had complete retention. A physician 
 catheterized him and left the catheter in for two or three days. 
 Since the morning before admission he had passed some urine with 
 difficulty. He voided last four hours before admission. Since the 
 onset of the acute retention he had had continued pain in the bladder. 
 
 Examination showed a man looking sick and old and showing 
 evidence of the loss of considerable weight. His color was fair, 
 his mucous membranes rather cyanotic. The location of the apex 
 impulse of the heart is not recorded. ‘There was no enlargement 
 to percussion. The radials were slightly hard. There was moderate 
 lateral excursion of the brachials. The action was regular, the 
 sounds faint but of fair quality. There were no murmurs. The 
 prostate was slightly nodular but not enlarged or tender. ‘The 
 examination was otherwise negative. The temperature and pulse 
 are Shown in Fig. 123. The respiration was normal until September 
 7, afterwards 24 to 30 with a rise to 40 on the last two days. The 
 urine was normal in amount, cloudy, alkaline at one of two examina- 
 tions, the specific gravity 1.006—1.018, a slight trace of albumin at the 
 second examination. The blood is not recorded. 
 
 The patient was put immediately upon constant drainage. There 
 was a residual of four ounces of slightly turbid urine. He complained 
 of considerable pain in the perineum. The catheter was removed 
 and the perineum found to be fluctuant and tender about the bladder. 
 Pressure expressed pus from the meatus. At operation September 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 623 
 
 5 a sound met obstruction in the deep urethra. Incision was made 
 in the perineum with the evacuation of two ounces of thick cloudy 
 urine. The urethral bulb was surrounded by slough. A rubber 
 catheter was passed through the perineum to the bladder. The 
 patient did not gain as he should have done after the operation. 
 The urine was kept up by rectal salt solution. September 13 he 
 was worse and markedly jaundiced. There was bile in the urine 
 and in the stools. The amount of urine was greatly diminished. 
 
 e 
 F Deecions | | | 
 
 iis 
 Da [S67 
 f aktouir Hoar lyse yinn (ie (10) Loman feet ex fet] iets | 
 7, emeeaimieca atta 
 | Je EEE 
 260 105° 
 (.oseeeeeee 
 250 |W} 104 
 2 lero i 
 240 |>| 103° f 
 : Saat tal othe 
 Fore cal al mie rNetaal it CAL AL 
 ae erarinee SAAN 
 WW 
 200 
 porilillve: Tel tal ed 
 laa Nee lies asia 
 peri ait Lele Rais cle le Wa feels alae 
 eked Rd a a Ca 
 m of Mima aaa 
 aie eal uites las) wasieala ie alea 
 Eeaaltene hws eal Slscl ar engl a| eT eh 
 She (eee 
 io fo ERC " 
 0 [2 of eT 
 90 90 eS < 
 ‘ o VY ara ae 
 so fe a Ml 
 
 Boal fc ie [nena UIE 
 
 ae 123.—Chart in Case 24309. 
 
 During the last few days of his life a tremendous systolic blow was 
 heard principally over the apex beat. September 14 he died. 
 
 Clinical Diagnosis —Perineal abscess. 
 
 Malignant endocarditis. 
 
 Dr. Edward L. Young’s Diagnosis Obstructing prostate. 
 
 Periurethral abscess. 
 
 Septicemia. 
 
 Acute endocarditis. 
 
 Anatomical Diagnosis ——Malignant endocarditis of the mitral 
 valve. 
 
 Septicemia, streptococcus. 
 
624 FACTS ON THE HEART 
 
 Infarcts of the spleen and kidneys. 
 Icterus. 
 Operation wound. 
 
 Dr. RICHARDSON: The incision in this case was a short one in the 
 
 anterior abdominal wall. We could not remove any of the organs. 
 Icterus was well marked. There was no evidence of peritonitis, 
 no stones in the gall-bladder. The hepatic, cystic and common 
 bile-ducts were free, the mucosa negative, the bile flowed freely. 
 The pancreas was not remarkable, the ducts of Wirsung free. There 
 was no evidence of new-growth in any of the organs seen, no ulcers 
 in the lower end of the ileum. There was a soft, hyperplastic spleen 
 with infarcts. The kidneys were of normal contour and size and 
 showed infarcts. The heart was somewhat enlarged and the mitral 
 valve presented a frank mass of vegetations, three by two cm. 
 The lungs were negative as nearly as could be made out. 
 
 The growth was streptococcus from the spleen. ‘The vegetations 
 on the mitral valve and endocardium showed the usual hyalin 
 material, blood plates and masses of micrococci. 
 
 Dr. Younc: Did you open the bladder? 
 
 Dr. RIcHARDSON: No. 
 
 Dr. Casot: As you hear the history, Dr. Richardson, would your 
 guess be that this endocarditis originated in the conditions of the 
 bladder and the instrumentation? He had had no heart symptoms, 
 had he? 
 
 Dr. Younc: There were none according to the record. They 
 report the location of the apex impulse not recorded, no enlargement 
 to percussion, the action regular, the sounds faint but of fair quality, 
 no murmurs till near death. 
 
 Dr. RICHARDSON: When was the first rise in temperature? 
 
 Dr. Younc: He came in with enough sepsis so that he had a 
 temperature the day after he camein. ‘The first rise was right after 
 the operation. I believe he came in with a septicemia. 
 
 Dr. RICHARDSON: But it shoots up on the day after operation. 
 I think that is fair enough, but there is also the other side, that he 
 might have had the septic condition mentioned and that following 
 the operation it extended and set up the endocarditis. 
 
 Necropsy 3336 
 
 A man of thirty-eight entered the hospital March 30. His past 
 history was negative except for recurring attacks of left lower 
 quadrant pain with alternating diarrhea and constipation. For a 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 625 
 
 year he had been subject to great mental and physical strain. He 
 used alcohol and tobacco in moderation. 
 
 A week before admission he had an attack of tonsillitis. On the 
 fourth day a peritonsillar abscess was opened with marked relief. 
 The next day his throat was much better, but he was chilly and 
 feverish. 
 
 Examination showed a well nourished man, bright, cheerful, 
 free from pain, but a little delirious at night. The throat showed 
 
 Duration 
 of Disease 
 
 Dejections 
 
 AES 
 
 103° 
 
 ae 
 ay 
 210 #h100° a 
 votes EAR BE 
 Hp BS SS aes 
 if et al Po Bs dal 
 170 SEE ota 
 
 . 2p Soeren 
 i ECCECCCE CA 
 
 =] RS Eo al 
 ees ee es da 
 z AP Et a ae 
 ee 
 ee AAT 
 es Ae eas We fu ai fo [a1 
 “AL (3) 9 SSG ea a 
 
 Fic. 124.—Temperature and pulse in Case 3336. 
 
 marked injection and swelling, especially on the right, where there 
 was a small whitish scar (incision for peritonsillar abscess). There 
 were several submucous hemorrhages in this area. Examination 
 was otherwise negative. 
 
 The temperature and pulse are shown in Fig. 124. The respira- 
 tion was 25 to 45. The blood pressure is not recorded. The output 
 
 of urine on the day of entrance was 165 ounces, after that 50 to 85 
 40 
 
626 FACTS ON THE HEART 
 
 ounces. The specific gravity was 1.010 to 1.017. There was the 
 slightest possible trace to a very slight trace of albumin, an occasional 
 red cell and a rare granular cast. There were 14,200 leucocytes, 
 go% polynuclears. The reds were normal. A blood culture showed 
 very large numbers of streptococct. 7 
 
 April 2 the patient was still delirious, with a temperature of 104°. 
 A painless red spot the size of a half-dollar appeared on the right 
 wrist. The next day this was painful. April 5 the patient seemed 
 better, slept well with opiates, and was delirious only occasionally. 
 The right wrist also was better, but a similar spot appeared on the 
 left calf. 
 
 April 6 both these spots were better, but the left wrist and eye 
 were now red and painful, and the patient more uncomfortable and 
 delirious. Next day the eye was worse, and was pronounced by an 
 eye consultant to be a case of embolism of the retinal artery. The 
 throat, the wrists, and the calf were better. Nevertheless the 
 patient seemed to be losing ground. A systolic murmur at the apex 
 was now noted as having grown more marked since being first observed 
 three days before. The pulse was going up, though of good quality. 
 Petechiae appeared over the back. With no new symptoms, but 
 constantly rising temperature, pulse and respiration, the patient 
 grew increasingly toxic, and April 12 died. 
 
 Clinical Diagnosis (from Hospital Record) —Pyemia. 
 
 Endocarditis. 
 
 Peritonsillar abscess. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Streptococcus septicemia. 
 
 Probably acute endocarditis, (left side of the heart). 
 
 Probably emboli in the kidney, perhaps in the spleen and liver, 
 possibly in the lungs, retina and subcutaneous tissues. 
 
 Probably acute glomerulo-nephritis. 
 
ACUTE ENDOCARDITIS—ILLUSTRATIVE CASES 627 
 
 Anatomical Diagnosis—1. Chemical or physical origin of fatal 
 illness. 
 Septicemia, streptococcus. 
 
 [ Acute vegetative endocarditis 
 of the mitral valve. 
 Hypertrophy and dilatation of 
 the heart. 
 (Weight 473 grams.) 
 Infarcts of the spleen and 
 kidneys. 
 2. Secondary or terminal lesions. Fibrinous pleuritis, double. 
 Soft spleen. 
 Central degeneration and foci 
 of necrosis of liver. 
 Suppurative nephritis. 
 Purpura. 
 Focal hemorrhage in wall of 
 small intestine 
 The kidneys weighed 512 grams. Wide cortex. There were 
 many purplish spots, and in the right kidney three yellow infarcts; 
 both these lesions embolic. 
 The cardiac hypertrophy is not explained. The patient was 
 athletic and took much exercise; but most athletes have no cardiac 
 hypertrophy. 
 
CHAPTER VIII 
 
 CHRONIC NON-DEFORMING VALVULAR SCLEROSIS OR 
 ENDOCARDITIS 
 
 After excluding cases characterized by soft or acute vegetations 
 on the valves, there remains a group of cases usually labelled by the 
 pathologist as ‘‘chronic endocarditis”’ on the basis of fibrous thicken- 
 ing of the valves, to which may be added stiffening and fibrocalcareous 
 changes. From the clinical point of view the important thing about 
 these lesions is to distinguish those which deform the valves and so 
 interfere with their function, from those which do noi. ‘This we have 
 attempted to do by the careful study of the records in all cases to 
 which our memory of the post-mortem examination did not extend. 
 After excluding the cases with definitely deformed valves believed to 
 cause stenosis or regurgitation, there are left in our 4000 necropsies 
 237 cases in which the valves, despite some endocarditis, remain 
 flexible and apparently quite capable of opening and shutting in the 
 normal way. There is apparently little if any interference with 
 their function. These cases of non-deforming sclerosis or fibrosis 
 of the valves we have further subdivided on the basis of the patholo- 
 gist’s judgment, into those which represent (a) “‘the usual sclerosis 
 of age,’’ and (b) those in which the changes seem greater in degree 
 or different in kind from anything that can be accounted for in this 
 way. 
 
 In our series Group a represents the condition of the valves in 
 almost every elderly patient, quite independent of the cause of his: 
 death, and recognizable only by careful comparison with the heart 
 valves of younger persons. Of these we have made no special enu- 
 meration or further study, believing that there is no considerable 
 chance of their being of any clinical importance. After setting 
 these on one side there remain as already said 237 cases which are not 
 to be included under Group a but yet which do not deform the 
 valves. 
 
 Further study of these 237 cases brings out the following facts 
 as to 
 
 628 
 
_ ETIOLOGY 629 
 ETIOLOGY 
 
 There appear to be two causal factors. One of these factors acts 
 especially on younger people, up to the thirtieth year, and acts 
 on both sexes alike. In this group there were twenty-five males and 
 seventeen females. But as this is almost exactly the relation (66 to 
 34) of male and female in the total group of 4000 necropsies in which 
 these fall, we believe that the figures do not represent any excess of 
 males. In this group there is very little cardiac enlargement or 
 arteriosclerosis, very little chronic passive congestion, and fewer 
 murmurs than in the other group. 
 
 The other factor is one which acts especially on persons over the 
 thirtieth year and which acts twice as often in males as in females. 
 There is certainly reason to suspect that this factor is arteriosclerosis. 
 Atvany rate it can be called an old man’s factor. This latter factor 
 (arteriosclerosis?) usually affects both the mitral and the aortic valves. 
 It was present in 73 males to 31 females, and especially in the decades 
 between the sixtieth and eightieth years. 
 
 On the other hand the cases in which the mitral valve alone is 
 affected are about equally males (36) and females (31), figures which 
 when properly weighted in relation to the distribution of males and 
 females in our necropsy statistics, as given above, seem to show that 
 females are somewhat more affected Ly this predominantly “mitral 
 factor,’’ which we may surmise to be rheumatism, as we know that 
 the infection associated with this syndrome has a particular tendency 
 for affecting the mitral valve alone and the female sex predominantly. 
 
 TABLE 139.—AGE, SEX AND VALVE INCIDENCE IN NON-DEFORMING. VALVE THICKENINGS 
 
 Pure mitral Mitralandaortic Pure aortic Other valves Total 
 Male | Female | Male | Female | Male | Female | Male | Female 
 
 Winger LOsyrse oe 
 
 ee ne, Oe | 
 
 Lael 
 
 I 
 fe) 
 I 
 2 
 3 
 (a) 
 
 louna 
 
 ease 
 Suleeibeo hoon Onno 
 lke pes Ma wee nso 
 
 ER Hea OL0-o 
 ploornnwnoocd 
 
 ies) 
 + 
 WwW 
 = 
 4 
 o 
 
 Ore lar Sos. hee 
 
 oO 
 “nN 
 = 
 oO 
 as 
 BS 
 aS 
 to 
 Ny 
 
630 FACTS ON THE HEART 
 
 There remains a third group affecting the aortic valve alone. In 
 this there are thirty-three males, eleven females, and only 11 out of 
 the forty-four cases were under the fiftieth year, 8 of these 11 
 being males and three females. This is presumably an arteriosclerotic 
 group of cases. 
 
 The cases with tricuspid involvement were eighteen of them in 
 males, four in females. These last groups are apparently like the 
 second group in respect to age and sex distribution. In other words, 
 when this disease gets beyond the mitral valve it is a lesion of elderly 
 males, i.e., arteriosclerotic (?). 
 
 My chief interest in the study of these cases has been not only 
 their possible etiology, just dealt with, but has concerned itself with 
 the following questions: 
 
 (1) Do these lesions cause functional impairment of the heart as 
 shown in chronic passive congestion post-mortem? 
 
 (2) Do these lesions produce cardiac murmurs? 
 
 (3) Are they associated with cardiac hypertrophy? 
 
 (4) Do they lead to cardiac symptoms and complaints recognized 
 by the patient himself (dyspnea, palpitation, pain, etc.) ? 
 
 1. Pursuing the first inquiry whether these non-deforming valvu- 
 lar lesions weaken the heart’s action so as to produce passive con- 
 gestion, we find that at necropsy there was present chronic passive 
 congestion in: 
 
 15 out of 44 cases affecting the aortic valve alone. 
 13 out of 67 cases affecting the mitral valve alone. 
 
 33 out of 104 cases affecting the mitral and aortic valves. 
 6 out of 22 cases affecting the mitral aortic and tricuspid valves. 
 
 Total, 67 out of 237 or 28%. 
 
 What can we conclude from these facts? Since only 28% showed 
 any passive congestion, we cannot say that these lesions usually cause 
 passive congestion, for a “‘cause’’ must act in more than 28% of the 
 cases in which it is present. But now analyzing further these sixty- 
 seven cases in which chronic passive congestion was present, we 
 find the following factors, other than the valve lesions, to account 
 for it: (See table 140.) 
 
 Since most of these complicating lesions are in themselves well 
 recognized causes for chronic passive congestion without the con- 
 currence of any valve lesions, I conclude that there is no reason to 
 believe that these non-deforming valvular lesions so interfere with 
 the heart’s action as to produce chronic passive congestion. 
 
ETIOLOGY 631 
 
 TABLE 140.—ASSOCIATED LESIONS IN THE 67 CASES OF NON-DEFORMING VALVE 
 SCLEROSIS, WITH STASIS AT NECROPSY 
 
 Arteriosclerosis 29 cases 
 Chronic nephritis II cases 
 Chronic pericarditis 8 cases 
 Fibrous myocarditis 6 cases 
 Syphilitic aortitis 4 cases 
 Acute endocarditis 3 cases 
 Acute pericarditis 7 cases 
 Acute nephritis 4 cases 
 
 Hypertrophy and dilatation without “‘cause”’ 6 cases 
 Pernicious anemia I case 
 I case 
 
 80 cases 
 
 2. Did These Lesions Produce Cardiac Murmurs?—Part of the 
 answer to this question can be given at once in statisticalform. Only 
 79 out of 237 cases, or 33%, produced any murmurs that were recog- 
 nized in life. These murmurs were systolic in 78 cases and diastolic 
 in 19; that is to say, all but one of the diastolic murmurs accompanied 
 systolic murmurs. One or both of these murmurs were heard in: 
 
 21 out of 67 mitral cases. 
 18 out of 44 aortic cases. 
 
 31 out of 104 mitral and aortic cases. 
 g out of 22 mitral, aortic and tricuspid cases. 
 
 79 237 
 
 Obviously then, as with the question of chronic passive congestion 
 in its relation to these lesions, so with the murmurs, we may say that 
 a lesion associated with murmurs in only 33% shows but a feeble 
 correlation and can hardly be said to be a cause of importance. 
 
 But now if we study further the 79 cases associated with murmurs 
 we find present the following conditions, all of them by themselves 
 often associated with murmurs and ordinarily believed to have a 
 causal relation to them. (See table 141.) 
 
 This table shows that in the twenty-one “‘pure mitral”’ cases with 
 murmurs there was no arteriosclerosis at all in the vessels post- 
 mortem. How about the ‘“‘pure mitral’’ cases without murmurs? 
 Six of the forty-seven cases without murmurs had arteriosclerosis. 
 
632 FACTS ON THE HEART 
 
 TABLE 141.—VALVES AFFECTED 
 
 Mitral Mitral, 
 and Mitral | Aortic | aortic and 
 aortic tricuspid 
 
 Arteriosclerosis with hypertrophy and 
 dilatation 
 
 Chronic nephritis 
 
 Hypertrophy and dilatation without 
 known cause 
 
 Chronic pericarditis 
 
 ACUTE eriCardl us alnctoke hae ee an aert 
 
 MV OCAECIEIS. wits: cts eet ee eae te en gee 
 
 Aneurism 
 
 Acute nephritis 
 
 Unknown or doubtful 
 
 Acute endocarditis 
 
 Pernicious anemia 
 
 et OF OUEO se eS emo 
 OO™N DN ORF HH DMN 
 OR ND HWW OO FW 
 Sb 30 OO Oe St cet OL & 
 
 In other words, arteriosclerosis was a very small factor in these 
 “pure mitral’? cases. (The six cases just referred to occurred at the 
 following ages: 78, 60, 56, 55, 54, 31.) This tends to show (what is 
 usually recognized) that arteriosclerosis has very little to do with the 
 lesions of the mitral valve. 
 
 Combining by causes the figures of the last table we see that 
 arteriosclerosis with enlarged heart was present in forty-two of the 
 cases with murmurs. Enlarged heart without arteriosclerosis, 
 nephritis or any other known ‘‘cause”’ was the only tangible lesion 
 in sixteen cases. Chronic nephritis (with enlarged heart), chronic 
 adhesive pericarditis, fibrous myocarditis, are also common lesions 
 in the cases showing murmurs. There were but nine cases 
 out of 79 in which no gross lesion of any kind could be found to 
 account for these murmurs, not even cardiac enlargement, which the 
 following table shows to be an outstanding fact in the whole series 
 except in the pure mitral cases which eyidently form a group by 
 themselves. : | 
 
 3. Is Cardiac Hypertrophy Associated with Cases of Non-deforming 
 Endocarditis? (See table 143.) 
 
 Obviously these figures need not mean that the often-associated 
 hypertrophy was due to the slight thickening of the valves. For first 
 of all the hypertrophy was present in but two-thirds of the cases 
 (160 out of 237) and in the pure mitral cases only in 28 of 67, or two- 
 fifths. Moreover there were present in the 160 hypertrophied cases 
 the following traditional ‘“‘causes’’ for such a condition. 
 
ETIOLOGY 633 
 
 TABLE 142.—ASSOCIATED LESIONS IN 160 CASES OF NON-DEFORMING ENDOCARDITIS 
 WITH CARDIAC HYPERTROPHY 
 
 Arteriosclerosis 72 cases 
 Chronic nephritis 24 cases 
 Chronic pericarditis II cases 
 Fibrous myocarditis 9 cases 
 NST SE GS TS PCS, i ee ee Eg gat ea oe | eo Ea A a . IO cases 
 Syphilitic aortitis 7 cases 
 Acute nephritis 2 cases 
 
 135 
 Counted more than once ni 
 
 No cause 
 
 No ‘‘cause”’ for hypertrophy (unless the non-deforming endocar- 
 ditis is so considered) was found in forty of the 160 hypertrophied 
 cases. If mere correlation is to be considered ‘‘causal,”’ these forty 
 cases could be held to indicate that non-deforming endocarditis leads 
 once in four times to cardiac hypertrophy, though not to chronic 
 passive congestion and not to murmurs. But there is no need of any 
 
 TABLE 143.—CARDIAC HYPERTROPHY AND DILATATION IN NON-DEFORMING VALVULAR 
 SCLEROSIS 
 
 ; Mitral 
 Mitral and ‘ : ie ria 
 ; Mitral Aortic aortic and 
 aortic 
 
 tricuspid 
 
 81 of 104 28 of 67 33 of 44 18 of 22 160 of 237 
 
 such conclusion. For it is well recognized that anatomical ‘‘causes”’ 
 for cardiac hypertrophy are not always to be found; 154 of 1209 in 
 our series were without any recognized ‘“‘cause.’? Many cases of 
 such enlargement exist not only without any of the ‘“‘causes”’ listed 
 in the last table but without any valve lesion, deforming or non- 
 deforming. Hence it seems to me probable that the correlation of 
 hypertrophy and non-deforming valve lesions in these forty cases is 
 a coincidence. ‘They may have been cases of hypertension without 
 known cause. 
 
 4. Does Non-deforming Endocarditis Produce in Life ‘‘Cardiac 
 Complaints”’ (Dyspnea, Palpitation, Edema, Etc.)?—In only fifty-one 
 of our 237 cases, or 21% were any such cardiac complaints recorded : 
 
634 FACTS ON THE HEART 
 
 TABLE 144 
 
 VALVE AFFECTED SYMPTOMS IN 
 Pure mitral 8 cases out of 67 or K%— 
 Pure aortic ro cases out of 44 or 444+ 
 Mitral and aortic....5.2.........2-2.:.5.0 25 Cases OUL Of TOs Bere 
 
 Mitral, aortic and tricuspid................ 8 cases out of 22 or 44+ 
 
 ot , 237 
 
 In these fifty-one cases other well recognized causes for cardiac com- 
 plaints were found (arteriosclerosis with hypertrophied and dilated 
 heart 17 cases, chronic nephritis ro cases, hypertrophied and dilated 
 heart without known cause 6 cases, fibrous myocarditis 5 cases, 
 chronic pericarditis 4 cases, acute pericarditis 4 cases, aneurism 2 
 cases, stomach cancer with anemia 1 case, pernicious anemia I case, 
 acute endocarditis 1 case). 
 
 In the mitral group in which other factors such as arteriosclerosis, 
 nephritis, myocarditis etc. are at the minimum, in which therefore 
 we most often find the non-deforming endocarditis standing out as 
 the only lesion in the heart, we find fewer cardiac complaints, fewer 
 murmurs, less chronic passive congestion and less cardiac hyper- 
 trophy than in the other groups. ‘These four evidences of disturbed 
 heart function fall off rapidly as we get nearer to isolating the non- 
 deforming endocarditis from confusing accompaniments. 
 
 CONCLUSIONS 
 
 1. It seems to me from these considerations that chronic non- 
 deforming endocarditis (or sclerosis) of the heart valves: 
 
 (a) Does not cause cardiac complaints (or symptoms). 
 
 (b) Does not cause chronic passive congestion. 
 
 (c) Does not cause cardiac murmurs. 
 
 (d) Does not cause cardiac hypertrophy. 
 
 And so it may be said to have no clinical significance. 
 
 2. Pathologically it is a result, I believe, either of a slight attack 
 of rheumatic endocarditis (especially when it occurs in young people 
 on the mitral alone) or (more often) of the general causes of bodily 
 wear and tear which are associated with advancing age, arterio- 
 sclerosis and the male sex. In the latter group of cases it usually 
 affects two or more valves. In both groups it is functionally and 
 practically insignificant. 
 
CHAPTER Ix 
 ACUTE PERICARDITIS 
 
 1. Age and Sex.—In 186 cases of acute pericarditis the outstand- 
 ing and altogether mysterious fact is the very decided excess of males. 
 More than three-fourths of all (141 out of 186) cases were in that 
 sex. This is all the more surprising because we have been in the 
 habit of thinking of acute pericarditis as frequently, at least, rheuma- 
 tic in origin, and it is certainly true that women are more prone to 
 
 TABLE 145.—AGE IN ACUTE PERICARDITIS 
 
 TABLE 146.—SEX IN ACUTE PERICARDITIS 
 
 rheumatic infection than men. But so far as our statistics go, the 
 
 fact seems to be that rheumatism in the ordinary sense—that is to 
 
 say, a generalizéd infection prone to attack the joints as well as the 
 
 heart—is only a minor factor in the production of pericarditis If 
 
 we put on one side the cases in which the pericarditis can be regarded 
 035 
 
636 FACTS ON THE HEART 
 
 as a terminal phenomenon and not as the main illness from which the 
 patient suffered, then it will doubtless appear that im the remaining 
 group of cases rheumatism is an important factor. That this group is 
 small appears at once probable from the fact that we have a clear 
 rheumatic history in only twenty-four cases out of 186, not much 
 more than 12%. 
 
 That pericarditis is primarily a terminal affair is further suggested | 
 by the ages of the patients in our series: only 62 of 186, or 33%, were 
 under the thirtieth year at the time of death. 
 
 2. Associated Lesions.—One of the facts which has surprised me 
 most in the study of this series of cases is that there are so few examples 
 of acute endocarditis occurring in connection with the pericarditis. We 
 find only sixteen undoubted cases in this series, or 8%. It used to 
 be taught that in acute pericarditis, underlying valvular murmurs are 
 often covered up by the noise of the pericardial friction, and that we 
 must always be on the watch for this association of acute endocarditis 
 and pericarditis. This series seems to prove that this 1s not the case. 
 There is, on the other hand, a rather small proportion of chronic endo- 
 carditis associated with acute pericarditis, which serves chiefly to 
 confirm our estimate of the amount of rheumatism in this group of 
 cases. In the history, rheumatism appeared clearly twenty-four 
 times, a figure remarkably close to the number of cases of chronic 
 endocarditis as found post-mortem,—twenty-eight cases in 186. 
 
 3. Fever and Leucocytosis.—Another surprise in the study of 
 these cases has been the absence of fever in 45, or 26% of the 172 
 cases in which a definite record was made. Many of these patients 
 were the subjects of wasting, debilitating diseases often associated 
 with subnormal temperature. The terminal nature of acute peri- 
 carditis is further emphasized by this group of facts. 
 
 The leucocyte curve corresponds very well with the temperature 
 curve; that is, we have leucocytosis in 115 out of 156 cases in which 
 a definite record is made. The absence of leucocytosis in 41, or 26% 
 may be reasonably held to indicate (like the 26% of afebrile cases) 
 that the patient does not sufficiently react against the invading 
 infection. } 
 
 4. Diagnosis.—In my previous studies of pericarditis I have 
 repeatedly called attention to the fact that our diagnostic resources 
 are very scanty. The reason for this is obvious if we remember 
 that the diagnosis of acute pericarditis rests in the majority of 
 cases on nothing but the presence of an audible or palpable friction 
 rub. When the diagnosis of any disease rests upon but a single sign 
 
- 
 
 ACUTE PERICARDITIS 637 
 
 or symptom, it is obviously insecure, and particularly so when, as is 
 shown in this series, that sign is very frequently absent in proved 
 cases of the disease. Only in 4o, or 21% of 186 cases was any fric- 
 tion heard. In many of these cases—though I cannot say exactly 
 how many—the pericarditis had been suspected owing to the presence 
 of an accompanying pneumonia or endocarditis. Therefore it was 
 searched for and listened for again and again, as in several of these 
 cases I can personally recall. 
 
 Only in ten cases was there evidence of pericardial fluid that could 
 be regarded as approximately distinctive. Seven of these cases are 
 included with the forty already mentioned as showing friction. 
 If therefore, we add together the cases in which pericarditis was 
 suggested either by the presence of friction or by signs suggesting 
 pericardial effusion, or by both sets of data, we get a total of forty- 
 three, the figure representing our percentage of diagnostic success, 
 23%. 
 
 Precordial pain was even less reliable as a clue to the existence of 
 pericarditis in this series. In only twenty-six cases or 14% was it 
 definitely complained of. 
 
 Of particular interest to me is the list of underlying causes of death 
 in this series of cases, as shown on page 642. First of all comes the 
 group of blood infections, septicemia or pyemia, whether associated 
 with a known focus of infection or not. Within this last group comes 
 the particularly interesting type of pericarditis occurring in children 
 with staphylococcus sepsis,—seven cases. All of these had abscesses 
 of the myocardium, so that the pericarditis may reasonably be 
 assumed to have spread through the myocardium. 
 
 In addition to these there is a considerable group of cases due to 
 the streptococcus, in which the pericardium is inflamed along with 
 other portions of the body; or, in other words, in which the pericar- 
 ditis complicates an empyema, an acute endocarditis, a general 
 peritonitis, an abscess of the lung. After septicemia three diseases 
 stand out in the etiology: pneumonia, chronic nephritis, and cancer. 
 
 Chronic passive congestion was found in sixty-seven necropsies 
 out of 186, or 35%. In twenty-four of these it was accounted for 
 by chronic nephritis; in seven by hypertension with arteriosclerosis, 
 in eight by valvular disease, in four by chronic pericarditis, a total 
 of forty-three out of sixty-seven. 
 
 Septic Heart Failure and Dropsy (Chronic Passive Congestion). 
 Beside these mechanical reasons for general stasis (applicable to 
 about two-thirds of our cases) there may be considered a septic- 
 
638 FACTS ON THE HEART 
 
 infectious group of causes which are not well recognized as causes of 
 poor heart function and so of dropsy. Even lesions like tonsillitis 
 or dental sepsis which seem small, local, and not septicemic, are 
 generally and I think correctly believed to weaken the heart’s action. 
 Even after a ‘‘cold” we are sometimes surprisingly feeble and dysp- 
 neic. But it is, I suppose, the more overwhelming and virulent 
 infections that might produce the most serious effect on the heart,— 
 such infections as show themselves simultaneously in several places. 
 
 In our sixty-seven cases of acute pericarditis associated post-mortem _ 
 
 with evidence of chronic passive congestion, there were sixteen which 
 showed in life only the following septic lesions as possible causes for 
 the circulatory failure: 
 
 TABLE 147.—SEPTIC LESIONS ASSOCIATED WITH STASIS AT NECROPSY IN ACUTE 
 
 PERICARDITIS 
 Acute pericarditis only ai, 5 ios; ac tghecn ee sls le ee 4 
 Pneumonia and empyema sa. 95,0 4. Oo ok «nos eee 4 
 Acute endocarditis: 4 pi aon a hd cee eee ee oe ee 3 
 Acute'empyemay sist Ursa os hee DO aa nt eee 2 
 Acute polyarthritis, #2). 25.4 nie ss: Vale ota ties eee oe I 
 Acute:pleuritis.and peritonitis (../-- Gola si) ken eee I 
 Acute-chorea and, phthisis $:).4..9'2. 2: tole yy. segue Ss ote eee ae L 
 
 16 
 
 Acute or Chronic Passive Congestion ?—In sixteen of the remain- 
 ing cases the pathologists recorded after death a chronic passive 
 congestion, although in life the entire illness (so far as the patient 
 or his friends knew) had lasted but a short time, e.g. two weeks (No. 
 921, pneumonia and acute endocarditis), one week (No. 1801, acute 
 pericarditis the only cause of death), three weeks (Nos. 3053, 3242, 
 acute polyarthritis and pericarditis). In the majority of these 
 sixteen cases, however, a chronic lesion such as chronic nephritis, 
 mitral stenosis, mediastinitis, was present before the acute symptoms 
 
 showed themselves, so that the pathologist’s findings are in all 
 
 probability correct. But in a few acute septic cases like those 
 just quoted, one wonders whether the pathologist was correct in 
 recording chronic rather than acute passive congestion. Can this 
 distinction be made in all cases from post-mortem evidence alone? 
 
 Pericardial Effusion.—Out of 186 cases twenty-seven showed 100 
 c.c. or more of exudate at necropsy. The fluid was measured with 
 the following results: 
 
 ' 
 
ACUTE PERICARDITIS 639 
 
 TABLE 148.—AMOUNT OF FLUID IN PERICARDITIS WITH EFFUSION 
 
 100 c.c. in 7 Cases 
 I50C.c. in 5 cases 
 200°C.c, In, ‘4 Cases 
 aCOC.Cm in 1 Case 
 200-300 in 2 Cases 
 300 c.c. in 4 Cases 
 300-400 in I case 
 406 'CiC: 1m) “T Case 
 OO... 1n _T Case 
 700 C.c. in TI case 
 
 — 
 
 27 
 
 In addition to these, nineteen showed a “‘considerable,” fourteen a 
 “moderate,” and two a “large” amount of fluid. In four cases the 
 sac is described as ‘‘ distended” or “‘full.’”’ One contained “‘an excess,”’ 
 and one “a quantity” of fluid. Together these make up sixty-eight 
 out of 186 cases In which we suppose that an effusion possibly capable 
 of producing physical signs was present. In the remaining 118 cases 
 (or over three-fifths) the fluid is recorded as. “‘a small amount,” a 
 “slight excess.” a “few c.c.,” or was absent and the familiar shaggy 
 or “bread-and-butter”’ exudate was described. 
 
 Of these sixty-eight cases 7 or 10% were recognized in life. 
 The terms used at necropsy to describe these cases are: 
 
 ‘“‘Distended”’ 
 ‘““Markedly distended”’ 
 ROO, Cee a 
 “Considerable amount” 
 oy BOONG.Cre 
 
 e280 Clr 
 
 300 C:Ce 
 
 In two other cases there was no excess of fluid in the pericardium 
 at the time of necropsy, but this does not prove the prior diagnosis 
 of effusion to be wrong. 
 
 The evidence used for diagnosis was in all cases a wide percussion 
 area in the third or fourth interspaces to the right and left of the 
 sternum, aided in one case by an X-ray picture. 
 
 Paradoxical pulse is mentioned in three of the nine cases. Its 
 absence is once noted. Muffled or distant heart sounds are recorded 
 in three other cases (also in one more with a diagnosis only of “dry 
 pericarditis”). In one all heart sounds were replaced by murmurs. 
 
 In some of the cases with the largest effusions (e.g. 700 c.c.) only 
 friction was noted in life. 
 
640 FACTS ON THE HEART 
 
 Weakness or muffling of heart sounds was noticed in nine of the 
 unrecognized pericardial effusions. Indeed in one of these the 
 sounds are recorded as “‘inaudible.”” But the presence of pneumonia 
 or other causes for poor heart action no doubt prevented these facts 
 from suggesting pericarditis. 
 
 Bacteriology.—I have already alluded to the well-known fact 
 that acute pericarditis 1s not usually or primarily a local lesion, like a 
 gum-boil or an inflamed hemorrhoid, but rather the manifestation 
 of a general septicemia. This is shown by its frequent association 
 with pneumonia, peritonitis, acute pleuritis, and arthritis. It is 
 further evident from the frequency of positive blood cultures 
 post-mortem. 
 
 113 out of 186 cases showed positive cultures, the details being 
 as follows: 
 
 TABLE 149.—ORGANISMS FouND IN BLOoD AT NECROPSY IN PERICARDIAL 
 
 INFLAMMATION 
 Streptococcus: dcce.. ¥ fea e Gesdlek ee ie One on ae een 39 
 Pneumococcus. ts Mer.chrde ool a ae eee auch eae anak, nr 33 
 Staphylococcus jdlireus:; 02S. 65.5 ieee See ee ee 14 
 Staphylococcus ‘albus: jee ese (9c - te pe ee eee 3 
 Staphylococcus unspecified ecm...) 672 asa Benes eee 4 
 Questionablevy owi.2. vba, ote coed eoeceeh cocker ee 9 
 Be COU Ses sins SR cos ae be aie lee che a ae net 3 
 Pseudo-Pnenumococeus sand colon 2.02 ett eee I 
 Streptococcus and colon.) .saien0s ee ae) ce I 
 Streptococcus and pnenumococcus.cug cult ers ee I 
 Steptococcus and staphylocqccus?.<. 2. vk ony ee 
 Streptococeus and smucosUS.\ FF kta ae se ewan 2 
 B. mucosus capsulatus..... Sind Opera b ow Maen Ma a Oe he 1 aie 
 Culture nerative yg N50 ve en ae Pee Re Oey ante eet 73 
 
 186 
 
 The staphylococci were oftenest found in the cases of juvenile 
 osteomyelitis with myocardial abscess, the pneumococci in the 
 pneumonic cases, and the B. coli in those associated with ulcerative 
 colitis. 
 
 Murmurs in Acute Pericarditis—In seventy of these cases, 
 murmurs, believed to be endocardial, not pericardial, were recorded. 
 In sixteen cases the cause of these murmurs can naturally be put 
 down as the valvular disease which necropsy showed was present in 
 addition to the pericarditis. But there remain fifty-four in which 
 this explanation will not hold. Of this fifty-four, thirty-nine showed 
 only systolic murmurs. 
 
ACUTE PERICARDITIS 641 
 
 TABLE 150.—DIASTOLIC OR PRESYSTOLIC MURMUR IN ACUTE PERICARDITIS 
 
 Chronic 
 Heart passive 
 Weight | conges- 
 tion 
 
 Murmurs Remarks 
 
 Presystolic at apex. 465 + Chronic nephritis accounts for 
 dyspnea (I yr.), cardiac hyper- 
 trophy with congestion. Mitral 
 
 8.5 cm. but not deformed. 
 
 | | | | 
 
 General arteriosclerosis. Mitral 
 Io cm. Aortic 8. ‘‘Atheroma- 
 tous endocarditis and dilatation 
 of aortic valve.”’ 
 
 | | 
 
 Pernicious anemia. 
 
 Diastolic at base. 
 
 1668 50 M | Diastolic near left 610 (a) Chronic nephritis. General 
 sternal edge. arteriosclerosis. Mitral FO.5; 
 aortic 7.4. 
 3206 61 M Diastolic, left sternal 696 + Chronic nephritis. 
 edge. 
 3603 18 M | Diastolic along left 566 + A cute glomerulonephritis. 
 sternal edge. Chronic non-deforming endocar- 
 
 ditis of aortic mitral and tricus- 
 pid valves. 
 
 _—— “| —— eS | 
 
 Chronic nephritis. 
 
 Faint diastolic at apex 
 and base. 
 
 eee ee ee ee eee SS ee ee See “ 
 
 General arteriosclerosis. Fib- 
 rous myocarditis. 
 
 Soft diastolic at apex 
 (transient). 
 
 Diastolic at the base, General arteriosclerosis. Mitrai 
 (2d right and 2d left Lie eaOrlicuso-3 ao tricuspiduil a: 
 interspaces). pulmonic 9. 
 
 15 remain in which diastolic or presystolic murmurs were heard in 
 cases without deforming valve lesions post-mortem. In six of these 
 fifteen there were acute vegetations (g21, 1814, 2800, 3242, 3561, 
 3797) which may have played some part in producing the murmurs, 
 though in four of these the acute vegetations were so small that it is 
 hard to imagine how they could produce a presystolic or diastolic - 
 murmur. (They are described as (1) ‘‘ Pin-point sized,” (2) ‘‘ Match- 
 end sized,” (3) ‘‘Flat ulcers 5 X 8mm. across,” (4) ‘‘ Minute or small 
 masses.”’ 
 
 In at least 9 cases, however, there is nothing whatever in the 
 endocardium to explain these murmurs. In Table 148 the facts are 
 presented in detail. 
 
 These nine cases include four of chronic nephritis and three of 
 general arteriosclerosis, lesions very commonly associated with an 
 
 41 
 
642 FACTS ON THE HEART 
 
 hypertrophied and finally insufficient heart. In such cases presys- 
 tolic murmurs at the apex (as in No. 233) have often been described. 
 Diastolic murmurs might well be produced in the same way, though 
 they have not been so often recorded so far as I know. 
 
 In Necropsy 1038 (pernicious anemia) the murmur may perhaps 
 be considered ‘‘functional.”’ I have elsewhere described such a 
 murmur in association especially with the anemia of chronic 
 nephritis. * 
 
 In Necropsy No. 3693 a boy of eighteen previously well is taken 
 with “‘grippe in the joints” five weeks before entering the hospital 
 and, after this infection, has dyspnea on exertion but no acute respira- 
 
 TABLE 151.—Main CAUSE OF DEATH IN ACUTE PERICARDITIS 
 
 General 'Septicemia*: s4(050 5 cvinoee ds. Maral able park ee 50 
 Pnetimonia and*pneumococcus sepsis... 4./.--4s..-c ps ee Pe 37 
 Chronic He pnritis 3.4 Scr. thse terns hs ees pcan 32 
 Neoplasms (and '1 case of leukemia): .425.. 2.) oo. 95 see 18 
 Valvularcheart: disease;...2: 0. ew..0 Sree eee ss ane " 
 Arterinsclérdsiss of 2. Rt es ee lee ee 3 
 AN@UrSIn Jey u ha es mieten ore ta eae 3 
 Syphilltic-ortitis,,. sees ae ae a ke 2 
 Tratima eee Tae i ks erage Seat oh ee 5 
 Meningitis! 0% 2 isteo. « Pema ye ee ae ee ‘2 
 Permicious anemiat oo. ¢e .ask Ono eae) ee ea 2 
 Hepatic cirrhosistis 2/0, tient ii ers esc leo cee Ri. 
 Cardiat infarction. 0 ..<2s 34h nea aa ad oe ee 3 
 Acute and subacute nephritia® 7... 0 ea niere oro 2 
 : Appendicitis: 3) Vp eaGe oe Sa 2 sage ae et ye 3 
 Status lymphaticus. 27h. =)5 sete eae ee I 
 Strangulated hernia s7texcgn See a ote oe eer I 
 ActINOMYyCOSISAe oes~ kee » tag eae aes aM he eet ee ae I 
 Pericarditis alone. «5 Jes ca ete ie Steen ek A 9 
 Pied Se ey Cd ees tg saga be aad ae SPIGA EE. GON EEN acca et se 2 
 186 
 
 *TI class here cases in which several serous sacs or other cavities were involved, i.e., peritoneum, 
 pleura, joints, endocardium, with or without positive blood cultures. 
 
 tory distress until two days before his death five weeks later. His 
 entire illness thus covered ten weeks only. Examination showed 
 pericardial friction and fluid (300 c.c. post-mortem) ; also a presystolic 
 thrill and roll at the apex and a diastolic blowing murmur along the 
 left sternal border. No murmur in the second right interspace. 
 
 * Richard C. Cabot, M. D. and Edwin A. Locke, M. D. of Boston: On the Occurrence 
 
 of Diastolic Murmurs without Lesions of the Aortic or Pulmonary Valves (Johns 
 Hopkins Hospital Bulletin, May, 1903. Vol. XIV, No. 146). 
 
ACUTE PERICARDITIS 643 
 
 Pulmonic second accentuated. After five weeks of febrile illness 
 with a leucocytosis of 12,700 to 3400 and a “‘picket-fence”’ tempera- 
 ture he died. 
 
 Necropsy showed in addition to the acute pericarditis a hyper- 
 trophied and dilated heart (566 grams), chronic passive congestion, 
 and ascites. There was a chronic non-deforming endocarditis of the 
 aortic, mitral and tricuspid valves. (Mitral 8.5 cm., aortic 6.5 cm., 
 tricuspid 12. cm., pulmonary 7.5 cm.) 
 
 No. 3797 presents a good example of the simulation of valvular 
 disease by this ‘“‘marplot’”’ pericarditis. In this case there was no 
 pericardial friction and no evidence of fluid in the sac though both 
 were searched for. There was a systolic murmur at the apex replac- 
 ing the first sound and widely transmitted. A diastolic was heard 
 in the second and third left interspaces near the sternum. One of 
 our best diagnosticians signed the record as “Acute endocarditis, 
 mitral stenosis and regurgitation, aortic regurgitation. Adherent 
 pericardium (?).” 
 
 Post-mortem there was acute endocarditis of the aortic and mitral 
 valves, chronic and acute pericarditis, but no deformity of the valves. 
 
 Cardiac Hypertrophy in Acute Pericarditis——In 117 out of 186 
 cases in this series cardiac hypertrophy is recorded after death. 
 In thirty-four of these the hypertrophy is associated with chronic 
 nephritis and in three with arteriosclerosis. Nine were associated 
 with valve lesions, two with chronic pericarditis in combination with 
 the acute process, and two with pernicious anemia. This accounts for 
 50 out of 117 cases, including all the largest hearts. 
 
 In the remaining 67 cases there are only nine hearts over 520 
 grams. ‘The two largest weighed 664 grams (male aet. 67) and 602 
 (male aet. 50). Nineteen other hearts weighed between 400 and 483 
 grams. ‘Thirty-one weighed under 4oo grams. Eight are recorded 
 merely as “‘large” or “rather large.” For the most part therefore 
 it is only a moderate or a rather slight hypertrophy that we must try 
 to explain in these cases. 
 
 Twenty-two of these patients died of pneumonia, the pericarditis 
 being presumably associated with this. Twenty-eight died of some 
 form of septicemia associated with acute peritonitis, arthritis, ulcera- 
 tive endocarditis, septic knee, urinary sepsis, etc. In five cases the 
 chief cause of death seemed to be a neoplasm, in three cases infarc- 
 tion of the heart, in two cases trauma, in one syphilitic aortitis, 
 in one cirrhosis of the liver. 
 
 In only five was the infection manifested in the pericardium alone. 
 
644 FACTS ON THE HEART 
 
 Twenty-eight of the 67 cases of cardiac hypertrophy without any 
 traditional ‘“‘cause”’ were thus associated with nothing more definite 
 than a wide-spread sepsis, and twenty-two with pneumonia, and re- 
 main totally unexplained unless we can conceive that an acute infec- 
 tion is itself a cause of cardiac hypertrophy, or unless we assume an 
 earlier permanent hypertension. 
 
 I do not see how the sepsis in the pericardium or elsewhere can 
 produce hypertrophy of the heart. My best guess therefore would 
 be that these 28 patients (like many others of the 67 above men- 
 tioned) had previously suffered from a ‘‘primary”’ hypertension, 
 had thus acquired cardiac hypertrophy, and had then caught a sepsis 
 and died. The necropsy then shows evidence of two stories: (a) a 
 long one in which ‘‘essential”’ hypertension built up some degree of 
 cardiac enlargement, and (b) a short one of sepsis and death with 
 acute pericarditis. These two stories need have no important con- 
 nection with each other. Neither need we assume any connection 
 between the pericarditis and the enlarged heart. (This subject is 
 also discussed under acute endocarditis.) The details in nine of 
 these.cases are shown in Table 152. 
 
 TABLE 152.—CARDIAC HYPERTROPHY WITH ACUTE PERICARDITIS AND WITHOUT OTHER 
 SUPPOSED ‘‘CAUSES”’ FOR CARDIAC HYPERTROPHY 
 
 Age Nec- Duration | Chronic 
 Heart : 
 and ropsy e of fatal passive Remarks 
 weight : 
 Sex No. illness congest 
 19 M 3930 483 I week + Syphilitic aortitis with no in- 
 
 volvement of the aortic ring. 
 
 50M} 2955 603 2-3 weeks ++ Traumatic death. Chronic inter- 
 stitial orchitis. Angina  pec- 
 toris. Coronaries free. 
 
 48 M 2675 LU ea ON Peete ae ° 
 iy 39 440 2 weeks ° 
 Dire 2290 389 11 days ° 
 ate 1711 420 10 days ° 
 Beant 1231 480 1o days fe) 
 
SUMMARY 645 
 
 Plastic Pericarditis.—Out of 110 cases of this type, eighteen were 
 correctly diagnosed in life. In nine more our diagnosis was of 
 pericarditis without fluid though at necropsy a considerable effusion 
 was found. A friction rub and nothing else was recognized in life. 
 
 Diagnosis of Pericarditis in General.—In all we recognized the 
 presence of some sort of pericarditis in forty-three cases or 23%. 
 In thirty-three of these the evidence was friction alone, in three 
 cases fluid, in seven cases both. The reason for our 77% of failures 
 is in part the terminal nature of the process and its frequent occur- 
 rence in surgical cases where attention was otherwise engaged. 
 But this is not the whole, or I believe the main reason. Even when 
 we expected pericarditis and sought for it again and again, we often 
 failed to find it, though it was there at necropsy, and not always a 
 recent affair either. I think we must conclude that in some, perhaps 
 in most, cases, there are no physical signs, no friction rub or any 
 evidences of fluid. 
 
 From my own and others’ clinical blunders I know it to be a fact 
 also that we often hear a friction rub and diagnose pericarditis when 
 the necropsy, shortly following, proves that pericarditis has never 
 occurred (See p. 684). Some of these frictions may be due to patho- 
 logical dryness of the tissues (uremia or pyloric obstruction). 
 
 SUMMARY 
 
 1. Acute pericarditis is three times as common in men as it is in 
 women. Why this should be so it is hard altogether to explain. In 
 part it is perhaps accounted for by the fact that chronic nephritis 
 and arteriosclerosis—both commoner in the male sex—often lead to a 
 terminal pericarditis. 
 
 2. Other cardiovascular lesions (except hypertension and its 
 results) are not often associated with acute pericarditis. The disease 
 occurs either alone or with chronic nephritis or arteriosclerosis. 
 Acute endocarditis is a complication in only 8% of cases. 
 
 3. A quarter of the cases are afebrile, presumably because of low 
 bodily resistance in terminal states. 
 
 4. Pericarditis itself was the main cause of death in only 9 cases 
 out of 186. In most instances pericarditis is only one localization 
 of a generalized septicemia (often with pneumonia), or else represents 
 a terminal infection in chronic diseases such as cancer, or nephritis. 
 
 5. Organisms of the streptococcus-pneumococcus group can 
 generally be cultivated post-mortem from the exudate or from the 
 blood. The staphylococcus—especially in children with myocardial 
 
646 FACTS ON THE HEART 
 
 abscess and general septicemia—is not an uncommon ‘ invader 
 (twenty cases in 186). 
 
 6. 117 cases of enlarged heart (hypertrophy and dilatation), with 
 chronic passive congestion in sixty-six cases, were present in our 
 186 cases of acute pericarditis. 50 or about 1% of these cases are 
 easily explainable by the other diseases present (chronic nephritis, 
 etc.). But there remains a majority not so easily explained. It 
 seems improbable that acute pericarditis is in and of itself a cause 
 for cardiac hypertrophy and congestive heart failure.. An earlier 
 unrecorded hypertension is more probably the explanation for these 
 hypertrophies. | 
 
 7. Pericardial exudates of considerable size were present in 
 36% of cases. 
 
 8. Cardiac lesions are often wrongly diagnosed in acute pericar- 
 ditis on account of murmurs believed to be of endocardial origin. 
 Fourteen cases were of this sort. In these diastolic or presystolic . 
 murmurs were heard or supposedly heard, though they can hardly be 
 accounted for by anything found in the endocardium. When there 
 is evidence or suspicion of pericarditis no diagnostic conclusions should 
 be based on murmurs no matier how clearly they seem to be of endocardial 
 origin. 
 
 g. As I have previously proved in a smaller series of necropsies* 
 we failed to recognize acute pericarditis during life in nearly four- 
 fifths of the cases in which it was present post-mortem. It is also a 
 fact, though not proved here, that a diagnosis of acute pericarditis is 
 often made in life when none is present at necropsy. Errors of 
 commission as well as of omission are frequent in the diagnosis of 
 this disease. 
 
 10. Pericardial effusion was recognized during life in nine cases 
 out of the sixty-five proved at necropsy. With more frequent use of 
 radioscopy this record can be greatly improved. An extraordinarily 
 wide area of transverse percussion dullness is our best diagnostic 
 sign when X-ray evidence cannot be had. The character of the 
 pulse and of the heart sounds gives but little aid. 
 
 POINTS OF SPECIAL INTEREST TO THE WRITER 
 
 1. It seems at least possible that in a few cases of this series 
 hypertrophy and dilatation and chronic passive congestion were due 
 to the acute pericarditis itself, though it is always possible to class 
 
 * Diagnostic Pitfalls Identified during a Study of 3000 Autopsies: Journal of the 
 American Medical Association, December 28, 1912, Vol. LIX, 2295-2208. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 647 
 
 these cases in the group of hypertensive cardiovascular disease with 
 complicating or terminal pericarditis. 
 
 2. Pericarditis (acute or chronic) is a diagnostic mar plot when we 
 are searching for valvular heart disease. 
 
 3. When there is no considerable effusion the diagnosis of acute 
 pericarditis is so often missed or falsely asserted that its correct 
 diagnosis may be said to be in many cases impossible. When effu- 
 sion is present in considerable amount it should usually be recognized 
 by the X-ray but not often otherwise. 
 
 ILLUSTRATIVE CASES 
 
 Necropsy 3418 
 
 An American painter of forty-four entered November 24. The 
 complaints were swelling of the legs and heart trouble. His father 
 died at fifty-six of heart trouble and dropsy, his mother at sixty-five 
 after two years of “pleurisy.”’ A sister died of tuberculosis. The 
 patient was living at home when the mother died. 
 
 At thirty-two he had a small growth in the rectum the nature of 
 which he did not know. There had been no recurrence. The same 
 year he had an attack of lead colic characterized by sharp pain in 
 the “pit of the stomach;”’ no paralysis or muscle weakness. He had 
 *‘malaria’’ and rheumatic fever nine years ago, sore throat every 
 winter, an ulcerated tooth a year ago. He had had a slight hacking 
 cough all his life. His stools were black. He had never seen blood 
 in them. He chewed one plug of tobacco every other day. He 
 slept poorly. He did both inside and outside painting. He was 
 not careful about washing his hands. His best weight was 210 
 pounds twenty-three years ago, his usual weight (one year ago) 170, 
 his present weight 179. 
 
 For nine years he had noticed that when he stood up all day his 
 ankles were slightly swollen at night. Six years ago he noticed 
 dyspnea on exertion. As the dyspnea progressed he became 
 conscious of his heart’s beating. For the past two years he had © 
 vomited after breakfast about once a week. The vomiting was 
 preceded by a dull pain which it relieved. The vomitus contained no 
 blood or food of the previous day. Sometimes during these attacks 
 his eyesight was blurred. For the past two years he had nycturia, 
 with marked urgency. One year ago he noticed that he stumbled in 
 the dark, his eyes were more frequently blurred, he had edema below 
 
648 FACTS ON THE HEART 
 
 the eyes, and severe frontal and occipital headaches on waking, at 
 times lasting several days and accompanied by nausea. His feet 
 felt heavy. Six months ago the headaches obliged him to give up 
 work. Since that time he had been at home, quiet, with no relief of 
 symptoms. For six weeks his legs and abdomen had been swollen, 
 with tenderness in the right upper quadrant. He now urinated 
 eight times a day, five times at night. For the past two weeks he 
 had had slight epistaxis in the morning. The dyspnea was now very 
 marked. 
 Examination showed a pale, slightly cyanotic man. Pyorrhea. 
 Mucosae pale. The apex impulse of the heart was felt in the fifth 
 space. The percussion measurements are shown in Fig. 125. The 
 
 8cm. rst rib 
 
 He Eben Firs Bad 
 
 Nipple 
 
 4.5 cm. TOseine as Te5e Cis 
 
 Fic. 125.—Cardiac percussion records in Case 3418. 
 
 aortic second sound was markedly accentuated. There was a slight 
 musical systolic murmur at the apex, a low, faint systolic at base. 
 
 The blood pressure was 200 /140-180/120. Theartery walls were 
 
 palpable. The lungs were negative except for coarse sonorous rales. 
 
 at both bases behind. The abdomen was held tensely. There 
 was dullness in the flanks, shifting slightly. The liver dullness 
 extended from the fifth rib to 3 cm. below the costal margin; the edge 
 was just felt. There was edema and tenderness of both ankles. 
 The knee-jerks were normal. The right pupil was greater than the 
 left; both were irregular, reacted to light and distance. 
 
 The temperature was normal except for an occasional rise to 100° 
 in the later days of life. The pulse was 60-102. The respirations 
 were normal. The output of urine was 40-90 ounces until December 
 26, when it fell from fifteen ounces to almost nothing. The specific 
 gravity was 1.o10-1.012. There was a slight trace of albumin at 
 all of five examinations, rare leucocytes at four; one finely granular 
 _ cast at one; a few hyalin casts at one. The renal function was 6%. 
 The hemoglobin was 55-80%. ‘The leucocytes were 6000—12,300, 
 the reds 3,408,000-4,736,000, with marked variation in size, some in 
 shape; no stippled cells or polychromatophilia. The polynuclears 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 6490 
 
 were 71%. <A blood culture was negative. The blood showed on 
 non-coagulable nitrogen determination 176 mgm. in 100 grams of 
 blood. A Wassermann was negative, a gonococcus fixation test 
 deeply positive. November 30 the fundi showed narrowing of the 
 retinal arteries, occasional hemorrhage; diagnosis, retinal arterio- 
 sclerosis. December 23 there was retinitis of both eyes. The right 
 eye was normal. ‘The left eye showed a few small hemorrhages seen 
 just above the optic nerve. A radial tracing showed no irregularity 
 or alternation. ‘There was a tendency to plateau pulse. X-ray 
 November 28 showed cardiac enlargement and dilated arch. 
 
 The patient felt very well in bed. December 4 and 5 he was 
 allowed to sit up. December 6 he felt weak, and was returned to 
 bed. December 12 his left thumb was swollen and tender. An 
 X-ray of the hand was negative except for thickening of the soft 
 tissues. December 16 his ankles were beginning to become infected. 
 December 21 he was very uncomfortable, requiring an occasional 
 dose of morphia. The throat and dental departments were consulted 
 to see if a possible focus could be found. The throat examiner 
 reported, ‘‘No probable source of infection.” X-ray of the teeth 
 showed definite thickening of the left antrum, and small pockets 
 about a number of teeth. 
 
 By December 25 the patient still required morphia and was 
 incontinent of urine and feces. The joints were swollen, tender and 
 hot. December 27 a friction rub was heard all over the precordia. 
 He was having anginoid attacks, relieved for an hour or two by 
 nitroglycerin gr. 409. The friction rub persisted. The joints 
 grew somewhat less painful. There was great diminution in the 
 urinary output. He gradually became more delirious, and December 
 31 died. 
 
 Clinical Diagnosis (from Hospital Record). —Uremia. 
 
 Arteriosclerosis. 
 
 Acute dry pericarditis. 
 
 Chronic nephritis, arteriosclerotic. 
 
 Enlarged aortic arch. 
 
 Dr. Richad C. Cabo#'s Diagnosts.—Arteriosclerosis. 
 
 Coronary sclerosis. 
 
 Arteriosclerotic nephritis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Acute pericarditis. 
 
 Terminal septicemia, streptococcus. 
 
650 FACTS ON THE HEART 
 
 Anatomical Diagnosis. 
 Arteriosclerotic nephritis. 
 Slight arteriosclerosis. 
 Hypertrophy and dilatation of 
 the heart. 
 2. Secondary or terminal lesions. Edema of the lungs. 
 Fibrinous pericarditis. 
 Septicemia, streptococcus. 
 3. Historical landmarks. Slight chronic pleuritis, right. 
 A cathether specimen of urine taken after death showed no 
 phthalein output. | 
 Note by Dr. Cabot.—I see no reason to modify the original opinion 
 that lead poisoning was at the basis of this man’s trouble. 
 
 1. Primary fatal lesions. 
 
 Case CXXXIX 
 
 A boy of twelve was seen May 1, 1920. 
 He had had an attack of measles of ordinary severity from which 
 
 Fic. 126.—Empyema, left, and pneumonia, right. (Roentgenological Department, 
 Massachusetts General Hospital.) 
 
 he was apparently convalescent April 26 and 27, with normal tem- 
 perature. April 28 he had a sudden chill with high temperature. 
 The temperature had remained about 104°. The white count was 
 11,200 on the 29th, 27,200 on the 30th. The pulse and temperature 
 
 had been constantly elevated and there had been considerable dry 
 cough. | 
 
ACUTE PERICARDITIS—-ILLUSTRATIVE CASES 651 
 
 Examination of the lungs showed respiration extremely limited. 
 Breathing shallow. Movement more restricted on the left. In the 
 left back from midscapula to base marked dullness, increased whisper 
 and tactile fremitus, loud bronchial breathing, crepitant rales. © The 
 left axilla showed slight hyperresonance with occasional fine rales. 
 
 May 3 there was severe pleuritic pain on the left. The tem- 
 perature was still about 104°. Examination showed flatness in lower 
 back and axilla suggesting the possibility of fluid. May 8 there was 
 flatness in the left axilla and back with faint distant breath sounds 
 and diminished tactile fremitus. A needle was inserted just below 
 the angle of the left scapula and 4 c.c. of straw-colored turbid serum 
 
 Fic. 127.—Shows tip of catheter draining left pleural cavity. (Note the axillary 
 position of the exudate.) Dr. Wyman Whittemore. (Roentgenological Department, 
 Massachusetts General Hospital.) 
 
 removed. The sediment showed an excess of leucocytes and many 
 bacteria, mostly in pairs, with occasional short chains of three or four 
 cocci. A few of the bacteria appeared to have pointed ends and to be 
 morphologically like pneumococci, but on the whole more suggestive 
 of streptococci. 
 
 May 9 the patient was moved to a hospital. X-ray (Fig. 126) 
 showed empyema on the left with pneumonia on the right. Opera- 
 tion was done. Forty-eight hours later the left ear was discharging 
 pus. The right ear was opened by an ear specialist. 
 
 May 15 X-ray (see Fig. 128) showed the heart shadow enormously 
 increased and the empyema cavity empty. Aspiration of the peri- 
 cardium in fifth left space just outside the nipple line and inside the 
 
652 FACTS ON THE HEART 
 
 border of dullness gave thin pus showing under the microscope many 
 leucocytes and a rare organism resembling the organism from the 
 empyema fluid. This organism proved later to be pneumococcus 
 type I. 
 
 The pericardium was drained. 1200 c.c. of pus was removed 
 during the first twenty-four hours following operation. Fig. 129 
 was taken about a week later. The amount of pus gradually dimin- 
 ished until at the end of about four weeks there was less than 2 c.c. 
 obtained by suction in twenty-four hours. Then drainage was 
 
 Fic. 128.—Acute pericarditis. Catheter still in left pleural cavity. Empyema 
 practically gone. Dr. Wyman Whittemore. (Roentgenological Department, Massa- 
 chusetts General Hospital.) 
 
 removed. Twenty-four hours later the drain from the pleural 
 cavity was removed. Smear taken from both cavities showed less 
 than one pneumococcus in five fields and a rare staphylococcus. 
 Both sinuses promptly healed up, and at the end of eight weeks the 
 patient was out walking around the hospital with a temperature no 
 higher than 99°. 
 
 The skin over both mastoids was found to be edematous at this 
 time. Both mastoids were immediately operated on under ether. 
 The patient made an uneventful convalescence, and left the hospital 
 at the end of three weeks. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 653 
 
 Dr. Wyman Whittemore’s Pre-operative Diagnosis.—-Double 
 pneumonia. 
 
 Empyema, left, encapsulated. 
 
 First Operation—Local anesthesia. Left pleural cavity drained 
 by a closed suction technique. 
 
 Dr. Whittemore’s Pre-operative Diagnosis.—Acute pericarditis. 
 
 Mastoiditis, double. 
 
 Fic. 129.—Catheter coming from left, going under base of heart, and draining 
 posterior sulcus of pericardium. Dr. Wyman Whittemore. (Roentgenological 
 Department, Massachusetts General Hospital.) 
 
 Second Operation.—Local anesthesia. Pericardium drained by 
 a closed suction technique. 
 
 Diagnosis.—(Measles.) 
 
 Pneumonia, double. 
 
 Empyema, left, encapsulated. 
 
 Mastoiditis, double. 
 
 Acute pericarditis. 
 
 Operations: drainage of empyema; drainage of pericarditis; 
 curettage of mastoids. 
 
654 FACTS ON THE HEART 
 
 Necropsy 4945 
 
 An American student of twenty-two entered August 19, 1922. 
 He had measles and whooping cough before he was a year old. Since 
 that time he had always been healthy and athletic. He was earning 
 his way through college as a musician, playing an hour and a half 
 every noon and four nights a week until one o'clock, afterwards 
 studying often until three. His best weight was 156 pounds, a 
 year before admission, his usual weight 150 to 155 during the summer, 
 about 140in winter. In the summer of 1922 it had remained at about 
 T4o. 
 
 Six months before admission he noticed a hard swelling on his 
 left forearm. It gave him very little discomfort except that it 
 sometimes interfered with rapid finger work. During the next 
 two months it gradually increased to its present size. One spot was 
 slightly tender to touch. Three months before admission he devel- 
 oped a dry cough which had persisted, with a little white sputum 
 occasionally in the morning, and dyspnea, worse when he lay down. 
 A month before admission for four days he had sharp cutting pain in 
 the right lower back only on deep inspiration or motion of the trunk, 
 and absent when he lay on his left side. A week before admission 
 he had gradual onset of severe dull aching pain in the right thigh, 
 . becoming so severe that he required several doses of morphia in two 
 days. After it subsided a slight pain remained on any motion which 
 put strain on the quadriceps group. He went to a hospital, where 
 50 c.c. of bloody cloudy fluid was withdrawn from the left chest. 
 
 Examination showed a poorly nourished man with slightly 
 cyanotic lips and an acneiform eruption over the face and upper torso. 
 The posterior pharynx was reddened. The tonsils were enlarged, 
 inflamed and cryptic. The left chest bulged slightly. The lung 
 signs, abdomen, and apex impulse of the heart were as indicated in 
 Fig. 130. The heart action was rapid. The sounds were of poor - 
 quality. The aortic second sound was greater than the pulmonic 
 second. The right pulse was greater than the left. The blood 
 pressure was 100/75 to 115/90. A firm fusiform tender non-inflam- 
 matory swelling apparently involved the left ulna, starting with the — 
 subcutaneous tissues. The skin could be rolled over the mass. The 
 tendons and muscles had normal function. The arm at the tumor 
 area was about one and a half times the diameter of the right arm. 
 Another tumor mass appeared from palpation to lie over the right 
 femur, more diffuse than the one in the arm, and tender. It could 
 be rolled over the femur. The pupils and reflexes were normal. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 655 
 
 The temperature was 96.3° to 104°, with periods of elevation 
 August 21 to 22, August 26 to September 7 and September rg to 23; 
 after September 24 there was no elevation. The pulse was 80 to 
 170; the greatest rise was August 27 to 30. ‘The respirations were 
 17 to 55. The amount of urine was normal, the specific gravity 
 1.015 to 1.028. ‘The urine was cloudy at three of five examinations, 
 alkaline at two, the slightest possible trace to a large trace of albumin 
 at three, leucocytes at three, red blood corpuscles at one. The hemo- 
 globin was 80%. There were 13,000 to 23,200 to g200 leucocytes, 
 with 55 to 87% polynuclears, and 6% eosinophils at entrance. 
 August 28 one examiner recorded, ‘‘ Mononuclears atypical. Many 
 granules of neutrophilic type. Nucleus slightly large and cell very 
 regular in outline.” Another recorded, ‘‘ The atypical cells are some- 
 what larger than a polynuclear, with a large nucleus filling most of 
 the cell, indented but not bean shaped. The cytoplasm contains 
 many neutrophilic granules.”’ The reds were normal August 19 and 
 
 Right chest hyperres- 
 Sg 
 
 out (compensa- 
 tory %) 
 
 Left chest bulges slightly. 
 Coarse rub as indi- 
 cated by dots. 
 
 13 ¢1 
 
 U\ 
 : 
 et: 
 
 wey 
 
 X 
 is 
 
 4 p> 
 
 Diminished voice, 
 breath sounds 
 and tactile 
 fremitus. Rales. 
 
 oe 
 
 To OV 
 
 my 
 SS 
 ae Sy: 
 
 eH | Heart's impulse. 
 
 Mase moving with 
 respiration. 
 
 2 
 
 Fic. 130.—Chest signs in Case 4945, Aug., 1922. 
 
 28; September 21 there was slight achromia and an occasional 
 polychromatophilic cell; September 27 slight achromia, anisocytosis. 
 A. Wassermann was negative. The non-protein nitrogen was 30.3 
 mgm., creatinin 1.68 mgm. ‘The sputum showed no blood or tubercle 
 bacilli; there were streptococci, occasional staphylococci, Gram-posi- 
 tive and Gram-negative bacilli, and a small amount of pus. August 
 20 a chest tap in the eighth interspace over a very dull area near the 
 posterior axillary line gave no fluid. Solid material was encountered, 
 grating against the needle and causing pain. Another tap in the 
 eighth interspace in the posterior axillary line gave 1o c.c. of bloody 
 fluid which clotted rapidly. There were 912,000 red blood corpus- 
 cles, 2100 leucocytes, 5% vacuolated mononuclears (pleural? 
 tumor?), 55% polynuclears, 38% lymphocytes, 2% large mono- 
 nuclears. A culture and a smear were negative. A blood culture 
 showed staphylococcus albus. X-rays August 21 are shown in 
 
656 FACTS ON THE HEART 
 
 pact aa ad 
 
 Fic. 131.—Forearm August 21, first admission, before treatment. Shows fusiform 
 thickening of the middle third of the ulna, apparently due to proliferative changes in 
 the region of the periosteum. Small but distinct ray formations on the outer aspect of 
 the ulna. Soft tissues in region of involved area considerably thickened. No definite 
 tumor outline visible. Bones show no evidence of atrophy or destruction. 
 
 Fic. 132.—Chest August 21, first admission, before treatment. Large dense sharply 
 defined shadows obscuring outline of heart and angle between it and diaphragm on 
 both sides. Similar small shadows well out in periphery of lung. No evidence of 
 cavity formation. Apices clear. 
 
 ¥ : 
 
ACUTE: PERICARDITIS—ILLUSTRATIVE CASES 657 
 
 Figs. 131 and 132. A plate of the femur showed a line suggesting 
 separation of the periosteum from the bone over the inner aspect of 
 the middle third. No soft tissue changes were visible. August 
 28 a plate of the chest was difficult to interpret because of, motion. 
 Apparently there was little increase in the size of the dull areas in 
 the chest. The outline of the diaphragm was still visible. Sep- 
 tember 5 and 7 there was no definite change in the appearance of the 
 chest or the forearms. The vital capacity September 11 was 3060 C.c.; 
 September 13 at a single reading only 1110. ‘The forced respiration 
 caused such violent coughing that a second determination was not 
 attempted. 
 
 August 27 the patient was given neavy radiation. This was 
 followed by severe reaction and the maximum rise in temperature, 
 pulse and respiration. He required two grains of morphia in less 
 than twenty-four hours. For two weeks he had dyspnea, marked 
 cyanosis, and paroxysms of cough, usually unproductive. 
 
 September 12 a biopsy showed an atypical specimen on which the 
 pathologists disagreed. 
 
 September 23 another X-ray treatment was given with no bad 
 results. He had had four by September 29, and showed remarkable 
 improvement. His nights were better than they had been at any 
 time. October 3 the lungs showed about the same dullness to per- 
 cussion as before, but striking absence of the showers of rales pre- 
 viously heard. X-ray showed some lessening of the areas of 
 involvement. October 6 he was discharged with advice for further 
 X-ray treatment. 
 
 After leaving the hospital he went for a month to the country, 
 where his weight increased from 125 pounds to 143. November 24 
 his vital capacity was reported as 3200 c.c. On his return to the 
 city he developed a “‘pleurisy”’ with severe pain in the left posterior 
 chest, constant, but worse on deep inspiration or movements of the 
 body. This persisted except for occasional remissions following 
 X-ray treatments. From June 20 to 27 it became more severe and 
 was associated with pain deep in the right thigh and knee joint, 
 becoming so severe that he was given morphia. June 26 this pain 
 made him cry out. June 27, 1923, he reentered the hospital. 
 
 Upon examination he was poorly nourished, with flushed face, 
 warm and moist skin, and cyanotic lips. There was brown pigmenta- 
 tion over the chest, very marked on the left. The bone beneath 
 the scar on the left forearm was roughened. There were pea-to- 
 
 bean-sized firm non-tender cervical lymph nodes. The left lower 
 42 
 
658 FACTS ON THE HEART 
 
 chest bulged posteriorly. The left chest moved very slightly. 
 The right was almost normal. The lung signs were as shown in Fig. 
 133. The apex impulse of the heart was in the fourth space 7 cm. to 
 the left, not forceful. The midclavicle was 8 cm., the right border 
 
 Emphysematous 
 breathing 
 
 Bronchovesicular 
 breathing 
 
 pebereye 
 
 Dullnees, diffuse 
 swelling and marked 
 tenderness. Breath 
 sounds very distant 
 to absent. Fremitus 
 diminished. 
 
 Fic. 133.—Chest signs in Case 4945, June, 1923. 
 
 Fic. 134.—Chest in July, eleven months after first admission, after X-ray treatment. 
 Looks practically clear except for an area of somewhat increased density at the right 
 base close to the heart border. Diaphragm on the left apparently high. Left costover- 
 tebral angle hazy. 
 
 of dullness 5 cm. The pulse was fair, the rate 110. The blood 
 pressure was 116/66. The abdomen was very tense. The spleen 
 was enlarged to percussion, the liver not enlarged. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 659 
 
 The temperature was 97.3° to 103.5°; there was no elevation 
 July 4 to 6 or 12 to 17. The pulse was go to r4o, the respiration 16 
 to 30. The output of urine was J 31 to 91, the specific gravity 1.010 
 to 1.024. The urine was alkaline at two of three examinations and 
 showed the slightest possible trace of albumin at one, occasional 
 leucocytes at one. The hemoglobin was 70 to 80%. The leuco- 
 cytes were 12,200 to 8800, the polynuclears 80 to 91%, the reds 
 normal except for slight anisocytosis at the first examination. 
 The X-ray is shown in Fig. 134. 
 
 A surgical consultant found no evidence of perinephric abscess. 
 The patient improved before as well as after his first X-ray treatment. 
 July 17 he was discharged, to return for X-ray treatment. 
 
 July 23, two days after his third X-ray treatment, he suddenly 
 developed ‘“‘shingles”’ involving the left side of the chest wall from 
 spine to midline over a breadth of four inches. This lasted three 
 
 Bronchial 
 réles. 
 
 felt on 
 respira- 
 tion. 
 
 Grating 
 sensation 
 
 Flat. Absent 3 
 voice and fremitu 
 
 Fic. 135.—Physical signs in Case 4945, Oct., 1923. 
 
 weeks, and continuous pain and tenderness or hyperesthesia two 
 or three weeks longer. September 15 he went to the country for 
 three weeks, and felt well and active until three days before leaving. 
 Then he developed dyspnea and a feeling of hardness in the left lower 
 chest. He went home and rested. The dyspnea disappeared, but 
 returned October 19. During the next few days he had severe 
 pain in the right upper chest and shoulder on deep inspiration. His 
 weight had remained the same; his appetite had been steadily fair. 
 The left forearm swelled at times for no apparent reason, becoming 
 swollen and firm with edema which in about a week subsided. Twice 
 since his discharge he had very distressing dull aching pain in the 
 outer thigh along the sciatic nerve (?) subsiding ina week or two. He 
 had been told that the prognosis was hopeless. When the pains 
 became too bad he took a pill with marked relief. 
 
 Examination at his third admission, October 26, 1923, showed 
 him emaciated, sweating profusely, lying on his left side in much 
 respiratory distress, with occasional attacks of cough with little 
 sputum. The skin over the left chest and abdomen was tense, shiny, 
 
660 FACTS ON THE HEART 
 
 and scaly. The left chest moved little with respiration. Two sub- 
 sternal glands were felt, also glands in the left axilla and both groins. 
 The lung signs were as shown in Fig. 135. The heart was apparently 
 pushed to the right. The left border was not determined. The right 
 border was 7 cm. to the right of mid-sternum. ‘The sounds were 
 heard only to the right of the sternum. There was a to-and-fro 
 rough murmur sounding likea pericardialrub. The belly-wall showed 
 almost board-like rigidity in the upper quadrants and considerable 
 in the lower quadrants. It was impossible to palpate through it. 
 The superficial veins were distended. There was no tenderness. 
 In the middle of the left forearm was an oval non-tender bony mass 
 with a smooth surface, merging with the bone. The right thigh was 
 slightly tender along the course of the sciatic nerve. 
 
 The temperature was 99° to 96.3°, the pulse 118 to 140, the 
 respiration 34 to 20. The amount of urine was normal. The urine 
 
 Fic. 136.—Forearm October 5, three weeks before third admission, after X-ray 
 treatment. 
 
 was cloudy, the specific gravity 1.034. There was a very slight 
 trace of albumin. The hemoglobin was 65%. There was 16,200 
 leucocytes, 85% polynuclears, 4,160,000 reds, slight achromia. 
 The chest was tapped October 26 in the eighth interspace at the 
 angle of the scapula and in the posterior axillary line. After an 
 hour of manipulation of needle and position with strong suction, 30 
 c.c. of thick slightly viscous bloody fluid which clotted almost 
 immediately was obtained. It showed 80% large mononuclears, 
 10% small fibroblastic (?) cell types, 5% polynuclears, 5% fragmented 
 cells, many red blood cells, four mitotic figures, 36,000 leucocytes. 
 The fluid clotted too quickly for a count of the red blood cells, but 
 it must have been very high—z2,000,000-3,000,000. October 28 a 
 tap in the eighth left interspace just below the scapula gave 2 c.c. of 
 thick bloody fluid which clotted quickly. On manipulating the 
 trocar it seemed as though there were adhesions along the chest wall. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 661 
 
 The patient was propped up in bed and kept comfortable with 
 morphia and caffein. October 28 he died. : 
 
 Pre-operative Diagnosis (Sept. 12, 1922).—Tumor of ulna. 
 
 Operation.—Local novocain. Incision made over middle of ulna. 
 Bone partly solid, partly moth eaten, surrounded by thickened 
 periosteum which did not appear characteristic of sarcoma, but sug- 
 gested syphilis or chronic osteomyelitis. Specimen of periosteum 
 and bone removed for examination. Wound closed. 
 
 Fic. 137.—Chest October 5, three weeks before third admission, showing recurrence 
 ; and displaced heart. 
 
 Pathological Report.—Microscopic examination of small fragments 
 of bone showing clusters of atypical cells suggesting osteoblasts, 
 with fibrils and areas of osteoid tissue. 
 
 Osteogenic sarcoma. 
 
 H. F. HARTWELL. 
 
 Bacteriological Report —Culture from bone negative. 
 
 Clinical Diagnosis (from Hospital Record).—Osteosarcoma of left 
 ulna with metastases to left lung and pleura. 
 
662 FACTS ON THE HEART 
 
 Dr. Richard C. Cabot’s Diagnosis —Osteosarcoma of the ulna with 
 metastases in the chest. | 
 
 Anatomical Diagnosis.—(Osteogenic sarcoma of left ulna.) 
 
 Metastatic osteogenic sarcoma of lungs, bronchial lymph glands 
 and paravetebral and retroperitoneal tissues. 
 
 Acute pericarditis. 
 
 Dr. RicHarpson: There was a large bulging area on the left chest 
 just above the costal border, and the cutaneous vessels of the anterior 
 wall of the thorax, the shoulders and along the sides of the abdomen 
 were prominent. There was no particular deformity of the left 
 forearm at the time of necropsy, and we were not allowed to go any 
 further with the examination. The organs had to be replaced in the 
 body. 
 
 There was a little thin pale fluid in the peritoneal cavity. The 
 mass had pushed down the stomach, spleen and intestines so that 
 the lower border of the stomach was six cm. below the umbilicus, the 
 small intestines practically in the pelvic cavity, and the transverse 
 colon skirting along the top of the bladder. Below the diaphragm, 
 except that this mass pushed down in the retroperitoneal tissues, 
 there was nothing except that on the right side of the pelvic cavity 
 there was a mass of new growth tissue similar to that in the lung. 
 It was hemispherical, rather discrete, and measured 7 XK 344 cm. 
 The diaphragm on the right was at the fifth interspace, on the left 
 at the eighth rib. A mass of new growth tissue in the region of the 
 left lung pushed the diaphragm down to within a few cm. of the crest 
 of the ilium; down along the retroperitoneal tissues. It pushed the — 
 spleen forward so that its long axis was parallel to the median line, 
 and its lower pole only eight cm. above the crest of.the ium. 
 
 There was no fluid in the pleural cavities, and no adhesions on the 
 right; the left was bound down to the tumor in that region. The 
 bronchial glands were slightly enlarged and some of them showed new 
 growth tissue. In places in the new growth tissue there were pecu- 
 liar rust-colored areas of necrosis. The right lung was voluminous 
 and showed metastases here and there, some of them of pretty good 
 size, but nothing in comparison with the other side. On the leit 
 side the ovoid mass of new growth tissue measured 31 X 24 X 24cm. 
 In some places the pleura was thickened and retracted, with possibly 
 some streaks and areas of fibrosis lying along the tumor tissue. 
 Scattered through the large mass of new growth tissue were in places 
 large rust-colored areas of necrosis. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 663 
 
 The pericardium showed acute pericarditis. The heart weighed 
 275 grams. ‘The left border was in line with the left border of the 
 sternum, the right at a line perpendicular to the junction of the 
 middle and outer thirds of the right clavicle. The valves and cavities 
 were negative, the aorta and branches negative except that the 
 ovoid mass flattened the ascending thoracic portion of the 
 aorta markedly. 
 
 The abdominal organs require no comment. The bones of the 
 body, as far as dissection permitted, were negative. 
 
 Microscopical examination ofthe kidney, liver, spleen, etc., was 
 negative. | 
 
 Dr. Casot: Have you any doubt that this man’s life was pro- 
 longed by radiation? 
 
 Dr. Hormes: No, I have no doubt of it. Without radiation he 
 would have died sooner; but what is more important, he was able to 
 carry on very comfortably until a very short time before death. 
 
 Dr. Casot: It was a prolongation not merely of existence but of 
 actual work. What seem to be the prospects for improving therapy 
 in cases of this kind? We have had one or two cases where you had 
 extraordinary temporary results in banishing from the chest great 
 masses of tumor, but with recurrence. Do you look for gain? Do 
 you think we are likely by the methods we now control to be able to 
 hold this lesion off longer? 
 
 Dr. Hormes: There is not a great deal of evidence that points 
 towards cure, but I think that we are going to be able to make 
 it easier for the patient while undergoing treatment; that there 
 will be less Roentgen sickness. As for the actual prolongation of 
 life, it does not look as though we were going to be able to accomplish 
 a great deal once widespread metastasis has taken place. There 
 are some interesting data in the recently published accounts of 
 German clinics. In the clinics where the radiation treatment is con- 
 trolled by the surgeon they are using radiation for all cases of malig- 
 nant bone tumor rather than surgery. I think there is some question 
 whether cutting into a tumor or even amputation of the primary 
 tumor does not shorten the life of the patient. It is better to treat 
 the primary growth with radiation rather than to remove it. It is 
 possible that work along that line may enable us to carry these 
 cases longer and more comfortably. 
 
 Dr. MERRILL: Dr. Holmes told us that when that appearance 
 was seen in the lung the question arose whether it was recurrence or 
 fibrosis. Knowing as we do in this case that it was not fibrosis, but 
 
664 FACTS ON THE HEART 
 
 recurrence, in another similar case, were we not deterred, what 
 would be the prospect of giving him another lease of life? 
 
 Dr. Hormes: I think it would be pretty good. 
 
 Dr. MERRILL: And even presuming that it was a condition of 
 fibrosis and there still remained a question of recurrence, what would 
 be the great harm in producing a condition of fibrosis? A man can 
 exist with a large amount of fibroid change in his lung. Suppose we 
 treated him, what harm would it do? 
 
 Dr. Hormes: I do not know that it would do any. I think we 
 were unduly scared. But there has been a good deal of experimen- 
 tal work recently that has given us a rather bad scare. Some of the 
 patients develop, for example, a Roentgen cachexia which goes on to 
 death. So that we feel rather shaky about going ahead. I think 
 perhaps if we had it all to do over again we should recognize we made 
 a definite mistake in not doing it. Of course the mass that developed 
 in the abdomen would probably have gone on and we should not 
 have been able to control it. Other cases similar to this have 
 developed metastases in the brain which we could not control. 
 The lymphoma cases, which are much more susceptible to X-ray, we 
 can control in the chest, but they die of metastases in the brain. So 
 that I think with metastasis we are going to lose the patient anyway. 
 
 Necropsy 4269 
 
 An American boy baby of four months entered October 11, 1921, 
 for relief of constipation and vomiting. His parents had lost one 
 child of pulmonary tuberculosis a year previously. The mother had 
 had one miscarriage. The child was normally delivered at eight 
 months, weighing less than five pounds. He was put at once upona 
 formula. He occasionally regurgitated, and then began to have 
 loose green stools. At seventeen days old he was taken to the 
 Floating Hospital, where he remained for three weeks. On the boat 
 he caught “‘impetigo.”’ At discharge he was still vomiting a little. 
 His weight had increased from four and a half pounds at admission 
 to five and three quarters. In a few days he began to vomit more 
 and then to have eight or nine loose green slimy stools a day. By 
 direction of a dispensary clinic he was put upon a different formula 
 and was well for three days, then began to vomit again with great 
 force, and one night had convulsions lasting five minutes in which 
 the face and mouth twitched more than the rest of the body. -The 
 temperature was 102°. He entered a hospital, from which he was 
 discharged September 30 against advice. 
 
ACUTE PERICARDITIS—ILLUSTRATIVE ‘CASES 665 
 
 Upon his discharge from the hospital his bowels were constipated 
 and his buttocks very raw. His mother started giving him an ounce 
 or prune juice at night. Since that time he had been having two or 
 three firm yellow stools a day until the day of admission when they 
 were looser. October to he vomited with great force five minutes 
 after each feeding and apparenly lost the entire feeding, which was 
 sour and contained curds. . 
 
 Examination showed a poorly developed and nourished baby with 
 excoriations over the lower abdomen, buttocks and inner sides of 
 the thighs. The mucosae were pale. There were white patches 
 in the mouth. There was umbilical hernia. There was well formed 
 rosary and slight enlargement of the epiphyses. 
 
 The urine was normal, the hemoglobin 50%. The leucocytes 
 gooo, the polynuclears 32%, the reds 3,232,000, six nucleated cells, 
 moderate variation in size and shape. A Pirquet was negative on 
 two occasions. A Wassermann was negative. 
 
 On admission the child was put upon whole milk 15, water 15, 
 55 every four hours. The next day two tablespoonfuls of malt soup 
 was added. He vomited once on each of the first two days, but not 
 at all after that, and after the first day the green watery stools became 
 soft solid. On the 18th the malt soup was increased to three table- 
 spoonfuls. On the 2zoth he had nasopharyngitis, with a tempera- 
 ture of 102.6°._ The right ear was opened on the 22nd. He vomited 
 twice on each of the two days before discharge without apparent 
 cause other than the otitis media. The stools, however, were normal. 
 At admission the weight was 6 pounds g ounces, on discharge October 
 24 7 pounds Ir ounces. 
 
 After the child’s discharge the mother was unable to get the 
 malt soup, so she gave him whole milk 32, water 32, cane sugar 1 
 tablespoonful; 38 every three hours. The baby took all of it, did not 
 vomit, had normal stools, and was well until November 20. 
 
 That day he began to have snuffles, with a nasal discharge. He 
 was very fretful and coughed. His temperature was about 103° 
 the whole week. November 24 and 25 he was worse. His bowels 
 were constipated. The night of November 24 he was given a dram of 
 castor oil. He cried much of the time. He took the bottle well until 
 the morning of admission, November 26. | 
 
 Examination showed a well developed and fairly well nourished, 
 very pale baby, not appearing very sick. The anterior fontanel was 
 3 X 4 cm., level. The head veins were large. There was slight 
 craniotabes. The sclerae and mucosae were very pale. The ears, 
 
666 FACTS ON THE HEART 
 
 nose and mouth were negative. The lungs showed diminished 
 resonance over the entire right back, more marked at the base, with 
 bronchial breathing, increased voice sounds and fine crackling rales. 
 The apex impulse of the heart was not seen or felt. The left border 
 was 4)4 cm., the right border not made out. There was sinus arrhy- 
 thmia. The epiphyses were enlarged. There was a suggestion of 
 clubbed fingers. ‘The pupils and reflexes were normal. There was 
 no Kernig or neck sign. 
 
 The temperature and pulse were as shown in Fig. 138. The 
 respirations were 84 to 46. The urine is not recorded. The hemo- 
 globin was 60%. ‘There was 13,000 leucocytes, 
 66% polynuclears, 3,680,000 reds, slight achromia. 
 The platelets were normal. A Pirquet was negative. 
 
 The day after admission the temperature was 
 104.6° and the child seemed dried out. He did 
 not eat well for the first time. The fontanel was 
 depressed. After 300 c.c. of normal saline was given 
 intraperitoneally he seemed much better. The 
 morning of November 28 he seemed in good condi- 
 tion. The temperature was 100.2°, the fontanel 
 level, the lower lobe showed fewer rales. He did 
 not however take his feedings well. At midday it 
 was noticed that he was spitting up a little milk 
 with foam and had a peculiar ash-gray look and 
 rapid and labored breathing. His whole body was 
 stiff, and the arms and hands twitched. The 
 
 Fides Mere constantly. Lumbar puncture gave fluid under 
 perature and pulse increased pressure, 2370 cells, 88% polynuclears; 
 Sears aides globulin positive; Fehling’s not reduced. Gram- 
 negative intra- and extracellular diplococci were found. 15 c.c. of 
 antimeningococcus serum was given intraspinously and 30c.c. intrave- 
 nously. The child stopped crying after it and seemed more comfort- 
 able. He would not take the bottle, so was tube-fed. At midnight 
 he began to fret again and breathed rapidly and with difficulty. 
 The fontanel was again becoming tense. Another lumbar puncture 
 gave 20 c.c. of fluid morecloudy than the first. 15 c.c. of serum 
 was given intraspinously. Two minutes after the needle was 
 withdrawn he began to have respiratory difficulty and was definitely 
 sicker. The needle was inserted again in order to withdraw some 
 fluid with the idea that the serum was causing increased pressure. 
 
 Ser bite a, sgl 
 
 fontanel had become tense and the child fretted 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 667 
 
 There did not seem, however, to be increased pressure, and the condi- 
 tion did not improve. Artificial respiration was given, but the child 
 died after a few breaths. 
 
 Clinical Diagnosis (from Hospital Record)—Lobar pneumonia. 
 
 Cerebrospinal meningitis. 
 
 Anatomical Diagnosis —Fibrinopurulent pleuritis (influenza bacil- 
 lus and pneumococcus). 
 
 Fibinopurulent pericarditis (influenza bacillus and pneumococcus). 
 
 Acute leptomeningitis (influenza bacillus). 
 
 Dr. RICHARDSON: A well developed and poorly nourished infant. 
 In the region of the anterior fontanel there was evidence of the 
 puncture mentioned. The vessels of Willis, the sinuses, the middle 
 ears, and the mastoids were negative. Was there a history of middle 
 ear? 
 
 Dr. TALszor: Yes. 
 
 Dr. RICHARDSON: Apparently he had got over that at this time. 
 The pia in the region of the convexities and scattered along the base 
 was coated with a thin layer of pale yellowish exudate, and there was 
 a small amount of thin cloudy fluid at the base, but there seemed to be 
 no excess of fluid in the ventricles. The brain weighed 550 grams, 
 and on section presented no lesions. Anatomically of course it was a 
 leptomeningitis, extending down presumably into the region of the 
 cord. In the anterior abdominal wall in the left lower quadrant 
 there were two brown puncture-like spots. 
 
 Dr. Tarsot: Normal saline had been introduced into the 
 peritoneum. 
 
 Dr. RicHArDsoN: On the back were the puncture spots mentioned. 
 The subcutaneous fat was small in amount, the muscles were pale, the 
 peritoneal cavity, appendix and gastrd-intestinal tract negative. 
 The mesenteric and retroperitoneal glands were negative. 
 
 The pleural cavities: on the right side there was a small amount 
 of yellowish purulent fluid and much membranous yellowish fibrinous 
 exudate. This was plastered over the visceral and parietal pleura; 
 on the left side there was nothing. Other than for the sticking of the 
 lung on the right by the fibrinous exudate there were no adhesions. 
 
 The thymus gland was present, rather small, negative. The 
 bronchial glands were negative. 
 
 The lung tissue generally was pinkish, spongy, yielding con- 
 siderable pale pinkish frothy fluid; negative. 
 
 The pericardium contained much yellowish purulent fluid, and 
 the two layers were thickly coated with membranous, opaque yellow- 
 
668 FACTS ON THE HEART 
 
 ish fibrinopurulent material. The circulatory apparatus generally 
 was negative. There was nothing in the liver, gall-bladder, pan- 
 creas, spleen, adrenals or kidneys. 
 
 Dr. Casot: Those intracellular diplococci—what were thee 
 
 Dr. RICHARDSON: They said they were not stained by Gram, and 
 they were probably influenza bacilli. 
 
 Dr. Tarsot: They must have been pretty small. 
 
 Dr. RICHARDSON: They were. Clinically which do you think 
 came first, the infection in the chest or in the meninges? 
 
 Dr. Tarsort: I think the clinical description there was of a lobar 
 pneumonia first, and although the description is not very detailed one 
 might infer that it had cleared up and we had a pleuritis either with it 
 or secondary to it, and that the meningitis came last. 
 
 Dr. RicHArDSON: When you tapped him the first time you got 
 the pus—it was pus the first time? 7 
 
 Dr. TAsBort: Yes. 
 
 Dr. RIcHARDSON: Anatomically here we have no evidence to 
 indicate which was first. 
 
 Dr. Casot: You cannot swear that he had not had pneumonia 
 and got over it? 
 
 Dr. RICHARDSON: He probably did not. The lungs did not look 
 like that. The condition found was infection of the pleura and 
 pericardium. 
 
 Dr. TALBot: How much fluid was there in the chest? 
 
 Dr. RicHAarRDsON: A small amount. Generally speaking the 
 character of the exudate in the pericardium and pleura resembled 
 more that of the pneumococcus. The exudate over the meninges 
 was different. It did resemble more, I think, the epidemic: form of 
 meningitis than it did the pneumococcus. The condition there was 
 not so marked. There was not so much membranous fibrinous exu- 
 date as on the pleura and the pericardium. I have been trying to 
 think if we have had a discussion before on an influenza meningitis. 
 
 Dr. Casor: I think not. 
 
 Dr. Tarsot: Of course we could not expect the antimeningo- 
 coccus serum to do any good to influenza. 
 
 Miss PAINTER: Why did the baby seem to be better after the first 
 injection? 
 
 Dr. TAtzot: J suppose the lumbar puncture relieved the pressure. | 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES 669 
 
 Necropsy 4174 
 
 An Italian-American schoolgirl of ten entered March 2, 1g2r. 
 She did not remember any illnesses or any attacks similar to the 
 present one. ‘The morning before admission she had a stomach ache, 
 which rapidly became worse and caused her to vomit. As the pain 
 increased it localized more or less in the lower quadrants and more 
 particularly on the left side. She continued to vomit during the day. 
 The day of admission the pain was intense 
 and the vomiting continued. Her bowels 
 had moved on both days. 
 
 Examination showed a well nourished 
 girl with reddened and injected tonsils and 
 slight cervical adenopathy. The lungs 
 were clear and resonant. The heart was 
 normal except for rapid action. There 
 was exquisite tenderness in both quadrants 
 and over the pubes, more marked on the 
 left side. There was definite spasm of 
 the muscle in the lower quadrants, while 
 the abdomen above was soft. No organs 
 or masses were palpable. The rectal 
 examination was negative except for slight 
 tenderness on movement of the uterus. 
 The extremities, pupils, and reflexes were 
 normal. 
 
 The temperature and pulse were as 
 shown in Fig. 139. The respirations were Peete eet areend 
 normal until the evening of March 3, then pulse in Case 4174. 
 28-50. The amount and the specific 
 gravity of the urine are not recorded. There was a trace to 
 a large trace of albumin at both of two examinations, diacetic acid 
 at the first. The hemoglobin is not recorded. There were 40,000 
 to 48,000 to 38,000 leucocytes, 89% polynuclears. 
 
 The evening of March 3 the patient vomited and was delirious. 
 A medical consultant thought the case might mean a crisis of pneu- 
 monia, but was not typical. March 4 the patient looked worse. A 
 medical consultant found no focus of pneumonia. He thought there 
 was a little suggestion of dullness at the left base. Another consul- 
 tant found some suppression of breath sounds over the right midlobe 
 and inferior lobe, but said the pulmonary signs did not explain the 
 temperature, etc. Fluoroscopic examination showed the lung fields 
 
670 FACTS ON THE HEART 
 
 clear. The right diaphragm did not move so freely as the left, 
 especially in the inner half. The costophrenic angles were clear. 
 The plate showed in addition a band of slightly increased mottled 
 density in the right chest in the region of the base of the upper lobe. 
 The child’s body was cold. She was not entirely oriented. There 
 were three pulse beats to a respiration. There was no sweating. 
 That night she was delirious and restless. A subpectoral was given. 
 March 5 the abdomen was stiff and rigid and tender throughout. 
 
 Late that evening operation was done. 
 
 Clinical Diagnosis (from Hospital Record) —Idiopathic peritonitis. 
 
 Ether. Incision and drainage of peritonitis. 
 
 Fic. 140.—Costophrenic angles clear. A band of slightly increased mottled density in 
 the right chest in the region of the upper lobe. 
 
 Next day two subpectorals were given, and March 7 two more. 
 A culture from secretions from the nose was negative. March 8 
 there was rapid breathing, the nostrils moving with each respiration. 
 The general condition was growing worse. ‘There was considerable 
 drainage. She retained a little rectal glucose. A sore was found 
 on the left buttock, and two blue streaks in the same region. There 
 was high color in her cheeks. March 9 she was distinctly worse. 
 She roused and cried occasionally. In the middle of the morning 
 she suddenly became cyanotic and had labored breathing. Next 
 day she died. 
 
 a 
 nt 
 x 
 . 
 v 
 a 
 * 
 
 5 
 : 
 3 
 me 
 
ACUTE PERICARDITIS—ILLUSTRATIVE CASES O71 
 
 Dr. Hugh Cabot’s Diagnosis.—General septicemia with widespread 
 generalized peritonitis. 
 
 Possibly pleuritis, 
 
 Possibly pneumonia, 
 
 Possibly pericarditis. 
 
 Anatomical Diagnosis.—General fibrinopurulent peritonitis. 
 
 Empyema, double. | 
 
 Acute pericarditis. 
 
 Operation wound. 
 
 Slightly defective closure of the foreamen ovale. 
 
 Note by Dr. Richardson.—Culture from the peritoneal pus showed 
 streptococcus. 
 
 It is not uncommon in cases of general peritonitis to find a culture 
 from the blood stream showing no growth. In this case a few diplo- 
 cocci were recovered from the heart blood culture,—beginning septi- 
 cemia. It is also not uncommon in cases of general fibrinopurulent 
 peritonitis to find fibrinopurulent pleuritis. This infection of course 
 comes either through the diaphragm or by the blood stream. At 
 times it is difficult to say which is the avenue. In this case there 
 are no definite lesions of the lungs,—only the empyema associated 
 with the peritonitis. 
 
 Further Discussion by Dr. Cabot—I am interested that Dr. 
 Richardson finds a streptococcus, as this is the organism which is 
 much more likely than any other to cause this picture. 
 
CHAPTER X 
 CHRONIC PERICARDITIS 
 
 Starting from the post-mortem facts as revealed in the 112 exami- 
 nations of this series, we find that chronic pericarditis shows itself, 
 in the first place, as the so-called “‘milk spot”’ or patch of superficial 
 fibrous thickening of the pericardium to which we have no reason to 
 pay any attention. When adhesions exist between the two layers 
 of pericardium, they may consist (a) of slight cases in which the few 
 loose bands of adhesions presumably do not interfere with the work 
 of the heart and are essentially historical landmarks, witnessing 
 the presence of some past infection. Next (b) we have the extensive 
 cases in which the whole pericardium is adherent to the surface of 
 the heart so that no pericardial cavity any longer exists. Here 
 there is at least the possibility of interference with the work of the 
 heart, though, as will be seen presently, it does not appear that such 
 interference can always be demonstrated. Lastly, (c) we have the 
 group of cases with mediastinitis in which, in addition to obliteration 
 ot the pericardial sac, we have adhesions between the external surface 
 of the pericardium and the mediastinal tissues,—pleura, sternum, 
 diaphragm. As a source of interference with cardiac function, this 
 group seems to be the most important. 
 
 In the first of these groups, wherein the pericardial cavity is not 
 altogether obliterated, we may find acute pericarditis associated with 
 the chronic process, just as the two are linked together in the endo- 
 cardium. Acute pericarditis with the chronic process was present 
 in 5 of 112 cases. Indeed it seems quite possible that we may have 
 a series of attacks or recrudescences of pericarditis, as we certainly 
 do of endocarditis, the membranes becoming with each attack more 
 extensively vascularized and therefore more subject to the invasion 
 of bacteria. 
 
 On the basis of these three types of pathological anatomy, we 
 should expect to find more than one clinical type or picture of the 
 disease, and as we run over the clinical histories corresponding with 
 these necropsies, this is to some extent the case. Clinically there are 
 three groups, I, Vestigial, II, Primary rheumatic, III, Secondary 
 rheumatic. 
 
 672 
 
CHRONIC VESTIGIAL PERICARDITIS 673 
 
 CHRONIC VESTIGIAL PERICARDITIS 
 
 In the largest group (see Table 154) the typical case is that of 
 an elderly man who has never had rheumatism, who complains of no 
 symptoms which can be in any way referred to the circulatory 
 system, but dies of cancer, of Addison’s disease, of urinary sepsis, 
 pulmonary tuberculosis, or some other disease outside the heart. 
 In the patients of this group no one suspects or ought to suspect 
 pericarditis during life, and no one would look especially for it post- 
 mortem. Only as a part of routine thoroughness in necropsy work 
 it is discovered at all. In the 64 cases of this group brought together 
 in Table 154, only 12 had any rheumatic history; more than 4% were 
 of the male sex; the average age at death was 53, the average weight 
 of the heart only 430 grams, most of the cases showing little or no 
 hypertrophy. In view of all these facts one would expect that in 
 this group of cases the pericardial adhesions found at necropsy would 
 be few and far between, in other words that we are dealing in this 
 group with some of the results of relatively mild attacks of the dis- 
 ease. But in fact the number of cases with extensive, practically 
 obliterating pericardial adhesions slightly outnumber those of the mild 
 and incipient type. There are 36 of the obliterating type to 28 of the 
 partial. Mediastinal adhesions, however, were present in only 8 out 
 of 64 of this series and this is the essential point. - 
 
 I have already pointed out that in this group we have had little 
 or no evidence of cardiac disturbance during life. Only 20 of the 64 
 cases, or 14, showed any dyspnea or other cardiac symptoms during 
 life. 6 of these patients had chronic nephritis, so that their dyspnea 
 might easily be accounted for, either as a result of the cardiac hyper- 
 trophy and dilatation which is linked with that disease, or as a uremic 
 phenomenon. 2 others had pneumonia to explain dyspnea and 6 
 others were explainable without regard to the pericarditis. Only 16 
 of the cases showed evidences of chronic passive congestion, i.e. of 
 poor heart function, post-mortem, while 48 showed none. 12 of 
 these 16 had other lesions post-mortem which would account for the 
 passive congestion without any relation to the pericardial adhesions. 
 The other 4 cases, however, are not as easily explained and deserve 
 some further description. One of these was a man of fifty-three 
 whose heart at necropsy weighed 628 grams, although the pericardial 
 adhesions were but slight and there was no nephritis or endocarditis 
 to explain this hypertrophy. His history stated that he had had 
 orthopnea ever since he was sixteen years old, an almost incredible 
 
 assertion. He had marked evidences of stasis both before and after 
 43 
 
674 FACTS ON THE HEART 
 
 death. I suppose that he really suffered from the hypertensive type 
 of heart disease though he happened to show only the chronic peri- 
 carditis post-mortem. 
 
 Another patient, strangely enough, had in her history the same 
 curious statement about prolonged dyspnea, which in this case was 
 said to have existed since the age of six. The patient, a woman of 
 twenty-two, died of cancer of the stomach. The heart in this 
 patient weighed 308 grams and was considered by the pathologist 
 to be but slightly hypertrophied. The pericardial adhesions were 
 extensive but there was no mediastinitis, no history of rheumatism, 
 no valvular or other lesion to account for dyspnea, and no evidence 
 of passive congestion at necropsy. The blood pressure was 110/50. 
 
 Of 2 remaining cases one was a post-operative death, the other a 
 crush. 
 
 Leaving out of account these 4 cases we may say that this group is 
 vestigial because chronic pericarditis is, in these instances, of no 
 clinical importance, a mere vestige of some early and apparently 
 harmless infection. It is merely an item conscientiously recorded in 
 the complete post-mortem findings. 
 
 PRIMARY RHEUMATIC GROUP 
 
 Sharply contrasted with this group we find a smaller series of 
 twenty-three cases, in almost all of which the pericardial disease 
 constituted an important obstacle to the normal function of the 
 heart. In 17 of these the pericarditis was clearly the main cause of 
 death by passive congestion. 3 had no passive congestion, 2 died 
 mainly of valvular disease, and 1 of pneumonia. 
 
 The end of life came relatively early in this type of the disease, the 
 average age at the time of death being twenty-eight years, contrasting 
 with the average age, fifty-three, in the vestigial group. ‘There were 
 15 men to eight women. 18 out of twenty-three of these cases had a 
 well-documented history of rheumatic fever, sometimes of many 
 attacks. 
 
 While in the ‘‘ vestigial group” described in preceding paragraphs, 
 the adhesions were extensive in a little more than half the cases, 
 they were extensive in 19 out of twenty-three of the group now under 
 consideration. On the whole, then, we may say that these ‘‘ primary 
 rheumatic”’ cases occur in young people and are characterized by exten- 
 sive pericardial adhesions. Mediastinitis was present in 11 out of 
 twenty-three. 
 
SECONDARY RHEUMATIC GROUP 675 
 
 That the pericarditis interfered with the work of the heart is 
 strongly suggested by the cardiac weights. In the primary rheu- 
 matic group the average weight was 655 grams. (Contrast this with 
 the average weight in the vestigial group, 430 grams.) As will be 
 seen in Table 155, this group contains some of the largest hearts seen 
 in the whole series of our 4000 post-mortem examinations since 1896. 
 In one case the cardiac weight, 1328 grams, was greater than in any 
 necropsy of the whole 4000, and in three others, it was also extra- 
 ordinary; 1205, 1150 and 1158 grams. ‘There was not a single case in 
 the series in which the absence of hypertrophy was demonstrable. 
 Moreover, 19 of the 23 cases showed no cause for cardiac hypertrophy 
 except the pericardial adhesions. In the remaining four cases there was 
 subacute nephritis in two, general arteriosclerosis in one, and in the 
 remaining case stenosis of the mitral, aortic and tricuspid valves. 
 
 SECONDARY RHEUMATIC GROUP 
 
 Besides these two fairly well delimited types, our series contains 
 an additional group of 25 cases characterized by the fact that other 
 ‘“‘rheumatic”’ heart lesions probably played the chief part in bringing 
 about death, while the pericarditis was of secondary importance. 
 This group affected relatively young individuals, the average age of 
 death being thirty-two years. There were 13 males and 12 females 
 in the group, suggesting, for reasons above alluded to, a slight excess 
 of females. The heart weights averaged 508 grams. The adhesions 
 were extensive in 12 while in 13 cases they were slight. Mediastinitis 
 was present in only 8 cases. The accompanying cardiac infections 
 are seen in the last column of Table 156. 
 
 AGE AND SEX 
 
 Looking at the whole group of 112 cases we find that there are 
 32 females to 80 males, so that—as in acute pericarditis—the males 
 make up 72% or nearly three-fourths of the whole series. The 
 ages and the sex are shown in the following table. 
 
676 FACTS ON THE HEART 
 
 TABLE 153.—AGE AND SEX IN CHRONIC PERICARDITIS 
 
 Females 
 
 Obviously the disease affects women earlier than men. 42% 
 of the males are over 50, while only 22% of the females exceed that 
 age (provided the ages are correctly recorded). At the other end 
 of the age scale, where there is perhaps less temptation to lie about 
 it, we have 37+% of the women under the 31st year, while only 
 18+ % of the men are of this age. 
 
 DIAGNOSIS 
 
 It remains to inquire whether there are any signs or symptoms 
 on the basis of which one may make the diagnosis of chronic pericar- 
 ditis during life. In answer to this question, the outstanding fact 
 is that in very few of these 112 cases was the diagnosis even sus- 
 pected before death, and in only six was it actually made (Nos. 2297, 
 3009, 3290, 3345, 3520, 3648). In three cases acute pericarditis 
 was the clinical diagnosis (1063, 3242, 3496) and in two cases this 
 diagnosis was correct, though insufficient. Among the 46 cases 
 in which some cardiovascular lesion was considered in the diagnosis, 
 chronic valvular disease was most often thought to be present. This 
 was the diagnosis in 22 cases. In 13 of these the mitral valve was 
 
DIAGNOSIS 677 
 
 accused (mitral stenosis 7, mitral regurgitation 3, both 3) and seven 
 of these were right so far, since there was mitral stenosis as well as 
 chronic pericarditis at necropsy. Myocarditis was the only diagnosis 
 in 5 cases, all of them wrong. Acute and chronic endocarditis was 
 predicted in 4 cases, all correct diagnoses as far as they went. Of 
 acute endocarditis alone there were six diagnoses, all correct though 
 partial. Arteriosclerosis was all we recognized in 2 cases and 
 aneurism (correctly) in one. 
 
 Thus we may say that in 66 or nearly 24 of the cases we failed 
 to consider any cardiovascular lesion, that in the 46 cases remaining 
 we got part of the diagnosis—the accompanying acute endocarditis, 
 acute pericarditis or valvular disease—in 25. Systolic retraction 
 of the interspaces near the heart or between the ribs of the left back 
 is a sign of little or no value in the diagnosis of pericardial adhesions. 
 It has been amply demonstrated by Tallant* and others that systolic 
 retraction of interspaces is a common phenomenon in patients who 
 show after death no evidence of pericarditis. Whenever a markedly 
 hypertrophied heart is acting strongly within a relatively thin and 
 elastic chest wall, the interspaces will fall in with each systole simply 
 as a result of negative pressure. On the other hand we have searched 
 in a number of these cases for systolic retraction of interspaces 
 because we had some more or less distinct suspicion that adhesive 
 pericarditis was present. But we usually failed to find it even when 
 such adhesions were present after death. 
 
 Radiologists tell us that pericardial adhesions can be recognized 
 by the X-ray, in case they are associated with chronic mediastinitis 
 and especially with diaphragmatic adhesions. In such cases we 
 are told that the respiratory movements of the diaphragm and the 
 contractions of the heart can be seen by the fluoroscope to be limited. 
 All this may well be the case, but I have yet to see an instance in 
 which a diagnosis of chronic pericarditis has been suggested by a 
 radiologist and then verified post-mortem. 
 
 Aside from these two signs, the falling in of interspaces and 
 the limitation of cardiac or respiratory movement as seen by the 
 fluoroscope, I know of no sign that even purports to give us any 
 direct evidence of chronic pericarditis. But some suspicion of its 
 presence may be aroused when, in a relatively young patient with a 
 rheumatic history and evidences of cardiac hypertrophy and poor 
 cardiac function, we are unable to account for them by any valvular 
 
 * Dr. Alice Tallant: Some observations on the occurrence of Broadbent’s sign, 
 Boston Medical and Surgical Journal, 1904, Vol. 151, p. 457. 
 
678 FACTS ON THE HEART 
 
 TABLE 154.—GroupP I. CHRONIC VESTIGIAL (“LANDMARK”) PERICARDITIS 
 
 or 
 
 x. Chronic 
 
 passive 
 Heart congestion 
 weight 
 
 Before | After 
 death | death 
 
 Rheumatism 
 Mediastinitis 
 
 Exten sive 
 slight 
 
 —) (Sex 
 
 ~ Slight Pneumonia. 
 
 S 
 
 Slight Rh. 3 years ago. Goitre. 
 
 = 
 
 Extens. 
 Slight 
 
 Extens. Addison’s disease. 
 General peritonitis. 
 
 BW) ss 
 
 < 
 
 Slight Chronic nephritis® 
 
 = 
 
 Slight 
 
 Very sl. General peritonitis. 
 
 5 
 
 Subac. Post-operative death. 
 
 <| 
 
 Shght Chronic nephritis. 
 Bronchiectasis. 
 
 Slight Obstruction. Cancer. 
 
 =| s 
 
 Slight Sl. hypertr. 
 
 = 
 
 Extens. 
 
 Extens. 
 
 M 
 F 
 
 Extens. 
 
 Slight 
 
 a 
 
 Extens. 
 
 = 
 
 Extens. 
 
 4 
 
 Extens. Amyloid nephritis. 
 
 = 
 
 Extens. Chronic nephritis. 
 
 s 
 
 Extens. ; Arteriosclerosis. 
 
 = 
 
 Slight Duodenal ulcer. 
 Chronic nephritis. 
 
 s 
 
 Extens. 
 
 hy 
 
 Extens. 
 
 5 
 
 Extens. 
 Slight 
 
 Slight Heart weight not ex- 
 plained. : 
 ““Orthopnea since 16.”’ 
 
 a 
 
 = 
 
 Extens. Weight not explained. 
 
 Yy 
 
 Slight Cancer of sigmoid. 
 
 < 
 
 Extens. 
 
 Slight 
 
 s/s 
 
 Slight - |Subac.glomerulo-nephritis. 
 Slight 
 
DIAGNOSIS 679 
 
 TABLE 154.—Group I. Curonic VESTIGIAL (“LANDMARK”’) 
 PERICARDITIS.—(Continued) 
 
 Chronic 
 
 passive 
 Heart congestion 
 weight 
 
 Before} After 
 death | death 
 
 Rheumatism 
 Extensive or 
 Mediastinitis 
 
 Coronaries occluded. 
 Arteriosclerosis. 
 
 Traumatic death. 
 Calcified peric. Pn. 
 
 Pneumonia. 
 
 Syphilitic aortitis. 
 Chronic nephritis. 
 Arteriosclerosis. 
 
 Chronic nephritis. 
 Apoplexy. 
 
 Subac. glomerulo-nephritis 
 
 Arteriosclerosis. 
 
 Pneumonia. Sudden 
 death. 
 
 Pneumonia. Phthisis. 
 Streptococcus sepsis. 
 
 Dyspnea since 6. Died 
 of gastric cancer. 
 
 Rheumatism 25 years 
 ago. Gangrene of leg. 
 Phthisis. 
 
 Cancer. Operation, 
 Sepsis. 
 
 Aneurism. Cardiac In- 
 farct. 
 
 Streptococcus sepsis. 
 
 Streptococcus sepsis. 
 Acute nephritis. 
 
 Prostate operation. 
 
~ 
 
 680 FACTS ON THE HEART 
 
 TABLE 155.—GRouP II. PRIMARY RHEUMATIC PERICARDIAL ADHESIONS 
 
 Chronic 
 passive 
 congestion 
 
 Extensive Heart weight 
 
 Ante | Post 
 
 No evidence of stasis ante 
 or post mortem. 
 
 + | Rheumatism 
 + | Mediastinitis 
 
 Hypertrophy Stenosis, mitral, aortic and 
 and tricuspid. 
 dilatation 
 
 Hypertrophy 
 _ and 
 dilatation 
 
 Hypertrophy Acute endocarditis. Sub- 
 and acute nephritis. 
 
 dilatation 
 Hypertrophy + |. Rheumatism 4 years ago 
 
 and ; and again six months ago. 
 dilatation 
 
 Subacute glomerular neph- 
 ritis 
 
 Acute endocarditis. 
 
 Hypertrophy | Acute endocarditis and 
 and pericarditis. 
 dilatation 
 
 General arteriosclerosis. 
 
 Diagnosis made in life. 
 
 + Acute rheumatism at end. 
 Acute endocarditis at. end. 
 
 + Mycotic aneurism. Acute 
 nephritis. 
 
 + Pick’s disease. 
 
 Extensive + Diagnosis made in life. 
 
 Extensive | + 600 4+ + Acute endocarditis. 
 
TABLE 156.—Grouvp III. 
 
 Adhesions 
 extensive? 
 slight ? 
 
 + | Rheumatism 
 
 Slight 
 
 Ext. 
 Slight 
 
 Ext. 
 
 Ext. 
 
 Sl. 
 
 Ext. 
 Ext. 
 Sl. 
 Ext. 
 
 Ext: 
 
 Extensive 
 
 DIAGNOSIS 
 
 681 
 
 SECONDARY CHRONIC RHEUMATIC PERICARDITIS 
 
 Mediastinitis 
 
 Heart weight 
 
 315 
 Slight 
 hypertrophy 
 and 
 dilatation 
 
 680 
 
 80 
 Hypertrophy 
 and 
 
 dilatation 
 
 360 
 
 567 
 558 
 
 170 
 
 640 
 
 Chronic 
 passive 
 congestion 
 
 Ante | Post 
 mortem 
 
 Valve lesions, etc. 
 
 Mitral stenosis. Acute 
 
 pericarditis. 
 
 Mitral stenosis. 
 
 Acute endocarditis, aortic 
 
 and mitral. 
 
 Subacute nephritis. 
 
 Chronic and acute endo- 
 carditis. 
 
 Ulcerative endocarditis. 
 
 Mitral stenosis. Acute 
 pericarditis (700 c.c. in 
 sac). 
 
 Mitral stenosis. 
 
 Mitral stenosis. 
 
 Mitral stenosis. Acute 
 
 endocarditis. 
 Mitral stenosis. 
 
 Mitral stenosis. Acute 
 
 endocarditis. 
 
 Mitral stenosis. 
 
 Mitral, aortic and tricus- 
 
 pid. Stenosis. 
 
 Mitral, aortic and tricus- 
 pid. Stenosis. 
 
 Mitral and aortic stenosis. 
 Mitral and aortic stenosis. 
 
 Mitral and aortic stenosis. 
 
 Mitral, aortic, tricuspid 
 
 and pulmonary stenosis. 
 
 Mitral stenosis. 
 
 Empyema, brain abscess. 
 
 Subacute glomerulo-neph- 
 ritis. 
 
 Chronic and_ ulcerative 
 endocarditis (aortic). 
 
 Acute endocarditis. 
 
 Mitral and aortic stenosis. 
 
 Acute endocarditis. 
 
 300 c.c. in pericardium. 
 
682 FACTS ON THE HEART 
 
 lesion, by chronic nephritis, congenital heart defect,—in short by any- 
 thing else except by supposing that the patient’s rheumatism has 
 obliterated the pericardium. In a few cases, by this concatenation 
 of facts, suspicions may certainly be aroused and those suspicions 
 are strengthened when the patient shows an unexplained, predomi- 
 nating, and recurrent ascites which, as has been pointed out by Pick 
 and others, is occasionally associated with chronic pericarditis when 
 the process works through the diaphragm to produce a capsular form 
 of cirrhosis,—the so-called ‘‘ Pick’s syndrome.” This was recognized 
 in one case of the present series and should have been recognized 
 in another which I published a good many years ago.* 
 
 There was very little pain in most of these cases, and when it 
 was present there was no good reason to associate it with the 
 pericarditis. 
 
 Cardiac murmurs were present in 64 out of 112 cases. 27 of 
 these could be accounted for by endocardial lesions. Not infre- 
 quently, however, one sees post-mortem cases in which a well-marked 
 diastolic or presystolic murmur has led to the diagnosis of valvular 
 heart disease in life, yet in which post-mortem no valve lesion is 
 found. 
 
 DIAGNOSTIC MARPLOTS 
 
 Leaving out the 27 cases in which systolic murmurs alone were 
 audible, we have left 37 cases in which one could hear a presystolic 
 or a diastolic murmur or both. At necropsy the endocardium was 
 normal in 5 of these. These presystolic murmurs were best heard at 
 the cardiac apex and the diastolics along the left sternal edge. 
 
 These 5 cases constitute the deceptive group, the diagnostic 
 mar plots of the series. There were 4 males, 1 female. Ages 18, 28, 
 37, 38, 58. 
 
 There were diastolic murmurs in 4 of the 5 cases, presystolic alone 
 int. The heart weights include the largest in our series (1328 grams) 
 and average 749 grams. The adhesions were extensive in 3 out of 5. 
 Mediastinitis was also present in one. 
 
 To increase the diagnostic difficulty of these cases a palpable thrill 
 accompanied the murmur in 2 cases. Acute pericarditis was also 
 present in 2. Three of these cases were included in the group called 
 Primary Rheumatic (above). ? 
 
 * Obliterative Pericarditis a Cause of Hepatic Enlargement and Ascites, Boston 
 Medical and Surgical Journal, May 19, 1898. 
 
DIAGNOSTIC MARPLOTS 683 
 
 TABLE 157.—DIASTOLIC AND PRESYSTOLIC MURMURS IN CHRONIC PERICARDITIS 
 
 slight or 
 
 extensive 
 Acute endocarditis 
 
 Necropsy number 
 
 Rheumatism 
 
 Age and sex 
 Heart weight 
 Mediastinitis 
 
 Acute pericarditis 
 Chronic passive 
 congestion 
 
 Blood pressure 
 
 Murmurs 
 Adhesions 
 
 Systolic Extensive 
 and 
 diastolic 
 
 Systolic 
 and 
 diastolic 
 
 Systolic 
 and 
 diastolic 
 
 Presystolic 
 at apex 
 
 Systolic 705 Slight 240/140 
 and 
 diastolic 
 
 The cause of these murmurs and thrills is a matter of speculation. 
 We can class them with the ‘‘Austin Flint” group first described in 
 connection with aortic regurgitation. But there was no evidence of 
 aortic regurgitation in any of them. We can call them “functional” 
 which merely covers up our ignorance of their cause. To me it 
 seems best to stress especially their association with the hypertrophy 
 and dilatation of the heart chambers, which is one feature of cases of 
 chronic pericarditis. 
 
 I believe that in the group of cases first noticed by Flint it was the 
 cardiac enlargement and not the aortic regurgitation which was most 
 clearly related to the murmurs. 
 
 Other causes of cardiac hypertrophy, such as chronic nephritis, 
 are also associated, now and then, with apical diastolic or presystolic 
 murmurs. 
 
 The only important conclusion seems to be that im cases of marked 
 cardiac hypertrophy, apical or left parasternal murmurs, whatever their 
 time, sometimes do not mean valve lesions and should be very cautiously 
 interpreted when occurring without other evidence of heart disease. 
 
 Arrhythmia was present in 25 cases out of 103 of this series, exclud- 
 ing 11 cases of arrhythmia associated with valve lesions, but was 
 of no special diagnostic significance in relation to the pericarditis. 
 
684 FACTS ON THE HEART 
 
 The pulmonic second sound was accentuated in 47 cases out of 82, 
 the aortic second in 17. 
 
 Feebleness of the heart sounds was recorded in 22 cases, but in 
 the great majority there was nothing remarkable about them. 
 
 Friction sounds were heard in g cases but in only one of these was 
 any acute pericarditis found at necropsy. (cf p. 645.) 
 
 We have no reason to believe that chronic pericarditis can of 
 itself produce pericardial friction, since this sign is not infrequently 
 recorded in our cases when post-mortem examination later shows no 
 pericarditis, acute or chronic, and no overlying pleuritis such as might 
 cause a pleuro-pericardial friction. In some of these cases of unex- 
 plained pseudo-pericardial friction, there was an abnormal dryness 
 of the tissues owing to persistent vomiting or other causes. Very 
 possibly the heart within the normal but desiccated pericardium is 
 capable of giving rise to friction sounds. 
 
 Ascites was present post mortem in 38 cases. In nine of these it 
 was probably the result not so much of the pericardial adhesions as 
 of the accompanying valve lesions. In the remaining 29, the ascites 
 was part of a general dropsy in 17 and in one of the remainder it was 
 presumably due to a pancreatic cancer with metastases. 
 
 Only in two cases of this whole series (Nos. 662, 1907) was there 
 present at the time of necropsy any predominating or solitary ascites 
 such as is seen in many cases of hepatic cirrhosis. Pick’s syndrome 
 is rare in chronic pericarditis. 
 
 The necropsy cultures were positive in 39 out of 112 cases, the 
 streptococcus being found in 29, the bacillus coli in 4, the pneumo- 
 coccus in 4, the bacillus mucosus capsulatus in 1, staphylococcus 
 albus in 1. These cultures have no special connection with the 
 subject under study and are to be regarded probably as evidence of 
 a decrease in the general bodily resistance owing to the patient’s 
 exhaustion with the approach of death. 
 
 SUMMARY AND CONCLUSIONS 
 
 I. (a) Chronic pericarditis, especially when extensive and accom- 
 panied by mediastinitis, may be the essential cause of an enlargement 
 and weakening of the heart which results directly in death. Such 
 cases are usually of known rheumatic origin and recur mainly in 
 youths or young adults. 
 
 (b) The pericardial adhesions may be part of cripppling rheumatic 
 infection which attacks also and perhaps with greater damage the 
 heart valves. 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 685 
 
 (c) More often the pericardial adhesions may be found post-mor- 
 tem in persons dying of some non-circulatory disease, so that the 
 pericarditis is of little or no importance—a mere historical landmark 
 or vestige of an earlier healed infection. 
 
 To these three types of the disease I have given the names: 
 
 1. Vestigial. 
 
 2. Primary rheumatic. 
 
 3. Secondary rheumatic. 
 
 The vestigial cases are mostly in elderly people (average age 
 53) and 46 of them were of the male sex with a relatively slight 
 development of the pericardial adhesion and without mediastinitis. 
 
 The primary rheumatic type averages 28 years at death. Two- 
 thirds of the patients are of the male sex. In the secondary rheu- 
 matic group the average age is 32 and the sexes are about evenly 
 divided. It is in these two groups (which make up together 48 or 
 nearly 14 of the 112 cases in this series) that the pericarditis is of 
 importance, sometimes dominating, always contributing to the 
 clinical picture. 
 
 II. Only 6 cases in 112 of all three types were recognized in life; 
 the X-ray thus far gives us no help. 
 
 III. Diastolic and presystolic murmurs occur in many of the 
 cases and lead to so many erroneous diagnoses that primary rheu- 
 matic pericarditis deserves the name of a ‘“‘diagnostic marplot.”’ 
 Most of these deceptive murmurs occur in patients with very large 
 hearts. 
 
 IV. Chronic pericarditis produces in young rheumatic patients 
 the largest hearts known. 
 
 V. Only in 2 cases out of 112 was the presence of ascites without 
 general dropsy a notable feature. 
 
 ILLUSTRATIVE CASES 
 Necropsy 4502 
 
 An American of seventy, formerly a whaler and fisherman, 
 for five years a laborer, entered March 15, 1923. One sister died of 
 tuberculosis. Except for the usual diseases of childhood he could 
 remember no illnesses. At fifteen he had a questionable chancre, 
 rash, sore patches in the throat and pustular scabs on the tibiae. 
 At thirty he had gonorrhea. 
 
 For four months he had had dyspnea and weakness accompanying 
 any emotion. Four weeks before admission his lower legs began to 
 itch and he noted an eruption of small papules, and some time after 
 
686 FACTS ON THE HEART 
 
 this of weeping and scaling lesions on the anterior surface of the 
 tibiae. This spread over the calves. Because of itching he pulled off 
 the scabs and some pieces of dead skin. ‘The ulcerations had ®een in 
 their present condition for three weeks. Since they had ulcerated 
 he had been unable to walk or to take care of himself and had become 
 very filthy. Slight efforts tired him, and the dyspnea and weakness 
 on emotion were much worse. His feet swelled occasionally. His 
 physician reported that a Wassermann by the State Board of Health 
 was positive. 
 
 Examination showed a thin man with dry, scaling and very hard 
 skin (fish skin), somewhat pigmented. The lesions on the lower 
 legs involved the superficial subcutaneous tissue. The edges, though 
 ragged, were not undermined, but rather sharply punched out and 
 precipitous. The shallow base was covered by desquamating dead 
 skin, crusts of dried serum and yellow dry doughy material. The 
 ulcerations were confluent and formed a large area extending around 
 the leg from just below the knee to the middle of the tibia. Several 
 narrow areas extended down the back of the leg to the heel. The 
 lesions had a vile odor. The mucous membranes of the pharynx were 
 injected and the tongue was covered with a dry brown coating. 
 All the superficial lymph nodes were palpable. The apex impulse of 
 the heart is not recorded. The measurements by percussion were, 
 supraclavicular dullness 5 cm., right border 5 cm., left border 8 cm.; 
 the midclavicular line was tocm. A loud systolic murmur was heard 
 all along the left border and across the sternum radiating to the right 
 axillary line, loudest at the xiphoid and stopping very sharply 5 cm. 
 to the left of the sternum, not heard at the apex. ‘The veins in the 
 neck and arms pulsated markedly at a different rate from that of the 
 brachial artery. The latter and all the visible arteries were markedly 
 tortuous and thickened. The blood pressure was 145/75. The 
 lungs were not abnormal except for occasional crepitant rales at the 
 apices and bases posteriorly. The abdomen was protuberant and 
 very tympanitic. Dullness was found rather high in the flanks. 
 The liver edge could be felt just below the costal margin, smooth, 
 not tender. There was a moderate amount of subcutaneous edema 
 over the back and chest, a slight amount in the legs. The extrem- 
 ities showed slight tremor. The pupils were irregular, reacted to 
 light and distance. The left was smaller than the right. The inferior 
 turbinates (?) obstructed the breathing through the nose somewhat. 
 The knee-jerks were equal. There was questionable Romberg; no 
 clonus, Babinski or Kernig. 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 68 7 
 
 The temperature was 96.7° to 100°, with a terminal rise and drop 
 to 104.3°-100.4°. The pulse was 77 to 98, with a terminal rise to 
 120. The respiration was normal except for a terminal rise to 30. 
 The output of urine was 32 to 30 ounces when recorded, the specific 
 gravity 1.030 to 1.018. There was no albumin. A few leucocytes 
 were seen at one of three examinations. The renal function was o. 
 The hemoglobin was 85%, the leucocyte count 10,800 to 33,000, with 
 89% polynuclears. There was moderate anisocytosis. Two Wasser- 
 manns were negative. 
 
 After three days’ use of Dakin’s solution the odor from the ulcers 
 had decreased remarkably. The application of the solution caused 
 some pain. The lips appeared slightly cyanotic. Dyspnea was 
 marked. All movements grew increasingly difficult. By March 20 
 the ulcers were quite clean and granulations were growing up from 
 the surface with great rapidity. The edges were smoothing off and 
 a delicate line of new epithelium was working over the sloping base 
 from the edges. 
 
 The next day the patient’s jowls were swollen. The potassium 
 iodid was immediately decreased. That day the heart weakness 
 was more evident than ever before. March 22 the patient was 
 failing rapidly.. The edema of the face, hands, back and chest was 
 somewhat increased. He was put in semi-Fowler position. The 
 heart sounds were less clear and the action weaker. That afternoon 
 he began to cough up frothy sputum, and moist bubbling rales were 
 heard in the lower chest, especially over the bases laterally. He 
 could not be moved without great discomfort, so the back was not 
 examined. The liver was not tender. There was marked passive 
 congestion of the lungs, but no pneumonic patches were noted. The 
 abdomen was distended with gas. The patient improved a great 
 deal after atropin and the respiratory discomfort subsided somewhat. 
 An enema and stupes also helped. 
 
 The night of March 25 the temperature rose suddenly. Nothing 
 was found. The next morning however a rather cyanotic red area 
 was found arising around the left ear and extending on the temple 
 involving the left eyelids, part of the cheek, and all of the ear. The 
 border was sharp and raised. ‘The area was tender. ‘The leucocyte 
 count rose toits maximum. That day the patient died. 
 
 Clinical Diagnosis (from Hospital Record).—Cardio-renal disease. 
 
 Syphilis? 
 
 Erysipelas. 
 
 Dr. Richard C. Cabot’s Diagnosis —Chronic nephritis. 
 
688 FACTS ON THE HEART 
 
 Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Erysipelas (streptococcus septicemia). 
 
 Passive congestion of lungs, posssibly of liver. 
 
 Pneumonia? 
 
 Acute pericarditis? 
 
 Anatomical Diagnosis. —Arteriosclerosis. 
 
 Chronic adhesive pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Serofibrinous pleuritis. 
 
 Serofibrinous peritonitis. 
 
 Fatty metamorphosis of the liver. 
 
 Marked edema of the lungs. 
 
 Chronic pleuritis. 
 
 Obsolete tuberculosis of a bronchial gland. 
 
 Tumor of right epididymis. 
 
 Dr. R1cHARDSON: The legs were bandaged, and I did not remove 
 the bandages. I have no doubt he had erysipelas and the other 
 things on the surface of his skin. 
 
 The peritoneal cavity contained 1500 c.c. of thin cloudy fluid 
 and fibrin and some reddish fibrin scattered over the peritoneum. 
 That is a serofibrinous peritonitis, terminal of course, in association 
 with the other expressions of infection. 
 
 In the right pleural cavity there was a serofibrinous pleuritis, 
 another expression of the same thing, and’a few old adhesions besides. 
 The left cavity was obliterated by old adhesions. 
 
 The gastrointestinal tract showed congestion, and we can leave 
 it that way. 
 
 One bronchial gland showed obsolete tuberculosis, and there was 
 a mass in one of the testes which was fibrocalcareous. And then the 
 the question arises, is it tuberculosis or is it syphilis. He had 
 tuberculosis somewhere else, and I think possibly that was an old 
 tuberculosis. 
 
 I could not make out any pneumonia in the lungs. There was 
 congestion. 
 
 The pericardium was obliterated by old adhesions,—chronic 
 adhesive pericarditis, which occurred many years ago. 
 
 The heart weighed 660 grams. The valves showed some of the 
 usual sclerosis associated with age, but otherwise were out of the 
 picture. The heart in general was hypertrophied and dilated. 
 
 _—— 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 689 
 
 The myocardium generally was rather thick, five mm. on the right, 
 fifteen mm. on the left. Back of that all I found was arteriosclerosis. 
 The sclerosis did not begin in the ascending thoracic, in fact was not 
 observed until we came to the descending thoracic. From there on 
 there was plenty of it. That distribution of course is rather against. 
 syphilis. 
 
 There were a few bands of adhesion between the liver and the 
 diaphragm, perihepatitis and congestion of the liver, but no definite 
 cirrhosis. The liver was a little enlarged, the vessels engorged. 
 
 The kidneys weighed 340 grams,—certainly not those of chronic 
 nephritis. Here the condition seemed to be chronic passive conges- 
 tion. The vessels were a little prominent. There was a good width 
 of cortex. The kidneys showed nothing that we could put our 
 hands on except as mentioned. 
 
 The prostate, seminal vesicles and testes were negative except 
 for the fibrocalcareous mass mentioned. As a matter of fact I did 
 try to decalcify that, and have some sections, but it would bother 
 us a little to say whether the sclerosis present was the end result of 
 tuberculosis or of syphilis. He had one tuberculous lesion, and I 
 do not see why we should not let it go as old tuberculosis. I think 
 the laboratory report of the kidney function must be wrong. 
 
 Dr. Casot: We are accustomed to divide our post-mortem into 
 three general groups, the underlying cause, the terminal infections 
 supplying the factor necessary to turn the scale,—erysipelas, pleur- 
 itis—and then the historical landmarks, things mentioned in a 
 conscientious account of everything that was found, having nothing 
 whatever to do with the case, such as this tuberculosis of the lymph 
 glands. In old times pathologists used to try to be entirely dis- 
 passionate and not arrange their findings at all,—put them in alpha- 
 betical order. It seems to me we are trying to do better in trying 
 to make these reports mean something and supply a basis for our 
 efforts during life. 
 
 Serofibrinous peritonitis was present. Nothing is said about 
 tenderness or about spasm, which we so often see as part of an infec- 
 tious process. We did not suspect in any way adhesive pericarditis, 
 and we shall do just the same thing next time probably. We do 
 not diagnose those things. 
 
 The zero reading in the renal function test was probably due in 
 
 part to failing absorbtion of the dye owing to edema. 
 44 
 
690 - FACTS ON THE HEART 
 
 Case 4475 
 
 An American slaughterhouse foreman of fifty-six entered January 
 19, 1923, for relief of weakness a year and a half in duration. 
 
 His father and one son died of diabetes. An aunt died of tuber- 
 culosis. His wife had three or four miscarriages. Several children 
 died in infancy. 
 
 Whooping cough was the only disease he remembered in childhood. 
 At fifteen and again at thirty-seven he had inflammatory rheumatism, 
 the first attack lasting two months, the second a whole winter. As 
 long as he could remember he had had attacks of “‘biliousness,”’ 
 formerly every two weeks, of late years rather infrequently. For two 
 or three days before the attacks his skin and eyes became yellow and 
 his urine very dark. The attacks began with dimness of vision, than 
 severe pain over botheyes. Ina few hours he vomited green material 
 and the attack was over. He had a cold sore removed from his lip 
 seven years ago. One gland on the left side of the neck swelled 
 occasionally. His bowels had always been constipated. He some- 
 times urinated once at night. 
 
 He took beer very moderately. Best weight 250 pounds, eight 
 years ago; usual weight 230-240, weight a week ago 205. 
 
 Four years before admission there was gradual onset of pain in 
 the lower back, fatigue, and a feeling of fullness and discomfort in the 
 epigastrium. This last was constant and was always made worse by 
 food. With it was marked jaundice. His bowels were constipated. 
 These symptoms lasted four months, during which time he did not 
 work. Finally on account of increasing severity of the symptoms he 
 went to an osteopath. After treatment the pain and jaundice 
 disappeared and he went back to work. The pain had never 
 reappeared. He was then entirely well for a year except that he hada 
 very sore tongue for three or four months. Three years ago following 
 domestic trouble he became very nervous and fretful and lost weight. 
 The nervousness and also the domestic trouble had persisted more or 
 less to the present time. He also began to have a feeling of weakness, 
 bad for a year and a half. Fifteen months ago he began to have 
 pain in midsternum, only after exertion or hard work. With this 
 there was also pain in the left forearm from the elbow to the wrist. 
 He was very weak, did not feel right, and he was told that he looked 
 queer. He felt chilly easily and got out of breath on moderate 
 exertion. After two months he recovered completely. Eight 
 months ago the symptoms returned, and with them jaundice. Again 
 after two months he was well. Very soon after this he had another 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 691 
 
 breakdown from which he quickly recovered. From six months ago to 
 four months ago he was well and worked every day. Four months 
 ago the present attack began with jaundice, weakness, dyspnea and 
 midsternal pain on exertion, palpitation and pounding in the ears. 
 With this attack his fingers and toes were numb. For the past two 
 weeks his appetite had been very poor and he vomited easily. For 
 ten days he had been coughing and raising thick yellow sputum. 
 
 Physical examination showed a well nourished white haired man 
 looking exhausted. Scattered tiny petechiae on the upper chest. 
 Small white round scars on the anterior chest wall. Pigmented scars 
 on the left lower leg and a purplish depressed scar on the right lower 
 leg. Skin and sclerae pale and yellow, the sclerae more yellow at the 
 periphery and slightly injected. One petechia noted under the 
 conjunctival surface of the lower lid. Slight pyorrhea. Tongue 
 margins very smooth. Papillae atrophied on margin. Atrophied 
 areas on under surface and a few petechiae. Moderate discrete 
 enlargement of the cervical and axillary glands. Chest: abnormally 
 wide intercostal angle with depression above a wide upturned xiphoid. 
 Apex impulse of the heart not localized. Sounds of rather poor 
 quality. Soft blowing systolic murmur all over precordia, loudest at 
 apex and base. Blood pressure January 19, 108/35, January 209, 
 132/60, February 3,90/45, February 16,112/50. Electrocardiogram. 
 Normal rhythm. Rate go. Diaphasic T:. Abdomen negative 
 except for slight retraction in the epigastrium. Pupils normal. 
 Fundi. Both showed pale, hazily outlined small hemorrhagic areas 
 scattered throughout, some apparently absorbing, others darker and 
 and fresher. Reflexes. Knee-jerks hyperactive, with clonic con- 
 tractions. Poor position and motor sense in both legs and arms. 
 Slight numbness of toes. 
 
 Temperature 96.9°-100.8° except for two periods of elevation, 
 January 19 102°, February 12-18 98.1°-106.5°. Pulse 71-160, rising 
 with the rise of temperature. Respiration 16-29. Urine 3 25-80. 
 Sp. gr. 1.015-1.020. Slight trace of albumin at one of two examina- 
 tions, rare to occasional leucocytes at both. Blood January 10. 
 Hgb. 40%, leucocytes 3200, polynuclears 56%, reds 1,030,000,— 
 1,120,000, marked anisocytosis and poikilocytosis, many large red 
 cells well filled with hemoglobin, considerable variation in staining, 
 many microcytes, platelets very rare, reticulated cells 1.9%. Jan- 
 uary 23. Hgb. 40%, leucocytes 2200, reds 1,500,000, reticulated 
 cells 1.7%. January 27. Before transfusion hgb. 40%, reds 920,000, 
 reticulated reds 2%. After transfusion hgb. 40%, reds 1,300,000. 
 
692 FACTS ON THE HEART 
 
 February t. Hgb. 50%, leucocytes 4400, reds 1,320,000, reticulated 
 reds 0.3%. February 7. Hgb. 60%, leucocytes 4100, reds 1,300,- 
 ooo, reticulated cells 2.8%. February 10. Before transfusion hgb. 
 50%, leucocytes 6400, reds 1,350,000. After transfusion hgb. 60%, 
 reds 1,750,000. February 14. Hgb. 60%, leucocytes 3500, reds 
 1,900,000, reticulated cells 1.1%. February 17. Leucocytes 2500. 
 Serum dilution 1:60. Clotting time 18-25-24-24-20 minutes. 
 Fragility. Hemolysis began at 0.46 and was complete at 0.26. 
 Throat exudate examination on dark field showed no spirochetes or 
 organisms of Vincent’s angina. Vital capacity 4300 c.c. Basal 
 metabolism +21%. Gastric analysis. Fasting contents. 33 c.c. 
 yellow-white mucous material. NofreeHCl. Totalacid5. Guaiac 
 positive. 3-4 red blood cells and 2-4 leucocytes to a high power 
 
 Fic. 141.—Pernicious anemia with hypertrophy and dilatation of the heart. Defin- 
 ite increase in transverse measurement both to right and to left. Cardiac shadow not 
 definitely abnormal otherwise. 
 
 field. Test meal. 24 c.c. whitish bread remnants. No free HCl. 
 Total acid 4. Guaiac positive. X-ray. Heart as in illustration. 
 No evidence of pathology in.any part of the gastro-intestinal tract. 
 February 17 left frontal sinus distinctly less radiant than the 
 right. Antrum on this side also a little cloudy. : 
 January 27 transfusion of 600 c.c. was done. There was very 
 slight reaction after it. Next day he felt great subjective improve- 
 ment which continued for several days. February 1o a second 
 transfusion was done. Following it he had fever. February 16 he 
 complained of sore throat and a very sore tongue. On the soft palate 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 693 
 
 were several small areas of superficial ulceration. The right half of 
 the tongue was markedly swollen, red, and extremely tender. The 
 next day the tongue was more swollen and there were several very 
 tender submaxillary nodes on both sides. During the day marked 
 edema of the neck developed. The saliva showed many streptococci. 
 That night he was much worse. The tongue filled the whole mouth 
 and pharynx, causing obstruction controlled by a tube. Early 
 the next morning, February 18, he died. 
 
 Clinical Diagnosis——Pernicious anemia. 
 
 Streptococcus septicemia ? 
 
 Acute glossitis. 
 
 Acute cellulitis, mouth and neck. 
 
 Dr. Richard C. Cabot’s Diagnosis —Pernicious anemia. 
 
 Streptococcus septicemia with glossitis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Anatomical Diagnosis.—Pernicious anemia. 
 
 Septicemia, streptococcus hemolyticus. 
 
 Hyperplasia of bone marrow. 
 
 Hematopoiesis of the liver and spleen. 
 
 Chronic adhesive pericarditis. 
 
 Arteriosclerosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Acute glossitis. 
 
 Edema of epiglottis. 
 
 Hemorrhagic edema of lungs. 
 
 Wet brain. 
 
 Fatty infiltration of the pancreas. 
 
 Myoma of stomach. 
 
 Chronic pleuritis, localized, slight. 
 
 Obsolete tuberculosis of one bronchial lymph node. 
 
 Cholelithiasis. | 
 
 Dr. Oscar RICHARDSON: I think we can put the anatomical basis 
 under most of the questions that have arisen. 
 
 We examined the head in this case. The pia showed a little 
 edema, but the vessels of Willis, sinuses, and middle ears were nega- 
 tive, and the brain tissue outwardly showed no definite lesions.. 
 
 The spinal cord outwardly showed nothing definite, but as Dr. 
 Cabot said, things can look all right outwardly. In this case how- 
 ever the cord showed no lesions either macroscopically or micro- 
 scopically. The bone marrow of the femur showed the typical 
 picture of the marrow of pernicious anemia. 
 
694 FACTS ON THE HEART 
 
 The skin showed a pale brownish-yellow sallow color, a peculiar 
 color—something of the pernicious anemia color and a little bit more, 
 but not what we should call a very definite jaundice. In the cubital 
 spaces there were purplish spots,—the transfusion punctures. In 
 a few places there were minute pale purplish spots. Just below the 
 jaw on the right the subcutaneous tissues were slightly swollen. 
 This man had a perfectly definite glossitis and a streptococcus septi- 
 cemia. The culture from the heart blood showed a typical growth 
 of the streptococcus hemolyticus. 
 
 The mucosa of the stomach seemed a little pale; but we have been 
 unable to demonstrate definite lesions in any of the examinations 
 made on stomachs in pernicious anemia. 
 
 The intestines and glands were out of the picture. There were a 
 few old pleural adhesions on each side; no fluid in the cavities. The 
 thyroid gland was negative. No thymic tissue was found. - The 
 bronchial glands were slightly enlarged, and one on the right showed 
 obsolete tuberculosis. The lungs were edematous, the tissue spongy, 
 saturated with thin red bloody fluid which streamed from the section 
 surfaces,—a frank hemorrhagic edema of the lungs such as is asso- 
 ciated usually with a streptococcus infection. 
 
 The pericardial cavity was obliterated by dense tough old mem- 
 branous adhesions,—a perfectly clear cut chronic adhesive peri- 
 carditis. The heart weighed 520 grams,—considerably enlarged. 
 (Normally 200-400.) There were three factors here. (1) The 
 chronic adhesive pericarditis. That inand of itself, with no associated 
 chronic mediastinitis or pleuritis, would not be sufficient to produce 
 a heart of 520 grams. (2) There was a little arteriosclerosis. (3) 
 The third factor responsible for the hypertrophy and dilatation of 
 the heart was pernicious anemia. 
 
 The arteriosclerosis in this case was interesting. There was a 
 slight amount in the aorta and great branches, but the coronary 
 arteries showed well defined fibrocalcareous sclerosis with much 
 thickening of the walls and some decrease in the lumen. The valves 
 were negative except for increase of the circumferences. 
 
 The liver was rather large and pale. The gall-bladder added 
 another interesting fact in this case. It was moderately distended 
 with bile and contained at least 200 small concretions. At the time of 
 necropsy the bile ducts were free and showed no particular dilatation. 
 
 The pancreas was of good size and on section was seen to consist 
 of fatty tissue in which were embedded here and there islands of 
 pancreatic tissue,—so-called fatty pancreas or lipomatous pancreas, 
 
> 
 
 CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 695 
 
 we used to think associated with sugar. We have got over that. 
 There was a soft hyperplastic spleen, due in part to the septic process 
 and for the rest to the pernicious anemia. 
 
 The kidneys were rather large, weighing 480 grams (normally 
 200-400), but they were normal. The gastro-intestinal tract was 
 out of the picture. 
 
 Dr. Casort: Dr. Holmes, I should like to ask you, with the facts 
 that you have on the fluoroscopic report and the X-ray plate here, do 
 you see any evidence from which you might have suspected adhesive 
 pericarditis? ! 
 
 Dr. G. L. Hormes: In the note there is just one statement; 
 that is the indefinite outline of the heart. The X-ray findings indi- 
 cative of adhesive pericarditis are: (1) Limited respiratory move- 
 ments; the left border of the heart as a rule does not move to the same 
 extent that it normally does. That is not indicated on this tracing. 
 Whether they were unable to get any motion or whether they failed 
 to make the record I do not know. (2) The next important finding 
 is the obliteration of the various chambers, so that we are unable to 
 differentiate the auricle from the ventricle. (3) The third is the 
 indistinct pulsation. Apparently they did get some of that. 
 
 Dr. Casor: But as to the chambers you did not make any obser- 
 vation. There is no reason why the respiratory mobility of this 
 heart should be diminished? It was not hitched up to the pleura or 
 mediastinum ? 
 
 Dr. RicHArpDSON: No. The great pull comes when it is hitched 
 up with mediastinitis and pleuritis. 
 
 Dr. Cazsot: There is no reason why this heart should not go 
 up and down as well as any other way? 
 
 Dr. Hormes: I may be wrong about this. I have never had any 
 definite proof. But I believe that as a heart moves up and downit 
 rotates, and any adhesion to the surface of the heart would limit its 
 movement. 
 
 Dr. RICHARDSON: You say rotation. One would think it would lift 
 up. 
 
 Dr. Capot: Can you see the rotation in the fluoroscope? 
 
 Dr. Hormes: We can see the change in shape which corresponds. 
 So I should think this case would have given some evidence of limita- 
 tions of respiratory movement. 
 
696 ~- FACTS ON THE HEART 
 Necropsy 3738 
 
 A physician of forty-seven entered March 30. One brother had 
 an arrested case of tuberculosis. The patient had had no definite 
 exposure. His general health had been good. For the past twenty- 
 five years he had never been ill. 
 
 Since March 3 he had had gradual onset of malaise, backache, 
 and pain in the head, with chilly sensations and irregular tempera- 
 ture, sometimes as high as 102°. He had been up and about most 
 of the time, growing steadily worse. March 21 he went to bed. For 
 the first three days his temperature was usually 1o1° to 102°, with 
 occasional rises to 104° and frequent sweats. March 24 the leuco- 
 cytes were 19,000. March 25 a Widal was negative (paratyphoids?). 
 March 26 the leucocyte count was g,ooo. <A blood culture was nega- 
 tive. He had severe pain in the abdomen, somewhat relieved by a 
 hot water bottle. Half an hour later he had a severe chill, after 
 which the temperature was 103°. After this he had repeated chilly 
 feelings and sweats, with temperature normal in the mornings and 
 ranging up to 103° in the evening. 
 
 Examination showed a fairly well developed, emaciated man, 
 unresponsive and apparently very ill. The skin was dry, with a small 
 firm purpuric nodule on the left thigh. The mucous membranes were 
 dry and pale. The lips showed sordes. The sclerae showed ques- 
 tionable slight icterus. The tongue had a furry white coat. The 
 heart showed no enlargement. The action was slow and regular. 
 The sounds were distant. The pulmonic second sound was greater 
 than the aortic second. The first sound at the left border of the 
 sternum was rumbling. ‘There were questionable systolic and pre- 
 systolic murmurs at the apex and the left border of the sternum. 
 The blood pressure was 95/70 to 78/45. At the apex of the left lung 
 anteriorly was slight dullness with diminished breathing and voice ~ 
 sounds; no rales’ The abdomen showed slight general spasm. The 
 right kidney was easily felt, not tender. The genitals, extremities, 
 pupils and reflexes were normal. 
 
 The temperature was 97.5° to 106°, the pulse 78 to 162, the respi- 
 ration 10 to 44. The amount of urinewastoto520unces. Theurine 
 was pink at entrance, cloudy at four of twelve examinations. The 
 specific gravity was 1.009 to 1.026. There was the slightest possible 
 trace of albumin at two examinations, a trace of sugar atone. The 
 sediment showed hyalin casts at two examinations, granular and rare 
 waxy casts at one, an occasional cylindroid with red blood corpuscles 
 attached at one, red blood corpuscles at another. The hemoglobin 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 697 
 
 was 90%. ‘There were 33,000 to 12,600 to 60,400 leucocytes. A 
 blood culture was negative. March 30 a Widal was positive in 49 
 and 169 dilutions. Loss of motility was slow and not complete. 
 Agglutination was complete. Paratyphoids a and 8 remained free 
 and motile. ‘The patient had had typhoid inoculation six months 
 before admission. ‘The renal function was perhaps 40%; the color 
 was very bad. The blood nitrogen was 30 mgm. per roo c.c. of 
 blood. A throat consultant found nothing in the nose and throat 
 to account for the symptoms. A dental consultant found no involve- 
 ment of the right antrum. The lower first molar showed large 
 definite foci for absorption. There were no other findings to account 
 for the temperature. X-ray showed enlarged dense glands at both 
 lung roots, mottled shadows at the right apex, and thickening of the 
 markings running to the apices on both sides. The excursion of the 
 diaphragm was fairly good on both sides. The left side was a little 
 higher than normal. The conclusion was, tuberculosis of the right 
 apex. Pus pockets were found at the roots of two teeth. The 
 right antrum and right frontal sinus were cloudy. 
 
 Two days after entrance the temperature was 103° and the pulse 
 140. A systolic murmur was heard definitely at the apex and the 
 left border of the sternum. April 8 a right lower molar was extracted. 
 A pus sac was found between the roots and a small osteomyelitic area 
 below the roots. It was thought this area might account for the 
 temperature. 
 
 April 13 the patient was irrational, then semicomatose. 
 Although he could not be roused he was sensitive to pain, and showed 
 very slight wincing on pressure of the right mastoid tip and more on 
 pressure over the right molar. The left knee-jerk was increased. 
 There was no definite Babinski. There was clonus on the left, not 
 well sustained, and very suggestive Kernig. The neck was stiff. 
 Lumbar puncture gave clear fluid showing 27 red cells, no white cells, a 
 few diplococci of pneumococcus morphology, possibly contamination. 
 Culture from. the spinal fluid was negative. After the lumbar 
 puncture the patient showed a somewhat clearer mental condition. 
 A friend now said that before entrance he had complained at times 
 of severe headaches and had said that he felt as he imagined a patient 
 with meningitis would feel. 
 
 April 15 he was unconscious (?). Later in the day he recognized 
 his sister. Fifteen c.c. of spinal fluid was removed and 30 c.c. of 
 anti-meningococcic serum returned. Next day 12-15 c.c. was 
 removed and 20 c.c. of serum returned. A slight chill followed the 
 
698 FACTS ON THE HEART 
 
 injection. April 17 18 c.c. of cloudy fluid was removed at a pressure 
 of 110. The fluid showed 500-600 cells, 909%-95% _ polynuclears. 
 The rest was largely made up of mononuclear cells resembling endo- 
 thelial phagocytes. No organisms were demonstrable. 
 
 April 18 the patient seemed brighter. Right facial paralysis was 
 more marked than at any time previously. The knee-jerks were 
 present and about equal. There was neck sign, marked Kernig, 
 and indefinite Babinski. Next day he was much brighter than at 
 
 5 | 
 
 ea 
 
 S| 
 
 Fic. 142.—Section of the heart valve in Case 3738, showing the masses of bacteria 
 impinging on the valve. (xX 225.) (Photomicrograph by Lewis S. Brown. Dr. 
 William H. Smith.) 
 
 any time since the 14th. He said he felt comfortable and had no 
 headache, though he had had some. Dr. Cushing thought the 
 condition due to obscure sepsis rather than brain abscess, and the 
 left facial paralysis a peripheral palsy rather than central. The 
 temperature was subnormal in the morning, the pulse roo. Lumbar 
 puncture gave ro c.c. of clear fluid at a pressure of 90. Next day the 
 patient had a chill. He voided without catheterization for the first 
 time in days. Lumbar puncture gave to c.c. of clear fluid. Ten c.c. 
 of serum was injected. General trembling followed. A_ systolic 
 bruit, possibly transmitted from the aorta or a transmitted murmur 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 699 
 
 from the heart, was noted. Between April 15 and 21 the white 
 count ranged from 19,600 to 60,400. 
 
 April 21 lumbar puncture gave 8 c.c. of slightly yellow fluid under 
 no increase of pressure, showing 11o cells. April 22 the temperature 
 again reached 102°. The breathing was somewhat Cheyne-Stokes. 
 April 23 the patient was bright and talkative. The temperature was 
 102°, rising in the evening to 104°. The patient was delirious. 
 April 24 750 c.c. of blood was transfused. Later the patient had a 
 chill, and next day three more. The temperature ranged from 98°- 
 105. The mental condition was at times cloudy, occasionally clear. 
 
 Fic. 143.—Detail of Fig. 142. (X 1000.) Small capsulated streptococcus. (Photo- 
 micrograph by Lewis S. Brown. Dr. William H. Smith.) 
 
 The urine showed occasional red blood corpuscles, no albumin, sugar, 
 or casts. One blood culture showed staphylococcus albus and ques- 
 tionable spore-bearing bacilli. Another showed no growth. The 
 rises in temperature after the chills were now as high as 106°. May 6 
 the lungs were full of non-consonating and consonating rales both 
 front and back, with no definite areas of dulness. A loud harsh 
 systolic murmur was heard over the back and in both axillae. The 
 patient grew progressively weaker, continued to have chills, and was 
 a little irrational. Purpuric spots developed at every point touched 
 by the bed clothes. The lungs gradually filled up. May 23 he died. 
 
7OO FACTS ON THE HEART 
 
 Clinical Diagnosis (from Hospital Record)—Malignant endo- 
 carditis. 
 
 Dr. William H. Smith's Diagnosis —Septicemia. 
 
 Purpura. 
 
 Endocarditis of the mitral valve, chronic or acute or both. 
 
 Terminal pneumonia or infarction of the lungs. 
 
 Anatomical Diagnosis.—Chronic adhesive pericarditis. 
 
 Chronic interstitial myocarditis with necrosis. 
 
 Slight chronic endocarditis of the mitral valve. 
 
 Acute endocarditis of the mitral valve. 
 
 Hypertrophy and dilatation of the heart. 
 
 Streptococcus infection (small capsulated form). 
 
 Infarcts of the spleen, kidneys, and brain. 
 
 Acute nephritis and arteriosclerotic degeneration of the kidneys. 
 
 Purpura. 
 
 Chronic passive congestion, general. 
 
 Hydrothorax. 
 
 Slight ascites. 
 
 Slight fatty metamorphosis of the liver. 
 
 Edema piae. 
 
 Decubitus. 
 
 Obsolete tuberculosis of the bronchial glands and the apex of the 
 right lung. 
 
 Slight chronic pleuritis, right. 
 
 Dr. RicHARDSON: This was a case of infection with a minute 
 capsulated streptococcus. 
 
 The culture from the blood stream in this case was taken from the 
 inferior vena cava, and was negative. Usually in these cases we get 
 cultures from the blood stream. Once in a while we do not, but may 
 at times get a culture from the spleen. I think the reason is that the 
 organisms get into the blood stream and then disappear from it. 
 The peculiarity about the organism from the anatomical standpoint | 
 Was its apparent association with septic infarcts produced in various 
 parts of the body. ) 
 
 Polypous endocarditis of the mitral valve means simply that there 
 was a large mass of vegetations there. As a result of this we found 
 infarcts of the spleen, kidneys and brain. 
 
 It was a straightforward, definite picture of infection and the 
 production of septic infarcts throughout the body. 
 
 The heart did not show much hypertrophy and dilatation; it 
 weighed 356 grams (normally 200-400). The most striking thing 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 7OI 
 
 about it was the condition of myocarditis. As far as the coronary 
 arteries could be examined they were negative. The myocarditis 
 was probably of infectious origin. That brings us to the question as 
 to how that was brought about. The vessels probably became 
 plugged with these bacteria, a metastasis of these masses of organisms 
 extending into the vessels, with consequent degeneration and replace- 
 ment of the muscle tissue by fibrous tissue. In some places the tissue 
 was cut off so sharply that it was necrosed. 
 
 The spleen in these cases usually shows the largest infarcts. 
 There was a large infarct in this one. I have seen a very large spleen 
 consist practically of one great infarct. 
 
 The microscopical examination of the cardiac valves showed 
 masses of these bacteria, beautifully stained by Dr. Smith. (See 
 Figs. 142 and 143.) 
 
 Examination of the myocardium showed the replacement by 
 fibrous tissue of the muscle, and in places necrotic material. 
 
 It was a typical picture of the end results of infection by this 
 particular organism, the character being that of the production of 
 septic infarcts, metastasis from some common source, which in this 
 case seemed to have had its main depot on the mitral valve. 
 
 Necropsy 4152 
 
 An unmarried American nursery governess of nineteen entered 
 November 5, 1919, for relief of exhaustion. Her general health was 
 not very good. She had had whooping cough, measles and varicella. 
 She had rheumatic fever four times between the ages of eight and 
 twelve, confining her to bed with painful, red, tender, swollen joints. 
 She had had tonsillitis four or five times, confining her to bed from 
 one to three weeks. A hospital reported that her tonsils and ade- 
 noids were removed in 1913. ‘At the time of discharge the rheu- 
 matism had cleared up, but the heart condition remained the same.”’ 
 
 She had always been subject to nosebleeds, and once a month had 
 severe attacks lasting intermittently for several days. These had 
 been less for the past year. Two years before admission she was ill 
 five weeks with “‘pleurisy.”’ Every week or two she was ill in bed 
 for a day with frontal headache, with vomiting at intervals all day 
 and swimming of the eyes. These attacks had been less frequent 
 recently. She had been told she was yellow after some of these 
 headaches. She had been at a nerve sanatorium for the summer. 
 Her catamenia were regular every three weeks, lasting five to eight 
 
702 FACTS ON THE HEART 
 
 days with profuse flowing. Previous to six months before admission 
 it sometimes ceased for a week and returned with four or five days of 
 further flowing. She was very weak after periods. There was no 
 family history of excessive bleeding of any sort. So far as she knew 
 she was normal at birth, with no bleeding from the cord. 
 
 A year before admission she began to have less strength and to be 
 tired all the time. She did not lose color. She found that her 
 gums bled easily on brushing her teeth. Often she found a blood 
 spot the size of a fifty-cent piece on the pillow in the morning. 
 She seemed to bleed easily. A small cut might bleed half an hour. 
 After her tonsillectomy (see below) she bled for several hours. 
 
 Examination showed a well nourished girl. The gums were not 
 spongy. There was no bleeding. The tongue was protruded in the 
 midline with slight tremor. The throat was red. The tonsils were 
 ragged, reddened, with pus pockets. The lungs were clear. The 
 apex impulse of the heart was seen and felt in the fifth space 7.5 cm. 
 to the left. The percussion measurements were 9g cm. to the left 
 of midsternum, 2.5 cm. outside the nipple line, 2.5 cm. to the right, 
 supracardiac dullness 4.5 cm. The pulmonic second sound was 
 slightly accentuated. The pulses and artery walls were normal. 
 The systolic blood pressure was 125, the diastolic 80. The abdomen, 
 genitals, extremities, pupils and reflexes were normal. 
 
 The temperature was 98° to 99.4°, the pulse 74 to 93, the respira- 
 tions normal. - The output of urine was 1g to 31 ounces, the specific 
 gravity 1.012 to 1.030. ‘The urine was cloudy at all of three examina- 
 tions, alkaline at one. The hemoglobin was 70%, the leucocytes 
 5000 to 8200, the polynuclears 82%, the reds 5,272,000, the smear 
 normal. There was 4% reticulated cells. A Wassermann was 
 negative. X-ray showed the respiratory movements of the dia- 
 phragm normal, its outlines regular. The costophrenic angles were 
 clear. The heart shadow was enlarged in the region of the left 
 ventricle. The hilus glands were increased and some apparently 
 were calcified. There was also considerable thickening of the 
 markings running upward and outward on the left side. The changes 
 did not reach the apex or the periphery of the lungs. The appearance 
 was that of a peribronchial process with enlarged bronchial glands. 
 
 A culture from the tonsils showed no hemolytic streptococci 
 or diphtheria bacilli. November to she was discharged unrelieved. 
 
 January 21, 1920, she reentered for examination and tonsillec- 
 tomy, having had a blood examination by Dr. Bock a month earlier 
 showing 6,696,000 reds, hematocrit reading 33% cells, 77% plasma; 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 793 
 
 hemoglobin (Palmer) 110%, polynuclears 64%, bleeding time 3 min- 
 utes, clotting time 17 minutes. 
 
 Examination was as before except as noted. The skin was very 
 dark. ‘The tongue was protruded without tremor. The pulmonic 
 second sound was not accentuated. The apex impulse of the heart 
 was 11cm. tothe left. The percussion measurements were 12.5 cm. to 
 the left of midsternum, 5.5 cm. outside the midclavicular line, 3.5 cm. 
 to the right, supracardiac dullness 6.5 cm. The blood pressure 
 was 130/95. The temperature was 98° to 100°, the pulse 72 to 100, 
 the respirations 16 to 24. The hemoglobin was 80%, the leucocytes 
 5200 to 15,800, the polynuclears 78%, the bleeding and clotting 
 time as in December. 
 
 January 22 tonsillectomy was done under ether. Pathological 
 examination showed no tuberculosis or tumor. January 27 she was 
 discharged relieved to a convalescent home. 
 
 July 6, 1920, she returned for her third admission with the 
 following note from a physician: “Since January 27 she has been 
 well except for severe headaches of migraine type for three or four 
 weeks. She has had less asthenia than before tonsillectomy. Her 
 handkerchiefs have however shown purulent and occasional bloody 
 mucus. This attack began July 1 after swimming, with headache, 
 malaise, July 2 some precordial pain, with pulse 130 and fever 
 102.3... Ice bag to chest relieved pain. Aspirin and aconite 
 brought down fever. July 3 fever in a.m. 102.5°, reduced in p.m. 
 to 99.8°. Pain severe in morning. At night severe precordial pain 
 required two doses of morphia gr. 14 by mouth. July 4 fever 
 between 101.5° and 99°, less pain. The ice bag kept on continuously. 
 July 5 fever in the morning, subnormal at noon. Pain—arches of 
 feet complained of July 3, shoulders and knees July 5. Aspirin 
 started, gr. x every two hours, July 4. Mixed vaccine given by a 
 physician July 5.” 
 
 Examination showed the throat and tonsils slightly injected. 
 The apex impulse of the heart was seen and felt in the fourth space 
 12 cm. to the left, coinciding with the left border of dullness. The 
 right border was 3 cm. to the right, the supracardiac dullness 6.5 cm. 
 The action was rapid (114). The sounds were of fair quality. The 
 pulmonic second sound was greater than the aortic second, not 
 accentuated. There was a slight systolic murmur at the apex, not 
 transmitted. The pulses and artery walls were normal. The 
 systolic blood pressure was 105 to 115, the diastolic 65 to 80. Both 
 shoulders, particularly the right, showed slight limitation and pain on 
 
794 FACTS ON THE HEART 
 
 motion. The knees and ankles were slightly painful on motion. 
 The examination was otherwise negative. 
 
 At entrance the temperature was 101°, the pulse go, the respira- 
 tions 28. Afterwards the temperature and pulse were as noted in 
 the history, the respirations 16 to 30. The hemoglobin was 90%, 
 the leucocytes 8400 at entrance, afterwards 5000 to gooo, the reds 
 3,950,000 to 5,120,000 the polynuclears 70%. A Wassermann was 
 negative. X-ray showed the frontal sinuses rudimentary; no 
 evidence of definite sinus involvement. Four molars were un- 
 
 Fic. 144.—Necropsy 4152. Chronic adhesive pericarditis with hypertrophy and 
 dilatation of the heart. Measurements by X-ray at seven feet six months before 
 death. (Roentgenological Department, Massachusetts General Hospital.) 
 
 erupted, two rudimentary. A seven foot plate of the heart is shown 
 in Fig. 144. There was moderate general increase in the heart 
 measurements with some prominence in the auricular regions. Fluo- 
 roscopic examination showed the lung fields clear, the diaphragm 
 moving freely on both sides; no definite evidence of active tuberculosis. 
 The hilus shadow was considerably increased on both sides. There 
 was evidence of enlargement of the bronchial and peribronchial 
 glands. <A throat consultant found nothing in the nose or throat to 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 795 
 
 suggest focai infection. A nasopharyngeal culture showed organisms 
 like diphtheria bacilli. A blood culture was negative. 
 
 The patient was given soft solids. Fluids were forced. She was 
 ordered aspirin gr. xv every two hours until toxic. The temperature 
 was normal by the second day and remained so. July 18 the apex of 
 the heart was 14 cm. from midsternum almost in the anterior axillary 
 line in the fifth space. The action was regular and not rapid. The 
 sounds were of good quality. There was a soft blowing systolic 
 murmur at the apex transmitted to the axilla; also a definite sugges- 
 tion of a diastolic at the apex in the left lateral prone position. In 
 the recumbent position the left border was not more than 12 cm. from 
 midsternum. The apex shifted normally with change in position. 
 The lungs were negative. July 25 Dr. Edsall advised absolute rest 
 in bed for a considerable period. Slight pain in the right shoulder 
 persisted, and July 26 there was pain and stiffness in the left shoulder 
 and right ankle. July 18 the patient was up for the first time, rather 
 weak. August 8 the temperature had been normal for three weeks. 
 When she began to get up for a few hours a day the temperature rose 
 slightly, between 99° and 100°, the pulse 85 to 95. August 14 the 
 systolic murmur at the apex was rougher than before. No diastolic 
 was heard. The pulmonic second sound was reduplicated. August 
 18 X-ray of the chest was negative. That day Dr. Paul D. White 
 found the heart practically as at the last examination. 
 
 August 27 she developed mumps, which had disappeared by 
 September 5. She began to get up slowly, but developed a slight 
 gastric upset with slight rise in temperature, passing off in a few days. 
 September 24 there was another rise of temperature and pulse and 
 she complained of an intermittent substernal ache lasting from a few 
 minutes to an hour. She was kept in bed again. By the end of 
 October she was able to be up three or four hours without elevation 
 of temperature above 99° or pulse above 90. November 29 she was 
 discharged. 
 
 On leaving the hospital she was taken in an automobile and was 
 carried upstairs and put to bed. Next day she dressed, but did 
 not walk about, and lay on a sofa without exerting herself in any way. 
 The following day she had some pain in the joints with precordial 
 pain and fever. The fourth day the pains increased, the tempera- 
 ture was 103°, and she felt very weak. These symptoms persisted. 
 
 December 4, 1920, she entered the hospital for the fourth time. 
 Upon examination the apex impulse of the heart was very definitely 
 palpable in the second space 8 cm. to the left of the midsternum in 
 
 45 
 
706 FACTS ON THE HEART 
 
 the third, fourth and fifth spaces in the anterior axillary line. The 
 cardiac dullness was increased. The action was rapid, with the first 
 sound weak, the pulmonic second sound accentuated. A soft systolic 
 murmur was heard over the precordia. There was no definite 
 diastolic. The right pulse was much greater than the left; the 
 latter was barely perceptible. The blood pressure was 100/60. The 
 large joints were tender, especially the ankles. As before there was 
 no swelling, redness or heat. She showed moderate jaundice. The 
 examination was otherwise as before. 
 
 Fic. 145.—Necropsy 4152. The same, one month before death. Heart shadow 
 still roughly triangular and distinctly abnormal. (Roentgenological Department, 
 Massachusetts General Hospital.) 
 
 The temperature was 97.4° to 104.1° with daily swings of one to 
 four degrees. The pulse was 100 to 166. The respirations were 25 
 to 51. The amount of urine was normal when recorded. The urine 
 was cloudy, the specific gravity 1.012 to1.020. There was the slight- 
 est possible trace to a trace of albumin at all of seven examinations, 
 bile December 11. The hemoglobin was 80%, the leucocytes 39,600— 
 I1,200—23,300, the polynuclears 75%, the reds and platelets normal. 
 A blood culture showed no hemolytic streptococcus. The X-ray 
 findings were not the same as before. The heart shadow was now 
 roughly triangular and distinctly abnormal. (See Fig. 145.) 
 
 a 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 7O7 
 
 December 15 the heart impulse was very forceful, visible in 
 the neck. There were crepitant rales at the bases, more on the left, 
 and signs of fluid at both bases. A left chest tap gave 20 c.c., the 
 first to c.c. cloudy, opaque, straw-colored, the remainder apparently 
 almost pure blood. The resulting fluid clotted within two or three 
 minutes; apparently a transudate. Culture was negative. Decem- 
 ber 18 the chest signs were more marked, and there was a definite 
 diastolic murmur. The respiration was very rapid, and there were 
 rales in the left upper chest in front. A right chest tap gave 480 c.c. 
 of deep orange opaque fluid, specific gravity 1.018, cells not counted; 
 smear, 52% polynuclears, 48% leucocytes, many red blood cells; 
 Esbach 0.7%. December 20 there was less pain and the tempera- 
 ture was lower. There were very few rales. Next day there were 
 many rales throughout both chests and peculiar rales in the left 
 front in the region of the fourth and fifth ribs. Two days later the 
 right base was very dull. The patient was kept under morphia. 
 When not under it she complained of pain in the joints and precordia. 
 The dullness at the right base increased to flatness with diminished 
 signs. December 29 there was a questionable soft diastolic in the 
 pulmonic area. January 9 the patient died. 
 
 Clinical Diagnoses (from Hospital Records) —¥irst ENTRY: 
 Secondary anemia. 
 
 SECOND EntTrRY: Chronic tonsillitis. 
 
 Metrorrhagia. 
 THIRD ENTRY: Endocarditis, subacute. 
 FourtH Entry: Acute infectious arthritis. 
 Acute endocarditis. 
 Hydrothorax. 
 
 Dr. Ricahrd C. Cabot’s Diagnosis —Chronic adhesive pericarditis. 
 
 Acute endocarditis? 
 
 Myocarditis? 
 
 Passive congestion of the lungs. 
 
 Right hydrothorax. 
 
 Chronic streptococcus septicemia. 
 
 Anatomical Diagnosis —Chronic adhesive pericarditis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Slight ascites. 
 
 Slight hydrothorax, right. 
 
 Chronic pleuritis. 
 
 Slight chronic endocarditis of the mitral valve. 
 
708 FACTS ON THE HEART 
 
 Subacute endocarditis of the aortic valve. 
 Slightly defective closure of the foramen ovale. 
 Dr. RICHARDSON: We were not permitted to examine the head in 
 
 this case. The gastro-intestinal tract, other than for some reddening ~ 
 
 of the mucosa, passive congestion, was negative. There was slight 
 ascites. 
 
 In the right pleural cavity there was about 200 c.c. of thin pale 
 fluid, and a sight amount on the left,—a slight hydrothorax on the 
 right. There were scattered fibrous adhesions on each side. The 
 lungs showed chronic passive congestion and nothing else. 
 
 The pericardial cavity was obliterated by membranous adhesions, 
 and the two layers were firmly bound together. The heart weighed 
 650 grams, markedly enlarged. There was considerable dilatation 
 and a slight amount of chronic endocarditis of the mitral valve, anda 
 patch on the aortic valve. 
 
 The liver and spleen showed chronic passive congestion, well 
 marked. The spleen weighed 313 grams. There was no definite 
 nephritis. 
 
 Dr. Casot: There was no deformity of either of those valves? 
 
 ~ Dr. Ricuarpson: A fibrous ridge extending along the mitral; but 
 
 the note specifies that the deformity was slight. The most extensive 
 lesion was of the pericardium. 
 
 The culture made at the time of necropsy was negative, but in | 
 
 these cases we may get a negative culture when there may be foci of 
 infection in the body. 
 
 Dr. MERRILL: It might not be out of place to mention that that 
 fluid was found several months after the last chest examination, 
 which was in August. The fluid found at the time of death was 
 undoubtedly a subsequent development. 
 
 Dr. Casot: Yes; the heart was doing fairly well when you exam- 
 ined her; later it gave out. 
 
 Necropsy 4470 
 
 An American drug clerk of twenty-nine was brought to the 
 Emergency Ward March 23, 1921. The history was given by his 
 father. The patient had measles and chickenpox in childhood. 
 At twenty he had an operation on his nose. He had rare moderate 
 headache and occasional head colds. Skating and running did not 
 trouble him. His best, usual and present weight was 160 pounds. 
 
 He had been doing some extra work and for the past few days 
 had not felt well because of cold in the head. A day or two before 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 709 
 
 admission after eating pork he felt nauseated. Since that time he 
 had eaten little. He had slight cough. March 22 he came to his 
 father’s house very weak and apparently very ill. 
 
 Examination showed a fairly well nourished man with dry and 
 cyanotic skin. The mucous membranes were cyanotic, with gray 
 pallor. There was slight pyorrhea. The veins in the neck were 
 dilated. There was dullness to flatness with diminished breathing 
 and many moist bubbling rales at both 
 bases posteriorly. The apex impulse of (-FS=|3S] 93] 3 =] 
 the heart was diffuse in the fifth space rz {]—a Se 
 cm. to the left of midsternum, 2 cm. _ |]>mrermoel23)9 Rs cla7b¢h7| 
 
 ia 
 
 outside the midclavicular line. The 
 
 right border of dullness was 5.5 cm. to ope eS 
 the right, the supracardiac dullness 6. 106° 
 : : ; od Ba PE ae 
 
 cm. The action was irregular, very 
 rapid (168). Thesounds were snapping. 
 The pulmonic second sound was accen-  [loa5 
 tuated. An explosive systolic murmur _ |lgeol#lio ea We a 
 was heard. A systolic thrill was felt at — {}2t0/F/100° INE: EB: 
 UNS AU ENENA 
 the apex. The pulses were normal. 44 BSENMC EYES 
 i Hae, 100] Josefa SESE eg 
 The artery walls were palpable. The Ma ESSERE 
 blood pressure was 150/90 to 125/40 to Iho] logt_1a9¢ 4 44S 
 120/30. The liver dullness extended Ilo SERRE REE 
 
 from the fourth rib to 5 cm. bélow the 150! |150 LL a ged eg 
 ; wl kA Sa 
 
 costal margin. The edge was felt. M0) )Mr~iriry——T—y— 
 There was edema of the sacrum. The __ ||? 7 CUS RS ey 
 
 genitals, extremities, pupils and reflexes = ne itm a 
 were normal. 100 | {100 lig] DRS BS 
 
 The temperature and pulse for the |] 90] | 90 Se Tt 
 first week were as shown in Fig. 146. _ || 80 
 Afterwards the pulse was 89 to42. After |] 7} |” 
 April 4 the pt at, was not above _~ © a 
 
 ; ; Fic. 146.—Temperature and 
 
 normal. The respirations were 47 to 15. pulse in Case 4470 (first entry). 
 The output of urine was 22 to 63 
 ounces, the specific gravity 1.017 to 1.025. The urine was cloudy 
 at three of six examinations, alkaline at three. It showed the 
 slightest possible trace to a trace of albumin at all, was loaded 
 with red blood corpuscles at the first, showed hyalin casts at two 
 and a few large cellular casts at one. The renal function was 35 
 to 55%. The hemoglobin was 80%, the leucocytes 31,800 to 5400, 
 the polynuclears 86%. A Wassermann was negative. A blood 
 
ul 
 
 71i0o FACTS ON THE HEART 
 
 culture was negative. The non-protein nitrogen was 73.2 March 24, 
 39.6 April 7. The sputum was slightly bloody, with many disinte- 
 grated red cells and occasional staphylococci in tetrads. The stool 
 showed blood and a positive guaiac at one of four examinations. 
 
 The patient showed marked orthopnea. Bleeding helped him 
 more than anything else at first. It was found that he had taken 
 digitalis for some time. By March 28 he was comfortable and his — 
 color was good. April 5 he had hardly any dyspnea and looked like 
 an entirely different man. Some edema of the ankles was developing 
 which disappeared four days later after bandaging. Edema of the 
 dorsum of the feet persisted, however, while the patient was abso- 
 lutely at rest in bed. April 13 he was discharged. 
 
 After leaving the hospital he lay in bed for over a week, then 
 got up for his meals, then began to walk a little, and improved 
 steadily for three weeks. After that he had to wait on himself 
 more or less, and was worried. He soon found he felt weaker and 
 had increased palpitation and dyspnea. His doctor ordered him 
 
 819 
 
 5 0146 - 334 
 
 Fic. 147.—Measurements by percussion. 
 
 back to bed. May 20 he began to have trouble with his digestion, 
 due he thought to eating a bad orange. May 21 he vomited his 
 breakfast. 
 
 That day he returned to the hospital. He was orthopneic, 
 had palpitation very noticeably when he lay on his left side, and felt 
 tired, weak, and slightly nauseated. He urinated once at night. 
 
 Examination was as before except for the points noted. There 
 was considerable dyspnea and orthopnea. The skin showed a slight 
 yellowish tint. The mucous membranes were rather pale. There 
 were some carious teeth; no pyorrhea. The lungs showed slight 
 dullness and a few moist rales at both bases posteriorly. The dia- 
 phragm excursion was equal. The apex impulse of the heart was 
 diffuse, seen and felt in the fourth, fifth and sixth spaces as far out as 
 the anterior axillary line. Percussion measurements in cm. are shown 
 in the diagram. The action was rapid, absolutely irregular in force 
 and rhythm. The sounds were not distant. The pulmonic second 
 sound Was greater than the aortic second but not markedly accen- 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES ype 
 
 tuated. The sounds were difficult to make out because of irregu- 
 larity, but there seemed to be a definite systolic murmur all over 
 the precordia, loudest at the apex, a sharp first sound, no definite 
 diastolic murmur, pulses equal, synchronous, of varying volume and 
 tension. The artery walls were not palpable. The blood pressure 
 was 130/75-110/60-135 /60. 
 
 The temperature and pulse were as shown in the chart (Fig. 148) 
 until June 3. Afterwards the temperature was 96.5° to 98.4”, the 
 
 N} 3 Ni ne ote as le Se RV IY), f 
 fd Sees 
 aes) al OA Ga Se Oa ew OL [| 
 Days of Month Ri 2a3sbyoshéla7 b39136/3/1 7 [2 [5 | 
 Four-Hourly woe he 
 ati eee g 
 
 ard a Se ie Le | SA | eg [a] 
 
 “Lee 
 
 | ‘TORE e 
 | loo fa 
 if Vd WAT 
 
 170} | 96° 
 
 tee eS ») ia Wah [ed ek a 
 : -* e, wy, nT 
 - : WN 
 “~! UY - 
 ~ 
 
 160 fae} 95° lene J 
 Hiso| |150 PAES ERS SES Ba Pe 
 140} 1140 PAPO ES EEG iol ed Ge Ba ES a 
 
 colblied Collet Sos Ws CSRS 3 
 
 120] fools i es | Bae 8 | | | 
 
 ood OO a 
 OIE bAC MN 
 oN MIA OPW 
 CeCe CNC IN 
 #111 2 fos es | Joe 
 
 Fic. 148.—Temperature and pulse in Case 4470 (second entry). 
 
 pulse 62 to 92 except for one rise June 7. The respirations were not 
 remarkable. The output of urine was 15 to 120 ounces, the specific 
 gravity 1.026 to 1.008. The urine was cloudy or muddy at two of 
 seven examinations, alkaline at two, showed the slightest possible 
 trace to a trace of albumin at all, very rare red blood corpuscles at 
 one, many at another, leucocytes at two, hyalin casts at two, granular 
 at three, cellular at two. The hemoglobin was 80%, the leucocytes 
 
712 FACTS ON THE HEART 
 
 13,200 to g600, the polynuclears 59%. The non-protein nitrogen 
 was 53.4 mgm. A blood culture was negative. X-ray is shown in 
 Fig. 149. 
 
 In the left lateral position there was limited excursion of the left 
 border of dullness and the maximum impulse; probably some fixation, 
 but no retraction at the back. At the apex were a sharp first sound, 
 a presystolic murmur, a high pitched early systolic, a rumbling 
 middiastolic with split second sound, and a systolic thrill. 
 
 By May 31 the patient felt well. The heart was still irregular 
 but slower. There was less deficit. The exact part played by 
 quinidine was felt to be uncertain. June 4 the pulse was down to 7o. 
 
 OU eWlest 
 
 Fic. 149.—-Heart shadow is very much enlarged and roughly triangular in shape. The 
 greatest increase is in the region of the right auricle. 
 
 There was headache, probably, it was thought, from digitalis, which 
 was discontinued. By June 8 there was no more headache. The 
 pulse was down and steadier and by June 12 there was no deficit, 
 though there was irregularity at times. June 22 he was discharged 
 relieved. | 
 
 At his third admission, February 23, 1923, the history was 
 unsatisfactory because the patient was in too poor condition to talk. 
 Since his discharge he had been on his feet most of the day, but had 
 not lost a day’s work until the onset of this attack. He had been 
 taking pills given him by Dr. Paul White regularly until the attack. 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 125 
 
 Two months before admission he found that he could not work 
 so hard as formerly. He tired easily and was troubled in climbing 
 stairs. He paid no attention to these symptoms however until the 
 first of February, when he had to go to bed because of a cold in which 
 the predominating symptom was a “‘tired feeling.” The second day 
 of his illness he was found lying with his head thrown over the side of 
 the bed, unable to speak, his right arm and leg paralyzed. Since 
 that time the arm had slowly improved until at admission he could 
 write with some difficulty. He could move his leg and could speak, 
 also with difficulty. Since his ‘‘stroke’’ his memory had been 
 poor, he had used three pillows instead of one, had been very dyspneic, 
 had had cough with about a cupful a day of tenacious sputum, had 
 urinated three times at night, and had felt his heart beat very force- 
 fully at times and at other times apparently stop beating. Since 
 his cold he had had edema of the legs. 
 
 Examination showed an extremely weak, well nourished man 
 propped up in bed, slightly cyanotic, dyspneic, coughing frequently, 
 
 Wee Ne compression sigue ; 
 
 in interscapular 
 region 
 
 Acute cardio- Dullness, dim- 
 hepatic angle. Duliness, b 22, iS h inished breath- 
 liver dullnese distant bron- SIS ing, decreased 
 
 5th rit above, fremitus, many 
 moderate and 
 coarse moist 
 
 rfles,. 
 
 absent fremitus,7| V 
 many mediur and 
 coarse moist 
 rfles. 
 
 SSS] 
 Soa RTRWAS 
 Sete ey ‘) 
 
 Say 
 
 Liver palpable at 
 level of urbilicus, 
 slightly tender. 
 
 Fic. 150.—Physical signs in Case 4470 (last entry). 
 
 raising sputum with great difficulty. He seemed to understand what 
 was said and to be rational, but was unable to express what he wanted 
 to say and had great difficulty in naming objects. The skin was 
 moist and clammy, the face decidedly dusky. The mucous mem- 
 branes were pale and slightly cyanotic. There were a few scattered 
 glands in the cervical region. The apex impulse of the heart was 
 diffuse and heaving, seen and felt in the third, fourth, fifth and sixth 
 spaces, maximum in the sixth, 14 cm. from midsternum in the 
 anterior axillary line. ‘There was a well marked systolic thrill at the 
 apex. No diastolic was made out. No cardiac pulsation could be 
 made out in the left back. In turning from the right to the left 
 lateral position the apex impulse stayed in the same spot. The first 
 sound at the apex was short and snapping but not very loud. There 
 was a rather loud and reduplicated second sound. ‘The sounds were 
 absolutely irregular in force and rhythm, very rapid (130). A loud 
 
714 FACTS ON THE HEART 
 
 high pitched blowing systolic murmur was heard at the apex following 
 almost immediately after the first sound and filling most of systole, 
 transmitted well out in the axilla. There was a questionable 
 rumbling middiastolic at the apex. The blood pressure was 165/75 
 to 145/75. The lung signs and the abdomen were as shown in Fig. 
 150. There was moderate edema of the dorsal surfaces of the feet 
 and slight edema of the ankles. Neuro- 
 ‘Daraton logical examination showed in addition to 
 " Deections | the previous findings normal fundi, ques- 
 tionable slight numbness of the right side 
 of the face, and weak grip on the right. 
 The abdominal reflexes and the jaw-jerk 
 were absent. The right triceps, biceps, 
 radial and wrist reflexes were increased. 
 The temperature and pulse are as shown 
 in Fig. 151. The respirations were 22 to 
 4o. The output of urine was 4o to 33 
 ounces, the specific gravity 1.020. There 
 | was a large trace of albumin at the single 
 Re a examination, occasional hyalin casts and 
 (70 mn RR red blood corpuscles and leucocytes. The 
 PSBSBe | renal function was 15%. The hemoglobin 
 ia EERE was 75 to 80%, the leucocytes 8800, the 
 ed Pe id ff Td | polynuclears 68%, the reds normal. A 
 Hien} {120 Ke r 1.43 | Wassermann was negative. The non- 
 110 [2] 0 ea protein nitrogen was 59.2 mgm. An 
 too | 100 aaa electrocardiogram showed auricular fibrilla- 
 YM VK | tion, ventricular rate 80 to 100, diphasic 
 lbs T2; aberration as before. The sputum was 
 Pyare i Toren ee eae mucopurulent. The presenting organism 
 pulse in Case 4470 (lastentry). was a Gram-positive lanceolated diplo- 
 coccus. There was an occasional strepto- 
 coccus-like chain of Gram-positive diplococci slightly curved 
 and well encapsulated. A few Gram-negative bacilli, moder- 
 ately thick, were seen, a few Gram-positive bacilli, long and straight, 
 and a few with a slightly narrowed center, a fair number 
 of diphtheroids, a slight to moderate number of influenza bacill, 
 extracellular, and one questionable endothelial phagocyte with phago- 
 cytized bacteria. 
 February 5 the heart rate was slower. ‘Two diastolic murmurs 
 were audible, a soft blowing early diastolic along the left border of 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 715 
 
 the sternum and a low-pitched rumbling middiastolic murmur heard 
 best at the apex. The general condition was much improved. 
 
 February 7 the temperature rose to 103° and the patient was 
 much sicker. Throughout the whole right lower back were many 
 moist rales different from the rales on the other side. There were no 
 definite areas of consolidation. There was considerable abdominal 
 distension. The abdomen remained distended in spite of strenuous 
 measures. February 8 the right base was full of moist rales obscuring 
 the respiratory sounds. A marked transmission of cardiac murmurs 
 suggested consolidation at both bases. That afternoon he died. 
 
 Clinical Diagnosis (from Hospital Record).—Rheumatic heart 
 disease with mitral stenosis and regurgitation and aortic regurgitation. 
 
 Adhesive pericarditis? 
 
 Auricular fibrillation. 
 
 Congestive failure. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 mitral and aortic valves with mitral stenosis. 
 
 Acute endocarditis. 
 
 Chronic adherent pericarditis? 
 
 Hypertrophy and dilatation of the heart. 
 
 Cerebral embolism. 
 
 Chronic passive congestion. 
 
 Terminal pneumonia? 
 
 Anatomical Diagnosis——Chronic endocarditis of the aortic and 
 mitral valves. 
 
 Chronic adhesive pericarditis. 
 
 Thrombi in the right auricular appendix. 
 
 Area of softening in the left cerebral hemisphere. 
 
 Hypertrophy and dilatation of the heart. 
 
 Chronic passive congestion, general. 
 
 Infarcts of left lung. 
 
 Wet brain. 
 
 Edema of the ankles. 
 
 Anasarca. 
 
 Chronic pleuritis. 
 
 Old infarcts of spleen and kidneys. 
 
 Dr. RicHarpson: This man was poorly nourished. The pia 
 showed marked edema and a slight excess of fluid in the ventricles. 
 The brain tissue was negative except in the places to be mentioned, 
 but generally wet. In the left cerebral hemisphere beginning in the 
 region of the outer margin of the optic thalamus and extending along 
 
716 FACTS ON THE HEART 
 
 the basal ganglia for three cm. where at its anterior tip it touched the 
 outer end of the internal capsule, there was a very pale circumscribed 
 area of frank softening and disintegration about 2!4 X 2 cm. in 
 the other dimensions reaching to within 214 cm. of the cortex. The 
 vessels of Willis were all normal as far as made out, but the vessel 
 that contained the embolus was lost in the area of degeneration. 
 The pineal and pituitary glands were negative. 
 
 The ankles were slightly swollen and pitted on pressure. There 
 was no marked evidence of any edema elsewhere in the body. Much 
 brownish granular fluid material run from the nose and mouth. 
 There were brown-red spots in the left cubital space and some beneath 
 the left pectoral. | 
 
 The peritoneal cavity and appendix were negative. There was no 
 ascites, no anasarca. The only edema was in the ankles. The 
 stomach showed some passive congestion. The intestinal mucosa 
 was rather pale. 
 
 The mesenteric and retroperitoneal glands were negative. The 
 liver at the time of necropsy was one finger below the costal margin. 
 The diaphragm was at the fifth interspace on the right, on the left 
 at the sixth. 
 
 The right pleural cavity was obliterated by old adhesions infil- 
 trated by much thin pale brownish fluid. That is, of course, the 
 cavity was obliterated, but the fluid saturated the adhesions. Still 
 on the left there were only a few c.c. of thin brownish fluid and a little 
 fibrin. Both lungs showed a few old adhesions, but were otherwise 
 free. The trachea and bronchi showed purulent bronchitis. There 
 was typical chronic passive congestion of the lungs, and in addition 
 to that, areas of bronchopneumonia at the time of necropsy, best 
 marked on the right. The lower lobe on the other side was negative 
 for areas of bronchopneumonia, but curiously enough on that side 
 there was an infarct. 
 
 The pericardial cavity was obliterated by thin membraneous 
 adhesions; consequently there was no space for fluid. The heart 
 
 weighed 917 grams. I think if I say that is an enormous heart I shall ° 
 
 be excused. The myocardium was of good consistence, pale brown- 
 red. The night ventricle measured four mm., the left thirteen; that 
 is, of course, rather thickened. The foramen ovale was closed, 
 consequently nothing could pass from one side of the heart to the 
 other. Thecavities were greatly dilated. The mitral valvemeasured 
 tr cm., the aortic 714 cm., the tricuspid 14 cm., the pulmonary 9 cm. 
 These are all full-sized circumferences, the mitral measuring eleven 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES ae | 
 
 cm. although there were changes on it. The mitral curtain showed a 
 moderate amount of diffuse fibrosis with thickening and shortening 
 of the chordae tendineae. The free margin was thickened and a little 
 nodular. In the region of the junction of the cusps there was a large 
 fibrocalcareous plaque. On the anterior aortic cusp there was a 
 small fibrocalcareous mass, and elsewhere fibrocalcareous change 
 and deformity of the valve. No recent endocarditis was made out. 
 The pulmonary and tricuspid valves were negative except that their 
 circumferences were increased. In the right auricular appendage 
 there were two small thrombi. 
 
 So that we have here chronic endocarditis and chronic adhesive 
 pericarditis. This combination of lesions gives us our largest hearts. 
 The aorta and great branches were perfectly good. It rules out any 
 question of arteriosclerosis playing a réle in the condition. 
 
 The liver showed nutmeg markings. The bile-ducts, gall- 
 bladder, pancreas, negative. The spleen weighed 190 grams, was 
 plump, dark red and elastic,—chronic passive congestion. The sur- 
 face showed an area of infarction. 
 
 The kidneys weighed 485 grams. ‘The pelves, ureters, bladder, 
 prostate, seminal vesicles, testes, were negative. The kidneys were 
 large but negative except for small infarcts. 
 
 Necropsy 3736 
 
 A metal worker of thirty-three entered March 27, 1917, for relief 
 of vomiting and loss of weight. He had always been strong. For 
 
 6 
 
 3:5 9 
 Fic. 152.—Dimensions by percussion. 
 
 seven years he had had painful hemorrhoids. For four or five years 
 his skin had been yellow. In 1913 he had rheumatism involving 
 several joints and later was told by his doctor that he had a “leaky 
 heart.”’ A year before admission he was ill in a hospital two months 
 with a severe attack of gastric ulcer with delirium and much abdom- 
 inal pain. While convalescent he had an acute attack of articular 
 rheumatism and was in the hospital again fora month. He had done 
 
718 FACTS ON THE HEART 
 
 no work for a year. Since an attack of gonorrhea eight months 
 before admission he had been unable to retain his urine. In 1915 he 
 weighed 134 pounds, his best weight. In the autumn of 1916 he 
 weighed 128 pounds. 
 
 Since his illness in 1916 he had felt ill and tired all the time. His 
 bowels had been irregular. A month before admission he was in. 
 bed for two days with sharp pain across the entire front chest. He 
 had vomiting, which persisted. His appetite was poor. For a 
 month he had had frequent chills, shaking all over, and felt cold 
 all the time. 
 
 Examination showed an emaciated man 5 feet 5% inches in 
 height, weighing 9714 pounds. The skin and mucous membranes 
 were pale, the former dry. There were hard, shot-like axillary, 
 inguinal and epitrochlear glands. The apex impulse of the heart was 
 felt in the fourth space 9 cm. from midsternum. The dimensions by 
 percussion and by X-ray are shown in Figs. 152 and 153. The action 
 
 5.8 was regular, slightly rapid. The aortic 
 second sound was slightly accentuated. 
 There was a blowing systolic murmur 
 transmitted to the axilla and the base, 
 with a slightly musical quality over the 
 lower sternum. There was a split 
 second sound followed by a thrill and a 
 short soft diastolic not transmitted to 
 the axilla or the base but heard well 
 
 12 ————— over the body of the heart. The artery 
 Fic. 153.—Dimensions by X- = 
 ray. Diameteratbase11.2. Ques- Walls wereslightly palpable. The blood 
 teats Er ce eae of the pressure was 95/45 to105/50. Theliver 
 dullness extended from the fourth space 
 to the costal margin. ‘The rest of the examination was negative. 
 
 The temperature was 94.3° to 104.8° usually elevated, the pulse 
 70 to 160, the respiration 20 to 36. The amount of urine was 9g to 
 35 ounces, the specific gravity 1.022 to 1.012. There was the slightest 
 possible trace of albumin at the last of seven examinations. One 
 specimen showed cellular and granular casts, two showed pus. The 
 hemoglobin was 85%. There were 18,800-5200-52,700 leucocytes, 
 89 to 70% polynuclears, 3,840,000 reds, slight variation in size and 
 shape, no stippling. A Wassermann and a Widal were negative, 
 a gonococcus fixation test strongly positive. 
 
 For nearly a month the patient showed little change. The 
 temperature oscillated between 98° and 104.8°. Lead was reported 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 719 
 
 in the urine and stools April 8.* Vomiting and chills persisted. 
 April 23 he had an attack of sharp substernal pain with marked 
 pallor. There was no change in the heart murmurs. 
 
 From this time on he complained of pain in the apical region. 
 May 3 a pericardial rub was heard. (See Fig. 154.) Thoracentesis 
 yielded no fluid. Pericardicentesis was done next day in the fourth 
 left and right spaces next to the sternum, and in the third space 3 cm. 
 to the right of the sternal border. Blood was obtained in the third 
 
 Dull. Bronchial 
 breathing and 
 egophony, distant. 
 Tactile fremitus 
 
 Pericardial 
 rub, 
 
 Dull. to flat. 
 
 Fic. 154.—Physical signs in Case 3736. 
 
 and fourth right spaces, nothing at the fourth left space. The heart 
 was felt at the end of the needle at each puncture, and the patient 
 complained of pain at each. 
 
 May 3 X-ray showed the chest as in the illustration. A Widal 
 was negative. May 12 the pericardial rub was faint, obscured by a 
 
 7°5 
 
 7-5 13 
 20.5 
 
 FIG. 155. 
 
 loud systolic murmur at the base. There was much pain in the side 
 and over the precordia. ‘The measurements by percussion are shown 
 in Fig. 155. May 21 there was a systolic murmur at the apex and 
 the aortic area, dullness at both bases, more on the right, with 
 diminished breath sounds and coarse rales. That day he died. 
 
 Clinical Diagnosis (from Hospital Record).—Ulcerative 
 endocarditis. 
 
 Cardiac failure. 
 
 Dr. William H. Smith's Diagnosis—Chronic endocarditis of the 
 mitral valve. 
 
 *The finding of lead in the urine and stools may explain his epigastric pain. 
 
 This emphasizes the importance of associating occupation (metal worker) with 
 abdominal pain. W. H. Smith. 
 
720 FACTS ON THE HEART 
 
 Presumably acute endocarditis of the mitral and aortic valves. 
 
 Dilatation of the heart. 
 
 Pericarditis, with little if any effusion. 
 
 Passive congestion. 
 
 Possibly acute glomerulo-nephritis. 
 
 Anatomical Diagnosis ——Ulcerative endocarditis of the aortic 
 valve. | 
 
 Chronic endocarditis of the mitral valve (stenosis). 
 
 Chronic adhesive pericarditis. 4 
 
 sm 
 
 Fic. 156.—May 3. Shows a shadow over the lower two-thirds of the left base, 
 higher in the axillary than in the median line. The shadow of the diaphragm is obliter- 
 ated. The heart shadow is very much enlarged. Its shape suggests fluid in the peri- 
 cardium. Pulsation is diminished. Conclusion: fluid in the left chest and probably 
 fluid in the pericardium. 
 
 Septic aortitis with thrombus formation. 
 
 Hypertrophy and dilatation of the heart. 
 
 Septicemia, streptococcus. 
 
 Suppurative infarcts of the spleen with abscess formation. 
 Infectious nephritis. 
 Acute glomerulo-nephritis. 
 Foci of pneumonia. 
 Fibrinopurulent pleuritis, left. 
 
 ~ ae > = 
 a | 
 
CHRONIC PERICARDITIS—ILLUSTRATIVE CASES 721 
 
 Chronic passive congestion, general. 
 
 Decubitus. 
 
 Slight chronic pleuritis. 
 
 Dr. RicHARDSON: There was not a luetic but a septic aortitis with 
 thrombus formation in this case. The heart weighed 315 grams. 
 There was some dilatation of the right cavities. The man was 
 slender and rather short. A normal heart for him would weigh 
 about 260 grams, so that the hypertrophy and dilatation was slight. 
 
 The condition at the mitral valve was a chronic one that occurred 
 years ago. There was fibrosis of the curtain and a shortening of the 
 chordae tendineae, with decrease in the circumference of the valve. 
 The endocarditis of the aortic valve was an acute process. Then an 
 area on the wall of the aorta was attacked and a septic aortitis was 
 set up, with formation over it of a large thrombus mass. The inter- 
 esting point about this is that it shows that some of the cases of aor- 
 titis may not be luetic but may be due to some of the other 
 micro-organisms. 
 
 There was a thick layer consisting of fibrous strands in the 
 pericardium. In the anatomical record I described it as a thick, 
 edematous layer. That means there is fluid there, and some coagula- 
 tion of the fluid, at least at the time of death. Sometimes with 
 transudates we get a fibrin clot; that may be the case here. There 
 was a layer of fibrous adhesions there, but much of the thickness was 
 due to the edema. 
 
 There was fibropurulent pleuritis on the left, perhaps too c.c. of 
 purulent fluid material. The right side was negative. 
 
 The infarct in the spleen came from the masses washed out either 
 from the aortic valve or else from that thrombotic material in the 
 situation of the septic aortitis. The spleen in this case was repre- 
 sented by a large ovoid mass about eight inches in diameter. That is 
 a pretty good-sized spleen. There was little splenic tissue left, and 
 that was wrapped around this large abscess filled with broken down, 
 necrotic material and pus. 
 
 In the kidneys there were some foci of infectious nephritis. 
 
 The cultures were taken from the blood of the inferior vena cava 
 because of the mass of thrombotic material on the aortic wall. We 
 obtained a profuse growth of a fine streptococcus which is more 
 closely related to the pyogenic than it is to the hemolytic strep- 
 tococcus. From the spleen we obtained a few streptococci and a 
 profuse growth of the staphylococcus aureus. ‘There was probably 
 
 a double infection which would account for the large abscess in the 
 46 
 
722 FACTS ON THE HEART 
 
 spleen and possibly for the small areas of infectious nephritis present 
 in the kidneys. 
 
 Here again we have the end result of an infection of years ago 
 illustrated by the chronic endocarditis of the mitral valve and the 
 chronic adhesive pericarditis. Besides that we have acute endocardi- 
 tis at the aortic valve, septic aortitis, the condition in the kidney, 
 pneumonia, and abscess of the spleen. One very interesting thing 
 was the septic aortitis. 
 
CHAT DERI] 
 THYROCARDIAC DISEASE 
 1. THE OVER-DEMONSTRATIVE HEART 
 
 One of the earliest cardiac manifestations of thyrotoxicosis and 
 one which, if we are on the watch for it, may give us the signal to 
 look deeper and so to identify the disease itself, is the extraordinary 
 demonstrativeness of the heart. It makes its presence strikingly, 
 to the patient distressingly, obvious to sight, to touch and to hearing. 
 There seems to be a great deal of the heart in contact with the chest 
 wall, so that (for example) a heart weighing only 365 grams bangs 
 against the ribs in the anterior axillary line and shakes the whole 
 thoracic cage. When we feel of this shock, we are amazed at its 
 violence and prone (mistakenly) to believe that we are feeling a 
 systolic or pre-systolic thrill. When we listen over it, the sounds 
 are almost painfully loud, louder than in any other condition except 
 one, presently to be mentioned. These surprisingly loud heart 
 sounds, with or without a systolic murmur, should always make us 
 suspect thyroid poisoning. 
 
 All this sound and fury is due presumably to the irritation 
 of the cardiac mechanism by the perverted thyroid secretion, com- 
 bined with the lowered vascular tension. These influences are shown 
 in the large pulse pressure (often a true ‘‘Corrigan pulse’’) the 
 capillary pulsation, jumping arteries and loud arterial sounds, as 
 well as in the flushing and sweating from which some patients 
 suffer much. 
 
 The only condition, so far as I know, that simulates the over- 
 demonstrative heart of thyrotoxicosis, is the so-called ‘‘effort 
 syndrome”’ (soldiers’ heart, neuro-circulatory asthenia) which is the 
 cardiac manifestation of great nervousness. By cardiovascular 
 examination alone the two diseases may be indistinguishable, but 
 luckily the history and the metabolism test—high in thyroid poison- 
 ing, normal in effort syndrome—make it easy to distinguish them in 
 almost every case. 
 
 723 
 
124 ‘FACTS ON THE HEART 
 
 2. EARLY CONGESTIVE HEART FAILURE IN THYROID DISEASE 
 
 In spite of the seemingly desperate exertion of the racing thyroid 
 heart, cardiac failure is rare in the acute exophthalmic goitre of 
 young persons. Even when the organ seems actually driven to 
 death, there is usually no sign of passive congestion before death orat 
 necrospy. It is usually'a toxic, not a congestive death. There are 
 but three cases of our series to illustrate congestive failure. 
 
 In necropsy 425 we were studying the organs of a patient who 
 three years earlier (1896) had been treated in our clinic for “‘rheuma- 
 tism’’? and for some supposed cardiac result of it. The thyroid 
 disease, if it existed, passed altogether unnoticed until six months 
 later when after her second period of hospital treatment (214 years 
 before her death) the diagnosis was changed to ‘“‘exophthalmic 
 goiter with chronic endocarditis.” She gave the history of an 
 illness interpreted as “‘rheumatic fever’? which had occurred a few 
 months previously and stated that every August for as long asshe 
 could remember she had had a peritonsillar abscess. With this 
 history, with an extension of cardiac dullness to one inch outside the 
 nipple line and with a loud apical systolic murmur, it was natural 
 enough to consider the case one of rheumatic endocarditis with 
 valvular deformity. But one point should have made us suspect 
 that we were wrong. ‘The record states that “the heart sounds were 
 very strong, sharp, quick and regular.”’ 
 
 Six months later (January, 1897) when the thyrotoxicosis 
 had been recognized, the record reads: ‘‘Cardiac impulse in the 5th 
 interspace, 3 fingers’ breadth outside the nipple, the right border of 
 dullness one finger to the right of the sternum. Pulse rapid, easily 
 compressed, regular. Rough blowing systolic murmur at the apex, 
 transmitted to the axilla. Pulmonic 2nd accentuated. Bruit de 
 galop in the 2nd right interspace.” 
 
 Two and a half years after this—at her 3rd and last hospital 
 entry—the cardiac apex was in the anterior axillary line (5th inter- 
 space). Otherwise the heart was as before. Necropsy, however, 
 showed no hypertrophy or dilatation of the organ (weight 365 grams) 
 although there were a few old pericardial adhesions in addition to the 
 thyroid poisoning. ; 
 
 In this case—and in only one other of our series (No. 3180, page 729) 
 there were signs of passive congestion before death and after it. 
 Ascites had developed and the abdomen was tapped three times for its 
 relief during the year preceding her death. The legs were edematous 
 during this period. Post mortem the spleen and kidneys showed the 
 
TOXIC DEATH spel 
 
 passive congestion especially well. The heart showed no myocardial 
 or valvular lesions and if the ‘‘rheumatism”’ of 1896 affected her 
 heart at all, it was in producing the pericarditis still recorded in the 
 localized adhesions found at necropsy. 
 
 No metabolism measurements are recorded in this case but 
 the continued fever without evidence of infection post mortem, the 
 exophthalmos, tachycardia, goitre, tremor, muscular twitchings, 
 insomnia and vomiting, leave little doubt as to the diagnosis. 
 
 3. TOXIC DEATH 
 
 Toxic death is much commoner than congestive failure in acute, _ 
 primary, exophthalmic goiter. In Hamilton’s* series there were 
 but seven congestive deaths among 18 fatal cases. The rest were 
 toxic. In our series there were 6 toxic to 2 congestive failures— 
 almost the same proportion. 
 
 In these patients who died a toxic death, the appearance of 
 cardiac enlargemeni during life, though necropsy showed none, was 
 sometimes as striking as in those ending by congestive failure. The 
 records contain such data as this: 
 
 t. (No. 2077) A woman of 24. Apex 6th interspace, 1 finger’s 
 breadth outside the nipple. Dullness 2 fingers’ breadth to the 
 right of the sternum. 
 
 Necropsy: Heart weight 260 grams. No enlargement. Normal 
 myocardium and valves. Persistent thymus. Bronchopneumonia. 
 Streptococcus sepsis. 
 
 2. (No. 3468) A woman of 29. Transverse dullness 27 cm. 
 Supracardiac dullness 9 cm. 
 
 Necropsy: Heart weight 220 grams. Myocardium and valves 
 normal. No enlargement. Status lymphaticus (with persistent 
 thymus). Purulent pleuritis. Purulent pericarditis. Pigmented 
 skin. 
 
 3. (No. 3731) A woman of 23. “Heart greatly dilated’’ just before 
 death (from lobar pneumonia). 
 
 Necropsy: Heart weight 270 grams. Myocardium and valves 
 normal. Hypoplasia of the aorta. 
 
 4. (No. 3825) A woman of 20. Impulse diffuse and forceful. 
 Sounds loud and snapping. ‘‘ Blowing systolic murmur and systolic 
 thrill at apex.”’ 
 
 Necropsy: Heart weight 315 (considered to be slightly enlarged, 
 as the patient was a girl of 20). Valves and myocardium negative 
 
 * Hamilton: Journ. of the A.M.A., Aug. 9, 1924. 
 
726 FACTS ON THE HEART 
 
 (note the mistake about the ‘‘thrill”). Status lymphaticus (with 
 persistent thymus). 
 
 In two other patients of this group (exophthalmic goitre with toxic 
 death) there was no apparent cardiac enlargement in life and none 
 post mortem. All these six patients had the typical manifestations 
 of fever, vomiting, diarrhoea, sweating and extreme tachycardia. 
 In one, the motor restlessness was so extreme that the skin had become 
 hyperaemic and morphia was needed to prevent her wearing it 
 through and forming bed sores. 
 
 Status lymphaticus with persistent thymus was present in five 
 
 out of six cases, a finding noted by many writers but ignored by 
 , many clinicians. 
 
 The characteristically high pulse pressure was well shown in one 
 of this group, a woman of 38, with very acute toxaemia leading to a 
 toxic, non-congestive death, four weeks from the first symptoms 
 noticed. The pulse averaged 166 but was regular. The blood 
 pressures, recorded three times in the 12 days of her life in the ward, 
 showed: 160/60, 170/65, 155/85. 
 
 5. (No. 3705) An American woman of 58 had noticed exophthal- 
 mos ever since her first pregnancy 20 years ago. Last summer she 
 noticed goiter, three months ago her daughter noted that her pulse 
 was usually above 120. Four weeks ago she had a sudden attack of 
 tachycardia, dyspnea and vomiting. Two weeks ago a fine tremor 
 of the hands appeared. She had been very nervous. 
 
 Examination showed moderate exophthalmos with lid lag and 
 diminished reflex winking. Moderate general thyroid enlargement 
 with a systolic bruit. The pulse was rapid (120-150) and absolutely 
 irregular, with sharp heart sounds and a soft systolic at the apex. 
 Slight edema of the legs with coldness and no pulse in the dorsalis 
 pedis. Fibrillation persisted despite rest and digitalis and she died 
 in 12 days. 
 
 Necropsy showed a sclerosis of the left coronary with marked 
 decrease in its lumen, slight fibrous myocarditis, general arterio- 
 sclerosis, thrombosis of the left auricular appendage and embolic 
 occlusion of the abdominal aorta. Streptococcus sepsis. No 
 general passive congestion. 
 
 This is probably a purely toxic case without heart failure though 
 the cardiovascular system (through thrombosis and embolism) was 
 immediately responsible for her death. 
 
TOXIC ADENOMA AND EXOPHTHALMIC GOITER 727 
 
 4. LATE CONGESTIVE FAILURE IN TOXIC ADENOMA AND EXOPHTHALMIC 
 GOITER 
 
 Plummer, Boothby, Hamilton,* Coller,f and others, have 
 recently aroused a much needed interest in another clinical picture 
 long ago described by Kraus tf as ‘‘Gotter heart.’”’ This term means 
 the development of cardiac failure in persons (usually women) who 
 have long had a goiter (or a small hyperfunctioning thyroid with- 
 out visible goiter) but no considerable symptoms until cardiac 
 manifestations appear. In Hamilton’s 50 cases (34 of primary 
 hyperthyroidism and 16 of adenomatous thyroid with secondary 
 hyperthyroidism) 42 were women with an average age of 50 (but look- 
 ing much older). 41 of the 50 had a history of severe prolonged heart 
 failure, confining them to bed or to a chair for months or years and 
 resisting treatment. ‘The heart rate was usually high, often 180-200, 
 falling below too with rest and digitalis in only 14 cases. Stubborn 
 tachycardia was thus a feature of 36 cases. Goiter and exophthalmos 
 were noticeable in only afew. Emaciation was notable in 43 (average 
 weight 1og pounds despite edema) and even in the other seven, there 
 had been a loss of 30 pounds or more. Pigmentation of the skin local 
 or general was present in 48 of 50 cases, mental apathy or exhaustion 
 in 28. 48 out of 50 had auricular fibrillation. The metabolism 
 tests, which one might expect to be quite characteristic, are not so in 
 fact for, though they show marked increase (16+ to 125++, average 
 61.8+), similarly high figures can be obtained in non-thyroid heart 
 failure. 
 
 We have here a clinical picture, the great importance of which 
 (despite its rarity in non-goitrous districts$) is obvious because 
 operation seems to offer some possibilities of relief and even of cure. 
 I venture to say that by most clinicians it is still overlooked; yet in 
 goitrous districts it is not rare, as the studies of Coller make apparent. 
 In 300 cases of endemic goiter without toxic symptoms, occurring in 
 persons past the 2oth year and with normal metabolism,|| Coller 
 records the following valuable observations: 
 
 * Hamilton: Op. cit. 
 
 { Coller: Journal of the A.M.A., May 31, 1924. 
 
 t Kraus, F.: ‘Uber Kropfherz: Wien Klin. Woch., 1890, XII, 416. 
 
 § Hamilton found but 50 cases of this type among goo patients with thyrotoxicosis 
 at a Boston clinic. 
 
 || Not over 15+ or15—. ‘These are selected non-toxic cases. About 14 of Coller’s 
 hospital cases of thyroid adenoma, between 30 and 50 years of age, show increased 
 metabolism. ‘ 
 
728 FACTS ON THE HEART 
 TABLE 158 
 
 Pulse Cardiac A necntte Palpi Signs of 
 rate* over| enlarge- P Dyspnea tracheal 
 
 fibrillation] tation 
 I0o ment pressure 
 
 Age 20-30 18% 
 
 Age 31-40 36% 
 
 24% 
 
 26% 
 
 * Counted at the heart’s apex during sleep. 
 
 In view of Hamilton and Coller’s findings it certainly behooves 
 us all to study more closely our cases of unexplained cardiac failure in 
 elderly women, especially when they are of the apathetic and pig- 
 mented type, not improving as one would expect under rest and 
 digitalis and maintaining a persistent tachycardia with fibrillation. 
 
 In our series there are a few which, though not recognized in 
 life as belonging to the thyrocardiac group, may perhaps retrospec- 
 tively be placed there. So far as I know, very few post mortem 
 examinations are yet recorded in cases of this type; therefore it seems 
 worth while to give our results in some detail. 
 
 t. (No. 2067) A woman of 47, seen in 1908, had noticed a goiter 
 since she was 11 years old. It enlarged with each of nine pregnancies 
 and grew somewhat smaller again between them, but on the whole 
 gradually increased in size. For the past two years she had been 
 growing ‘“‘nervous”’ and felt too warm much of the time, so that she 
 preferred cold weather. Tremor of the hands had been noticed for 
 six months. 
 
 Examination showed slight exophthalmos, considerable emacia- 
 tion, marked tremor and goiter (1614 inches circumference), a very 
 rapid heart with a presystolic roll at the apex, a congested liver and 
 swollen legs. ‘The urine three times examined showed a gravity of 
 toro to 1012, traces of albumen and, in one specimen alone, a few 
 hyalin casts. She died in five days, the heart rather suddenly 
 giving out a few hours before the end. Necropsy showed a heart 
 weighing only 405 grams but considered the seat of hypertrophy and 
 dilatation. ‘There was also hydrothorax, hydropericardium, ana- 
 sarca and general passive congestion, with a thyroid adenoma and a 
 chronic glomerulo-nephritis (the latter an astonishing feature in view 
 of the negative urine). Possibly the congestive failure in this case 
 
TOXIC ADENOMA AND EXOPHTHALMIC GOITER 729 
 
 may be attributable to the nephritis and its effects on the heart, 
 rather than to the thyroid. 
 
 2. The other congestive failure of this series was in a woman of 32; 
 heart No. 493 grams. In 3189 the heart was not at all enlarged (285 
 grams). But the clinical picture was characteristically one of very 
 considerable cardiac enlargement. ‘Though the heart was not enlarged 
 post mortem the apex impulse was “‘heaving”’ and extended 3.5 cm. out- 
 side the nipple linein the 5th interspace. There was also visible systolic 
 pulsation along the left sternal margin and in the 2nd right interspace, 
 as is often the case in exophthalmic goiter. This is due inpart, per- 
 haps, to the lack of normal pulmonary expansion, the heart’s surface 
 being less covered by lung than normal. This patient had auricular 
 fibrillation during the three days of her life inthe hospital ward. 
 There was also a loud rough apical systolic murmur and a very loud 
 tst sound, with great accentuation of the pulmonic 2nd. Yet the 
 valves were negative at necropsy and there was no evidence of the 
 cardiac dilatation and hypertrophy which had seemed so obvious in 
 life. This patient was 45 years old, had had goiter for 17 months, 
 exophthalmos and “nervousness”? for two years, tremor for 7 
 months. In 214 years her weight had fallen from 140 pounds to 86 
 pounds. Her skin was generally pigmented. Palpitation had been 
 noticed for two months and diarrhoea for the same period. 
 
 Histologically the thyroid showed tubular elements of varying size 
 formed of cylindrical cells, sometimes with short papillary ingrowths. 
 No colloid. 
 
 3. (No. 3739) A negress of 50 was seen in May, 1918, complaining 
 that for years she had had a bad heart and at times been disabled 
 by it, but never so severely as in the past six months when her 
 dyspnoea increased toorthopnoea. Dropsy appeared a few weeks ago. 
 
 On examination she was found to be poorly nourished, cyanotic, 
 with evidence of much edema in the lungs, legs, liver and subcu- 
 taneous tissues generally. There was moderate symmetrical thyroid 
 enlargement. The heart’s dullness reached 10.5 cm. to the left and 
 5.5 cm. to the right of mid-sternum; its action rapid and regular. A 
 rough systolic murmur and a suggestion of a presystolic was heard 
 at the apex. The pulses and artery walls normal. The pulse ranged 
 from 110 to 200 during 10 days’ observation, usually above 150. 
 The systolic blood pressure 170, diastolic 80. At times there was 
 fibrillation. 
 
 Necropsy showed a heart weighing 280 grams but as the 
 woman was but 4 feet, 1034 inches high, this weight was considered 
 
730 FACTS ON THE HEART 
 
 about 60 grams beyond her normal, i.e., moderate hypertrophy and 
 dilatation. The aorta was capacious, fibrous and inelastic and in 
 its abdominal portion there were some fibrous and fibrocalcareous 
 areas. The myocardium and valves were normal except for slight 
 fatty degeneration in the myocardium, such as is often associated 
 with infection or anemia (both of which were absent). The rest 
 of the body showed nothing, except general passive congestion, to 
 explain the death, although there was a slight degree of chronic 
 interstitial hepatitis, obsolete tuberculosis in the bronchial glands 
 and a few small foci of fibrosis in the kidneys—not sufficient to affect 
 their function. 
 
 Mitral stenosis and regurgitation and possibly a similar lesion 
 at the aortic was the diagnosis in life, with chronic hyperthyroidism 
 and auricular fibrillation. 
 
 Possibly an operation on the thyroid early in this patient’s 
 illness might have saved her from the fatal decompensative attack. 
 
 4. (No. 3961) A woman of 46 gave in 1919 the history of a goiter 
 which she had noticed for 15 years, increasing and decreasing in — 
 size. Her eyes, she said, “chad always been prominent.” ‘Two 
 years ago she began to notice dyspnea and palpitation; later 
 edema of the legs and loose cough. For six months she had had 
 diarrhoea (3-5 movements daily). For nine weeks she had been 
 orthopneic and for four weeks vomiting had occurred almost every 
 day. Recently tremor of the hands, increased circumference of the 
 neck, increased edema of the feet, nervousness and restlessness 
 had been noticed. In five weeks her weight had fallen from 145 
 pounds to 100 pounds. 
 
 Examination showed poor nutrition, nervous restlessness, a 
 warm moist skin, a questionable slight exophthalmos and lid-lag, 
 a smooth elastic enlargement of the thyroid, more marked on the 
 left but without thrill or bruit, and coarse tremor of the fingers. 
 The heart showed no enlargement or arrhythmia; rate 77-131; a 
 snappy first sound and a slight systolic murmur. At this time 
 there was no evidence of passive congestion in the lungs, liver or 
 legs. Two weeks after entrance she became drowsy and ate but 
 little. Next day auricular fibrillation began and persisted until 
 death a week later. There is no record of a metabolism test. 
 
 At necropsy the left ventricle showed slight hypertrophy. There 
 was a suppurative nephritis (of which there was no evidence’ in 
 life), regarded by the pathologist as a terminal infection. No 
 signs of passive congestion so that the death in this case probably 
 
THYROCARDIAC DISEASE—ILLUSTRATIVE CASES 731 
 
 belongs in the toxic-infectious group, though earlier in the disease 
 swollen legs and loose cough suggested congestive failure. 
 
 These necropsies suggest: 
 
 1. That in the toxic deaths of fulminating or untreated thyro- 
 toxicosis, the toxemia is apt to be associated with infection, as is 
 the case of most of the ‘‘toxic”’ death in diabetes, in uremia, and 
 cholemia. Terminal acute pericarditis (two cases), acute endo- 
 carditis and suppurative nephritis and streptococcus sepsis were 
 among the infections found. / 
 
 2. That chronic passive congestion is a relatively rare cause of 
 death in thyrotoxicosis. 
 
 3. That characteristic, cardiovascular change is not here demon- 
 strable either in the toxic or the congestive deaths. The heart is 
 very slightly, or not at all, hypertrophied or dilated, the valve orifices 
 are seldom relaxed. The myocarditis demonstrable in one case was 
 in all probability due to coronary sclerosis rather than to the 
 thyrotoxicosis. 
 
 4. Persistent thymus, with or without status lymphaticus 
 (found in six out of our ten necropsies), is doubtless a factor in the 
 symptomatology. 
 
 5. Two cases were markedly pigmented at the time of necropsy. 
 
 SUMMARY AND CONCLUSIONS 
 
 1. In exophthalmic goiter the characteristic cardiovascular 
 changes are an over-demonstrative heart, which seems enlarged but 
 usually is not, and a low peripheral blood pressure. 
 
 2. Congestive heart failure is rarely the cause of death. Most 
 deaths are toxic, infectious, or mechanical. 
 
 3. In long standing quiescent goiters of the adenomatous type 
 heart symptoms of the congestive type may gradually develop and 
 though resistant to treatment by rest and digitalis may be greatly 
 benefited by operation. Post-mortem no definite pathology is 
 established. 
 
 ILLUSTRATIVE CASES 
 
 Autopsy 3189 
 
 A widowed American book-keeper of forty-five entered May 3 for 
 relief of diarrhea, edema of the legs, and skin eruption. 
 
 Her husband had died of tuberculosis. 
 
 She had been well except for malaria ten years ago. 
 
732 FACTS ON THE HEART 
 
 Until the present illness her micturition and catamenia were 
 normal, her bowels somewhat constipated. Her weight was 140 two 
 and a half years ago, 115 a year ago, 86 two weeks ago. 
 
 Two years ago she began to feel nervous, her neck began to 
 swell, her eyes to become prominent, and her heart to beat so that 
 
 she could feel it. She developed a great desire for cold fluids, and 
 still has it. She began to have frequency, sometimes a 
 A year and a half ago she began to have tremor. Two months later 
 she entered a hospital and had an operation. After it the tremor 
 increased, her heart became more rapid, and she developed edema of 
 the legs and feet. After four months in the hospital she went home 
 to the country for five months. All the symptoms persisted. In 
 September she began to have dull to sharp pains, first in the right 
 arm, then in both, worse on lying down. She entered the hospital 
 again. By December the pains left, and had not returned. In 
 February she went to a convalescent home. Her eyes, twitching, 
 and nervousness improved, but the tachycardia remained the same. 
 The middle of February she had a “‘relapse,’’ developed a cold in the 
 head, and had ever since had cough with sputum, several times blood- 
 tinged. She had also had persistent diarrhea, at first 12-15 watery 
 stools a day, more recently 7-8. Swelling of the legs and feet also 
 developed and persisted. For two months she had had brown spots 
 on her legs. She had been dyspneic for a month. Ten days ago 
 she left the hospital, feeling no better. The night before admission 
 her legs began to get red. 
 
 The patient was a wild-eyed, fluttering, emaciated wreck of 
 humanity with a brownish pallor. The skin of the legs, chin, etc., 
 showed scattered shallow brown blister-like lesions the size of a dime, 
 several showing scratch-marks. Over the lower abdomen and the 
 inner aspect of both thighs, most marked over the veins, were numer- 
 ous uniform red-blue areas of capillary stasis. The general nutrition 
 of the skin seemed impaired; a subcutaneous injection of morphia 
 gr. 16 caused a wheal to form rapidly. Sclerae were injected, the 
 mucosae pale. ‘Tongue dry, rough, and pale, with a white coat. 
 Marked exophthalmos, loss of convergence and lagging of the lids. 
 Brownish circles of pigmentation about the eyes. Thyroid very 
 much enlarged, the right lobe more than the left. Marked thrill. 
 The apex impulse of the heart was heaving, in the 5th space. There 
 was visible impulse, systolic, in the 2nd space at the right sternal 
 margin. ‘There was absolute irregularity. The first sound was loud, 
 
 ® 
 
THYROCARDIAC DISEASE—ILLUSTRATIVE CASES 733 
 
 P. accentuated. There was a rough high-pitched double murmur at 
 the apex, probably not endocardial; the action was too rapid to 
 differentiate. ‘The pulses were rapid, thready, irregular in force and 
 rhythm. The lungs were negative. The abdomen was tympanitic 
 except for induration in the wall of the left lower quadrant at the 
 margin of the discoloration. ‘There was some tenderness over this 
 area. ‘The liver dullness extended from the 5th rib to two cm. below 
 the costal margin, where a smooth, rounded, insensitive edge was felt. 
 The genitals were not examined. Extremities: The hands showed 
 nodular enlargement of the finger-joints and fine tremor. The legs 
 showed a good deal of edema and induration, with the discoloration 
 described. The pupils were normal. The reflexes were not 
 attempted. 
 
 T. 104.4°, falling to 100.2°.- P. 132-160. R. 28-40. Urine: 
 Amount normal. Sp. gr. toro. A very slight trace of albumin at 
 both of the examinations, a very rare red blood corpuscle and hyalin 
 
 8 
 
 4-5 o Sue ers. 5 
 
 Fic. 157.—Percussion dulness in cm., Case 3189. 
 
 cast at the first. Blood: Hgb. 65%, leucocytes 5700, polynuclears 
 87%, reds 2,824,000, showed considerable achromia. Wassermann 
 negative. Stools, (two examinations): All elements undigested. 
 No ova or parasites. Guaiac negative. Report of skin consultant: 
 “The lesions on the legs might be specific or traumatic. I cannot 
 make a positive diagnosis or suggest treatment. The left thigh 
 shows subcutaneous extravasation of blood. This might also be 
 traumatic.”’ Report of surgical consultant: “I am inclined to think 
 the skin picture is part of the circulatory disturbance associated with 
 the goiter, possibly posterior mediastinal in location.”’ 
 
 Following the application of ice-bags to the heart and cold com- 
 presses to the left leg and lower abdomen there was a fall in tem- 
 perature and rapid improvement. ‘The edema of the legs decreased. 
 The diarrhea was less evident. Morphia had, however, been given 
 to the physiological limit (gr. 14 two doses; gr. 14 one dose). In 
 spite of sedatives the patient grew more and more excited and had 
 ideas of persecution, until finally she required restraint with sheets. 
 She was given another dose of morphia gr. 1, and triple bromides 
 gr. 30, hyoscin gr. 1499, atropin gr. 1490, caffein gr. ii without effect. 
 
734 - FACTS ON THE HEART 
 
 She went into coma, the bronchi filled with numerous coarse audible 
 rales, and May 6 she died. 
 
 Clinical Diagnosis (from Hospital Record).—Exophthalmic goiter. 
 
 Thrombosis of the pelvic veins. 
 
 Dr. Richard C, Cabot’s Diagnosis —Thyrotoxicosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Anatomical Diagnosis.—1.Chemi- 
 
 cal or physical origin of. fatal Exophthalmic goiter. 
 
 illness. [ 
 
 Septicemia, pneumococcus. 
 
 Amyloid nephritis. 
 
 Slight chronic interstitial hepa- 
 titis, with fatty metamor- 
 phosis. 
 
 Serous atrophy of the fat tissue 
 of the pancreas. 
 
 Hypertrophy of the spleen. 
 
 | Double hydrothorax and 
 slight ascites and anasarca. 
 Hypoplasia of the adrenals. 
 Foci of pigmentation of the legs. 
 Punctate hemorrhages in the 
 skin of the left thigh. 
 ( Old salpingitis. 
 3. Historical landmarks. | Cicatrices of operation wounds. 
 Myomata of the uterus. 
 
 The heart weighed 285 grams and showed no hypertrophy or 
 dilatation, no myocarditis. | 
 
 The eyeballs protruded. 
 
 On the anterior aspect of the neck and extending from the larynx 
 to the suprasternal notch and to the sternocleidomastoid muscles 
 on each side was a bulging firm tumor mass beneath the skin. 
 
 The thymus was absent. 
 
 The tumor mass beneath the skin showed on section of its inferior 
 portion near the suprasternal notch a grayish translucent firm tissue 
 as well as some hard calcareous matter. A piece of the former was 
 taken for microscopical examination. 
 
 Microscopical examination. Thyroid. The tissue was com- 
 posed chiefly of tubular elements of varying size and formed of 
 cylindrical cells. Sometimes a tubule showed short papillary 
 ingrowths. There was no colloid. 
 
 2. Secondary or terminal lesions. 
 
 -_ sal 
 
THYROCARDIAC DISEASE—ILLUSTRATIVE CASES 735 
 Necropsy 3468 
 
 A married American woman of twenty-three entered November 
 28, 1908, for the relief of recurrent attacks of tonsillitis for several 
 years. Her tonsils and adenoids were removed. She became very 
 cyanotic during the operation, and her pulse was of very poor 
 quality, so that shock treatment had to be given. The temperature 
 was 98.4° to 100°, at discharge 97°. The pulse was 109-145-120. 
 She was discharged relieved December 4. The Out-Patient Depart- 
 ment records show at this time she had tremor and swelling of the neck. 
 
 In February two years later she had had a “‘cold”’ all winter with 
 slight expectoration, occasionally blood-tinged. The sputum was 
 negative. 
 
 May 8, 1915, she reentered for the relief of pain and swelling in 
 the neck and nervousness. She now gave a history of the diseases of 
 childhood, including scarlet fever. Ten years ago she had ‘“‘ malaria,” 
 and ‘‘rheumatism”’ in one joint of the hand. She had tonsillitis 
 every winter. She had one child, in good health. She had had one 
 miscarriage. Her best weight was 110 pounds, her usual weight 
 100, her present weight 7614. 
 
 She had always been nervous and weak, and had tired easily. 
 Since girlhood she had had “‘sour stomach,” sour eructations, and 
 a slight burning sensation in the epigastrium after eating. For 
 ten years she had had paresthesia, a numb “‘creepy”’ feeling starting 
 in her left thumb and in the course of two or three hours extending 
 over the hand and arm and the left side of the face and sometimes 
 down the other side. The arm felt dead, and when lifted dropped 
 heavily. After an attack she had a dull, heavy feeling in her head. 
 For eight years she had at times been so nervous that she shook all 
 over and had to take to her bed. For the same period she had had a 
 bilaterial swelling in the front of the neck, varying slightly in size 
 and hardness. Occasionally she had had sharp, severe pain starting 
 in this swelling and running up into her head, beginning and ending 
 suddenly, apparently brought on by excitement or over-fatigue. 
 For seven or eight years she had had attacks of diarrhea brought 
 on by fatigue, excitement or chill and lasting from a few days to four 
 weeks. For seven years she had had rapid heart on emotional 
 disturbance, with sometimes the dropping of a beat; fine tremor of the 
 hands; and when very nervous, tremor of the lips and lower jaw; 
 at times a little protrusion of the eyes. She occasionally had sick 
 headaches, rarely vertigo. For four years her hair had been coming 
 out. She urinated every fifteen minutes by day and three or four: 
 
736 FACTS ON THE HEART 
 
 times at night. For two months her skin had been growing browner 
 all over the body. During the past month she had lost twenty 
 pounds. She perspiredagreatdeal. Lately she had had someitching. 
 
 Examination showed a poorly developed woman weighing 7614 
 pounds, yellowish-pale, with brown pigmentation around the eyes, 
 which showed marked exophthalmos, imperfect convergence, and 
 Von Graefe’s sign. Except over the face the skin was markedly 
 pigmented, most deeply on the lower abdomen. The tongue pro- 
 truded with coarse tremor. There was a large pulsating thyroid 
 tumor measuring 33.5 cm., moving on deglutition and showing 
 marked thrill and a loud venous systolic hum. The apex impulse of 
 the heart was in the fourth space. The left border of dullness was 
 13.5 cm. from midsternum, the right border 3.5 cm. to the right. The 
 supracardiac dullness was 9 cm. The first sound was sharp and 
 ringing. The rate was 126. A roughened systolic murmur was 
 heard at the apex, along the left border of the sternum, and over 
 the pulmonic area. The blood pressure was 130/70. The lungs, 
 abdomen, rectal and vaginal examinations were negative. The arms 
 showed evidence of muscular atrophy, and the fingers fine tremor. 
 The pupils were slightly irregular. Their reactions and the other 
 reflexes were normal. 
 
 Until operation the temperature was usually normal, with 
 occasional rises to 99°—99.8°. The pulse was 80-125. ‘The respira- 
 tion was normal. The output of urine was normal. The urine 
 was cloudy, alkaline at entrance, acid later. The specific gravity 
 was 1.016-1.010. ‘There was the slightest possible trace of albumin 
 at one of three examinations. The hemoglobin was 70 to 80%, 
 the leucocytes 7600, the polynuclears 45%, the reds 4,560,0c00- 
 5,348,000. The smear showed slight variation in size and shape, an 
 occasional large stippled cell, an increased number of plates, and one 
 normoblast. A Wassermann was negative. The stools were 
 negative to guaiac at three examinations. Bile was present at three 
 of eight examinations, many fatty acid crystals at seven. 
 
 The patient was given hydrobromate of quinine gr. v t.i.d. 
 from entrance, changed May 21 to tincture of opium gr. v t.i.d. 
 p.c. She grew quieter, but had marked diarrhea, and by May 21 had 
 lost three pounds in spite of a tremendous appetite and extra diet. 
 May 21 X-ray treatment was started. May 23 she took 6550 
 calories, though she weighed only seventy-four pounds. Dr. Means 
 found the basal metabolism + 63. The diarrhea and the pigmenta- 
 tion persisted. Nothing was found to account for the latter except 
 
THYROCARDIAC DISEASE—-ILLUSTRATIVE CASES 737 
 
 the thyroid. June 2 tannalbin gr. v and fel bovis gr. iv were given 
 t.id. They stopped the diarrhea so effectually that the tannalbin 
 had to be omitted after two days because of constipation. 
 
 June 14 the left superior thyroid vessels were ligated under 
 novocain anesthesia. The patient was much excited after the opera- 
 tion, but was quieted by bromides. Next day she was very nervous, 
 but in fair general condition. The temperature was 99.5° the evening 
 of operation, then normal until the second operation. ‘The pulse was 
 120 June 14, 86 June 19, 120 June 21. By June 21 the general condi- 
 tion was good. 
 
 June 22 the right superior thyroid vessels were ligated under 
 gas and oxygen. The breathing stopped during the early part of 
 the operation, but was restored after a little artificial respiration. 
 The patient became cyanotic after the operation and could not 
 be aroused. The pulse was rapid and irregular. She was given 
 morphia freely. Her color gradually cleared up, and the pulse 
 became of better quality, but she was very restless. The next 
 morning she seemed a little better, but by night was worse, very 
 restless and weak, with a pulse of 208. She was given digitalis 
 intravenously. Next morning she was found very cyanotic, with 
 feeble and irregular pulse. The right border of the heart was out. 
 After being bled ten ounces her color cleared up and the pulse became 
 of better quality. June 24 she was semiconscious and died. 
 
 Clinical Diagnosis.—Exophthalmic goiter. 
 
 Mitral disease. 
 
 Acute dilatation of the heart. | 
 
 Ligation of the superior thyroid vessels. 
 
 Dr. Richard C. Cabol’s Diagnosis.—Thyrotoxicosis. 
 
 Hypertrophy and dilatation of the heart. 
 
 Anatomical Diagnosis ——(Exophthalmic goiter and ligation of 
 the superior thyroid vessels.) 
 
 Status lymphaticus. 
 
 Purulent pericarditis and pleuritis. 
 
 Pigmentation of the skin. 
 
 Chronic appendicitis. 
 
 The heart weighed 200 grams and showed no hypertrophy or 
 dilatation and no myocarditis. 
 
 There is no pathological report on the thyroid. The neck was 
 covered with a surgical dressing which was not removed. 
 
 The thymus gland was present in the form of an elongated flat- 
 tened mass about 8 cm. in greatest length. On section it was found 
 to be composed of a grayish, translucent, fairly firm tissue. 
 
 47 . 
 
CHAPTER XII 
 CONGENITAL HEART DISEASE 
 
 In our four thousand necropsies which include a good many in 
 children, there were but seven cases of congenital defects or lesions 
 such as seemed of actual or possible damage to the circulation. 
 These comprise three cases of pulmonary stenosis, one complicated 
 by an interventricular septal defect and another by an apparently 
 independent post-natal endocarditis on the tricuspid. There were 
 four cases of septum-defect alone, three between the ventricles, one 
 between the auricles.* 
 
 The diagnosis of some congenital lesion was suggested by the 
 presence of clubbed fingers in one case and by a deep, unexplained 
 cyanosis in another. The rest were unrecognized. The details 
 are given in the case-reports to follow. 
 
 For this book the chief importance of these scattered data is to 
 show how rare congenital lesions are in a twenty-three-year hospital 
 experience. Only seven in a series that comprises 1906 cases were of 
 the congenital type. Unless seen in infancy or childhood, these 
 lesions then are naturally very rare. 
 
 Their ages, seven, nine, nineteen, twenty-two, twenty-four, 
 thirty, forty-nine, are what one might expect. But these early 
 deaths are not due wholly to the severity of the cardiac lesion since 
 four of the seven patients died of disease unconnected with the heart, 
 and passive congestion was found at necropsy in only three cases, two 
 of which showed post-natal (rheumatic?) valve lesions as well. 
 So that in only one case of the seven was death due clearly to the 
 congenital lesion. 
 
 The cases are too few in number to justify any conclusion except 
 the rarity of congenital lesions after early infancy. 
 
 Detailed histories follow. 
 
 * Beside the seven cases there were five with harmless anomalies of valve-cusps: 
 In two cases the aortic had but two cusps, in one case it had four. In another case the 
 cusps were slightly fenestrated. In a fifth case the pulmonary valve had four cusps. 
 
 I may also mention here the 19 cases of hypoplastic or small-sized aorta. Ten of 
 these apparently produced no effect on the heart. In nine others there was cardiac 
 hypertrophy, occasionally very considerable. 
 
 738 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 739 
 
 ILLUSTRATIVE CASES 
 Necropsy 106 
 
 A mentally defective girl of nine was brought to the Accident 
 Room March 17. She had had measles and chickenpox, and had 
 always been nervous and easily excited. She did not walk well 
 until she was four. She had always complained much of pains in the 
 legs. For the past three weeks she had had cough. Five days before 
 admission she began to feel stupid and to complain of pain in the 
 stomach. March 15 she had a little vomiting of watery material 
 with the cough, which was very severe. The night before admission 
 there were several blood spots on her pillow. The night of admission 
 she had a hemorrhage of liquid and clotted blood and some fecal 
 material from the bowels, fully a quart altogether. An hour later 
 she had another movement of about the same amount. 
 
 Examination showed a pale, fairly well nourished child looking 
 older than her years, tossing about on the bed with sighing respiration 
 and convulsive movements of the hands, head and facial muscles 
 but no suggestion of exhaustion. She was said to do this commonly, 
 especially when excited. There was a loud systolic murmur at the 
 apex of the heart transmitted to the axilla, and heard also all over the 
 back and at the aortic area transmitted upward. At the apex was a 
 presystolic murmur. The pulmonic second sound was accentuated. 
 The abdomen, pupils and reflexes were normal. The output of urine 
 was not recorded; the findings were normal. 
 
 The child had two bowel hemorrhages in the first night and early 
 the next morning, perhaps five ounces in all, with a few clots and 
 some loose fecal material. She continued to have slight hemorrhages 
 for the next three days. She was very nervous, and screamed with- 
 out apparent cause. She had troublesome cough at first which 
 improved. April to she was discharged relieved. 
 
 After leaving the hospital she was well until the morning of June 6, 
 when she had another intestinal hemorrhage (amount?). She was 
 brought to the hospital that day, pale, restless, and frequently crying 
 out, with scarcely perceptible pulse. The heart action was rapid. 
 There was a loud systolic murmur heard everywhere over the chest 
 and back. The day of admission she had a hemorrhage of about 
 sixteen ounces, during the night another of eight ounces, and next 
 day one of five ounces. Just before each hemorrhage she cried out 
 and threw herself about on the bed. Her respiration varied greatly. 
 Sometimes it was quick and short, sometimes.sighing. Restlessness 
 
740 FACTS ON THE HEART 
 
 was the most marked feature of her condition. June 7 her pallor 
 was much greater than at admission. That afternoon she had two 
 movements of the bowels containing considerable fecal material 
 mixed with blood. Her pulse was very poor. Her respirations grew 
 more rapid and the pallor extreme. She became, however, less 
 restless. The evening of June 8 she was much weaker, with Cheyne- 
 Stokes respiration. Just before the infusion of eight ounces of salt 
 solution the heart sounds were short and no murmurs could be heard. 
 Twenty minutes later the general condition seemed better and the 
 murmur was heard again. She seemed better during the rest of the 
 night, with fair pulse and quiet respiration. Early the following 
 morning when apparenly in good condition she suddenly collapsed 
 and died. 
 
 Clinical Diagnosis.—Intestinal hemorrhage. 
 
 Anatomical Diagnosis——Congenital malformation of the heart 
 (partially defective interventricular septum and defective mitral 
 valve). 
 
 Chronic mitral endocarditis? 
 
 Slight cardiac hypertophy. 
 
 Fatty degeneration of the myocardium. 
 
 Bronchopneumonia and atelectasis of the inferior lobe of the 
 right lung. 
 
 Purulent bronchitis. 
 
 Meckel’s diverticulum with localized dilatation of the ileum lead- 
 ing to 
 
 *Intestinal hemorrhage. 
 
 General anemia. 
 
 Old pleural adhesions. 
 
 The heart was somewhat larger than normal, weighing 163 grams. 
 The left ventricle had a capacious cavity with rather thick pectinate 
 muscles. In the ventricular septum just below the insertion of the 
 mitral valve and under one of the cusps of the aortic valve was a 
 semicircular defect in the muscle tissue, its convexity pointing down- 
 ward toward the apex and measuring 18 by 12mm. This defect was 
 filled up by an irregular membrane of yellow fibrous tissue which 
 in places was diaphanous and separated the cavities of the ventricles. 
 This membrane of fibrous tissue seemed to represent and to be con- 
 tinuous with one of the curtains of the tricuspid valve. The mitral 
 valve opposite the defect in the ventricle over a length of 3.5 cm 
 showed a marked shortening and almost obliteration of its curtain 
 in an irregularly crescentic form with the convexity upward. The 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 741 
 
 edges of the valve along this defective portion were markedly thick- 
 ened but smooth. The median portions of what remained of the 
 valve were attached to the margin of the defect in the septum by 
 short branching chordae tendineae. The remainder of the valve 
 seemed normal and was not thickened. At the extremities of the 
 crescentic shortening of the valve were long rather thick chordae 
 tendineae. The mitral valve measured 9 cm. in circumference, the 
 tricuspid 9 cm. ‘The wall of the left ventricle was 1 cm. thick, the 
 right 4-5 mm. The myocardium generally was pale yellowish brown 
 with fine mottling of the pectinate muscles of the left ventricle. The 
 endocardium of the left auricle showed yellowish irregular fibrous 
 
 Fic. 158.—Congenital, defective interventricular septum and defective mitral valve. 
 (Photograph by Lewis S. Brown. Dr. Oscar Richardson.) 
 
 patches. The foramen ovale was closed. In the pericardium there 
 
 was some clear fluid with fibrinous clots. The bowel bleeding which 
 
 was the main cause of death, is not clearly explained but was apparently 
 
 connected with the Meckel’s diverticulum. 
 
 Necropsy 238 
 
 A Swedish cook of nineteen entered March 15, 1898. She said 
 she had never been ill before. The friend who came with her however 
 said that at twelve years of age she was in bed a year with bloody 
 vomiting and great epigastric pain. For the past two months she 
 had felt weak, had often vomited after eating, and had gradually 
 
742 FACTS ON THE HEART 
 
 become pale, losing appetite and some weight. ‘Two weeks before 
 admission she had severe sore throat. After being in bed a week 
 she was up for four days. March 12 her legs began to swell and 
 were so painful that she could not walk. Her hands also swelled 
 and were painful. She still vomited after eating and had some 
 epigastric pain. Her bowels were very constipated. 
 
 Examination was negative except for extreme pallor, an occasional 
 faint systolic murmur at the apex of the heart and over the pulmon- 
 ary area, and swelling, heat, and tenderness of both ankles. 
 
 The temperature was 102.8° falling steadily to 97.7°, the pulse 
 115-88, the respiration 28-32. ‘The output of urine is not recorded. 
 The specific gravity was 1.037. There was a slight trace of albumin 
 at the single examination. The hemoglobin was 45%, the leuco- 
 cytes 20,000, the reds 3,248,000. 
 
 The patient vomited everything taken by mouth. She com- 
 plained of great pain in the arms. On examination nothing was 
 found but tenderness. The evening of March 16 she started to vomit 
 and very suddenly died. 
 
 Clinical Diagnosis (from Hospital Record)—Acute articular 
 rheumatism. 
 
 Anatomical Diagnosis.—Ulcer of the stomach. 
 
 Anemia. . 
 
 Verrucose endocarditis of the mitral valve. 
 
 Acute degeneration of the myocardium. 
 
 Partial defect of the ventricular septum. 
 
 Slight acute hyperplasia of the spleen. 
 
 Small cysts of the right ovary. 
 
 Dr. RicHarpson: The skin seems to have been noticeably pale 
 and waxen. The brain and meninges were frankly negative. There 
 were some old adhesions in the peritoneal cavity and some of these 
 were about the stomach. 
 
 The heart showed slight hypertrophy. There was a partial defect 
 in the interventricular septum just below the aortic cusp and some 
 acute degeneration of the myocardium. On the mitral valve there 
 was a row of minute granulations. Other than that the heart, the 
 aorta and great branches were negative. : 
 
 The liver, spleen, and kidneys called for no mention, and the 
 microscopic examination of the kidney was negative. 
 
 That brings us to the gastro-intestinal tract. About midway 
 between the cardia and the pylorus in the posterior wall was an ulcer, 
 rather deep, five to six mm., and the other dimensions two by three 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 743 
 
 cm. On the peritoneal aspect there were adhesions, and at the base 
 of the ulcer the pancreas was visible. ‘There was no evidence of new 
 growth. It was frankly an ulcer of the stomach. 
 Dr. Casor: Of course she died of the gastric ulcer. Those mitral 
 granulations were terminal things and not the cause of all this anemia? 
 Dr. RICHARDSON: I should think so. 
 
 Necropsy 303 
 
 An Italian housewife of twenty-two entered April 20. She 
 had had two children and one miscarriage. She had had no cata- 
 menia for four months, and during that period had had dyspnea 
 and cough. For the past two weeks the cough had been worse and 
 she had had bad color, pains in the joints and very little urine. 
 
 Examination showed cyanosis of the whole body, marked about 
 the lips, cheeks, tongue, ears and nails. The hands and feet were 
 cold. There was slight glandular enlargement. The lungs were 
 normal except for slightly harsh respiration at the left apex. The 
 apex of the heart was in the fifth space in the mammillary line. The 
 left border of dullness was just to the left of the nipple line, the right 
 border three finger-breadths to the right of the sternum. There was 
 no thrill, but a duplicated impulse was felt. At the apex was a 
 harsh systolic murmur transmitted to the axilla and heard over most 
 of the cardiac area. Just at the end of the murmur two short sharp 
 sounds were heard faintly. At the base the sounds were very feeble, 
 with accentuation of the pulmonic second. © The liver extended to a 
 hand’s breadth below the costal margin and was somewhat tender. 
 No enlargement of the uterus was made out. There was slight edema 
 of both legs. _ 
 
 During her thirteen days in the hospital she ran an irregular 
 temperature, 97-101.5° with one drop to 95.6°, followed by two 
 days of subnormal temperature. The pulse was 83-113, the respira- 
 tions 22-36. The output of urine was 13-70 ounces, the specific 
 gravity 1.013-1.028. All of three examinations showed albumin 
 1449-16%. The sediment at one examination showed a few abnormal 
 red blood cells. There is no record of the blood except “leucocytes 
 8200.”’ 
 
 Under rest and purgation the patient made marked improvement. 
 The edema decreased, her color improved, and the liver became 
 smaller. May 2 she was discharged relieved. 
 
 After leaving the hospital she was fairly well until early in June, 
 when edema of the legs and dyspnea returned. At her readmission 
 
744 FACTS ON THE HEART 
 
 to the hospital June 22 she was unable to use the right half of the 
 body. 
 
 Examination showed her very cyanotic, with right hemiplegia. 
 The whole surface of the body was cool and the extremities cold. 
 The left pupil was larger than the right and the left eyelid opened 
 wider than the right. The face was drawn slightly to the right, 
 and in laughing the muscles of the right side of the face were more 
 active. Over the back and the sides of the chest was a brownish 
 maculo-papular eruption. The bases of the lungs showed edematous 
 rales and the left apex slightly harsh respiration. The apex impulse 
 of the heart was felt in the fifth space two inches outside the mamil- 
 lary line, forcible and very diffuse, coinciding with the left border of 
 dullness. The right border was three finger breadths to the right. 
 The systolic murmur was heard all over the cardiac area except in the 
 aortic region. Over the tricuspid area it seemed to have a higher 
 pitch. The heart sounds were confused, rapid, and at long intervals 
 intermittent. The pulse was rapid and very slightly intermittent. 
 The liver dullness extended to a hand’s breadth below the costal 
 margin. The right leg was much more edematous than the left. 
 No knee-jerks were obtained. 
 
 The temperature was 97.7-—99.7°, the pulse 80-107 until July 3, 
 then July 4 and 5 swinging from 53 to 108, dropping to 67 the day of 
 death. The urinary output was 10-33 ounces except one day when 
 it reached 45 ounces; cloudy, specific gravity 1.025-1.009. The 
 sediment showed leucocytes at both examinations and a few red 
 blood corpuscles at one. 
 
 The edema and hemiplegia gradually decreased and the cyanosis 
 cleared a little. The cardiac condition remained unchanged. July 
 4 the patient’s sister died of heart trouble. July 7 the patient 
 insisted upon going home. 
 
 After leaving the hospital she grew more cyanotic and became. 
 
 blind except for recognizing light. Pain developed about the liver 
 and she became unable to lie down. 
 
 Upon examination at her third admission, July 29, she showed exter- 
 nal strabismus of the right eye and internal strabismus of theleft. She 
 could bring the eyes to the median line but not to the left side. She 
 appeared wholly blind. The pupils reacted to light. The lungs 
 were negative. The cardiac impulse was very weak, scarcely felt. 
 The percussion measurements were as before. The systolic murmur 
 was faint at the apex, transmitted into the axilla. At the tricuspid 
 area was a faint systolic blow of higher pitch than the apex systolic. 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 745 
 
 The pulmonic second sound was slightly accentuated. The sounds 
 were much fainter than at her last stay in the hospital. The base 
 sounds were very weak. The liver was three finger breadths below 
 the costal margin, hard, somewhat tender. The legs showed no 
 edema. The left upper thigh was larger than the right, tender 
 along the femoral vein, hard, resistant. The patient cried out 
 with pain upen pressure over Scarpa’s triangle. No paralysis was 
 made out, merely equal sided weakness. The rash was generalized 
 over the body. No urine could be obtained for examination. The 
 blood is not recorded. 
 
 During her three days in the hospital she ran a temperature 
 of 101.3°-103.4-, the pulse 120-130, the respirations 30-15. The 
 day after admission the tenderness and swelling over the left femoral 
 vein had largely cleared up. The general condition however was 
 worse. There was much more cyanosis. The systolic murmur was 
 large at the apex. She gradually failed, became purple, yet showed 
 no edema of the lungs, abdomen or legs. July 31 she died. 
 
 Clinical Diagnosis —Mitral regurgitation. 
 
 Congenital heart lesion. 
 
 Dr. Richard C. Cabot’s Diagnosis ——Chronic endocarditis of the 
 mitral and tricuspid valves. 
 
 Mitral stenosis. 
 
 Embolism and thrombosis. 
 
 Anatomical Diagnosis.—Stenosis of the pulmonary valve of the 
 heart (congenital malformation ?). 
 
 Verrucose endocarditis of the tricuspid valve. 
 
 Hypertrophy and dilatation of the right ventricle and the right 
 auricle. 
 
 Partially patent foramen ovale. 
 
 Thrombosis of the right auricular appendix, of the right ventricle, 
 and of the left ventricle. 
 
 Infarctions of the kidneys. 
 
 General chronic passive congestion. 
 
 Dr. RICHARDSON: There was no edema of either upper or lower 
 extremities. There was some ascites, moderate hydropericardium, 
 no fluid in the pleural cavities. There was some congestion of the 
 lungs, and old pleural adhesions on the right side. 
 
 The liver was one hand down. 
 
 The heart weighed 631 grams,—marked hypertrophy. The 
 right ventricular wall measured from twelve to fifteen mm., the left 
 
740 FACTS ON THE HEART 
 
 ventricular wall ten mm. There was slight dilatation of the right 
 ventricular cavity, much dilatation of the right auricle. 
 
 Dr. Casot: That is, the right ventricle was actually thicker than 
 the left? That is extraordinary! 
 
 Fic. 159.—Stenosis of pulmonary valve (congenital?). (Photograph by Lewis S. 
 Brown. Dr. Oscar Richardson.) 
 
 Dr. RICHARDSON: The wall of the right auricle was four to five 
 mm. thick; the left negative. There was slight dilatation of the 
 left cavities. 
 
 The aortic and mitral valves were negative. There were mural 
 thrombi in the left ventricle. On the tricuspid valve there were a 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 14] 
 
 few small firm fibrous granules,—the so-called verrucose endocarditis 
 The cusps of the pulmonary valve generally were fused, thickened, 
 a smooth fibrosis, and from them three bands extended on the 
 pulmonary artery, the whole process producing pulmonary stenosis, 
 congenital. There was also a partially patent foramen ovale. 
 There were mural thrombi in the right ventricle and night auricular 
 appendix. 
 
 The liver, spleen, and kidneys showed chronic passive congestion. 
 From the mural thrombi on the left side there were infarcts in the 
 kidneys. 
 
 The mucous membranes were markedly purple. 
 
 Dr. Casot: Pulmonary stenosis is one of the severe congenital 
 lesions. I do not believe for a moment that that child had failed to 
 show cyanosis and heart murmurs much earlier. I entirely believe 
 that if we had got a decent history here I should not have gone so 
 entirely wild as I did. 
 
 Necropsy 2453 
 
 A boy of seven who had been found deserted and starving in a 
 tenement was brought tothe hospital October 5. Nothing was known 
 of his history except that he had been ill about a week. 
 
 Examination showed a fairly well developed, poorly nourished, 
 sick looking child with marked rosary and prominence of the super- 
 ficial veins of the chest and abdomen. The tonsils were somewhat 
 enlarged. Therewere slightly enlarged glands in the neck and groins. 
 
 The precordia showed slight prominence. The apex impulse 
 of the heart was barely palpable in the fifth space just outside the 
 nipple line, 214 inches from midsternum, corresponding to the left 
 border of dullness. There was no enlargement to the right. The 
 action was regular and slow. A loud harsh blowing systolic murmur 
 was heard all over the precordia entirely replacing the first sound, 
 loudest in the third and fourth spaces to the left of the sternum, 
 transmitted deep into the axilla and into the vessels of the neck. © 
 The pulmonic second sound was accentuated and louder than the 
 aortic second, which was also accentuated. The pulses were poor in 
 quality. Both testes were undescended. ‘The fingers were some- 
 what clubbed, the nails cyanotic. Examination was otherwise 
 negative. 
 
 The child lived only a day in the hospital. His temperature rose 
 from 98.4° to to1.9°. The pulse and respirations were not remark- 
 able. The urine was normal except for a trace of albumin. The 
 
748 FACTS ON THE HEART 
 
 hemoglobin was 100%, the leucocyte count 26,000. Early the 
 morning after admission he vomited and immediately stopped breath- 
 ing. After fifteen minutes of artificial respiration the breathing 
 began again, deep, slow, stertorous, of the air hunger type. During 
 the artificial respiration vomitus was expressed through the mouth 
 and nose. The type of breathing suggested the possibility of thymus 
 —though no thymic enlargement could be determined—or of some 
 ~ metabolic or some central nervous affection. Air hunger breathing 
 continued for about three hours. The respirations ceased before 
 the heart. 
 
 Clinical Diagnosis.—Congenital heart disease. 
 
 Aspiration of vomitus. 
 
 Persistent thymus? 
 
 Anatomical Diagnosis—Abscess of brain (streptococcus). 
 
 Leptomeningitis (streptococcus). | 
 
 Stenosis of the pulmonary valve (congenital). 
 
 Incomplete closure of the interventricular septum. 
 
 Dilatation of the heart. 
 
 Right ventricular hypertrophy of heart. 
 
 Chronic pericarditis. — 
 
 Chronic perihepatitis. 
 
 Chronic tuberculosis of the mesenteric lymph glands. 
 
 Dr. RICHARDSON: The age is given here as five. At the base of 
 the brain there was frank meningitis. On the left side—the absolute 
 boundary is not given, but I should think about in the left parietal 
 region—there was a large abscess which extended into the left lateral 
 ventricle,—frank abscess of the brain and leptomeningitis at the base, 
 the organism streptococcus. 
 
 The skin and mucous membranes were purplish, the fingers slightly 
 clubbed. 
 
 The heart weighed 135 grams. The organ was not remarkable 
 except for a congenital stenosis of the pulmonary valve and a per- 
 foration, incomplete closure of the interventricular septum, rather a 
 common type of congenital condition. 
 
 Culture from the heart blood yielded streptococcus. 
 
 There was some slight chronic tuberculosis of the mesenteric 
 lymph glands. 
 
 Dr. Cazot: How do you feel about the air-hunger? What caused 
 it? ) 
 
 Dr. FREMONT-SMITH: I think he had increasing intravenous 
 pressure. 
 
 ee ee ee ee ae, een er ee eee ee ee. 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 749 
 
 Dr. Casort: That is, he did not have any air-hunger, he had 
 breathing mistaken for that. 
 
 Dr. RICHARDSON: The thymus gland was present and weighed 
 four and a half grams,—negative. 
 
 Necropsy 2599 
 
 A Nova Scotian housewife of forty-nine entered April 25. She | 
 remembered no serious illnesses or injuries. She passed the meno- 
 pause six years before admission. Three weeks and a half before 
 admission while working in a factory her hair was caught in some 
 machinery and her scalp torn almost completely off. Twenty min- 
 utes after the injury she was taken to a hospital where the wound was 
 dressed without ether. The pain had increased somewhat but had 
 not been unendurable. 
 
 Examination was negative except for: obesity and the injured 
 area, which was covered with healthy looking granulation tissue with 
 fresh epithelium growing in about its edge. There was no pus and 
 not even a red angry look. 
 
 The heart was not enlarged. The action was regular, the sounds 
 clear and of good quality. No murmurs were heard. The pulses 
 were of fair volume and tension. 
 
 The patient slept fairly well and complained of nothing. — April 
 30 a Tiersch skin graft was done under spinal anesthesia, skin being 
 taken from the thighs. The patient stood the operation well and 
 returned to the ward in good condition. Except that some of the 
 grafts at the back of the head floated off with pus she seemed to be 
 doing very well until May 7, when she suddenly became very cyano- 
 tic, with extreme air hunger and thready pulse. She failed to 
 respond to stimulation or artificial respiration and died that day. 
 
 Clinical Diagnosis.—Avulsion of scalp. 
 
 Pulmonary thrombosis. 
 
 Anatomical Diagnosis ——Absence of the scalp (avulsion) with 
 granulation tissue formation and skin graft. 
 
 Thrombosis of the posterior tibial veins, left and right. 
 
 Embolism of the right auricle and the pulmonary arteries, right 
 and left. 
 
 Perforate interventricular septum. 
 
 Open foramen ovale. 
 
 Fatty metamorphosis of the liver. 
 
 Fibromyoma of the uterus. 
 
75° FACTS ON THE HEART 
 
 Heart: Weight 314 grams. The epicardium contains abundant 
 fat. On section the cavities of the left side empty. Myocardium 
 brownish red and limp. Wall of left ventricle 1.4, of right 0.4 cm. in 
 thickness. Mitral valve 9.6, aortic valve 6, pulmonary valve 6, 
 tricuspid valve 10.5 cm. in circumference. Depth of left ventricle 
 9.3 cm. The aortic curtain of the mitral valve contains several 
 small, smooth, yellowish patches; the endocardium and valve curtains 
 otherwise normal. The interventricular septum at a point 3 cm. 
 below the anterior curtain of the aortic valve shows an oval depres- 
 sion about I cm. across, at the bottom of which is an opening 0.2 cm. 
 across; a probe introduced into this passes obliquely downward and 
 to the right, emerging in the cavity of the left ventricle at a point 5 
 cm. above the apex. Coronary arteries contain small, soft, yellow- 
 ish patches. At the site of the foramen ovale, along the anterior 
 border of the membrane, is a slit-like opening about 1 cm. long, well 
 guarded.* 
 
 Dr. RicHARDSON: This case was examined by the Medical 
 Examiner, and we have the anatomical diagnosis and a note through 
 the courtesy of Dr. Magrath. 
 
 There was a thrombosis of the posterior tibial veins, left and right. 
 That of course is the important statement, because that is the prob- 
 able source for the pulmonary embolism which was present. 
 
 Dr. Casot: How much did the congenital heart lesion enter in? 
 Do you think it is of any importance? 
 
 Dr. RICHARDSON: Not as a cause for death. 
 
 Dr. Caport: She would have got along all right with that? . 
 
 Dr. RicHarpson: Yes. It is not a thing we like to have in a 
 heart, but we should not expect death to result from it. It was an 
 additional load, but the death here was due to frank pulmonary 
 embolism, and the only source we have for it is in the thrombosis of 
 the posterior tibial veins. 
 
 Dr. CHURCHILL: It would look as though the skin-grafting might 
 have been the cause of death rather than the avulsion. They took 
 the skin from the thighs according to the record. 
 
 Dr. Casot: Why should that bring about a thrombosis in the leg 
 veins? 
 
 Dr. CHURCHILL: There is no reason whatsoever. There is no 
 mention made of sepsis, and the wounds of a skin graft are really 
 intradermal. | 
 
 * The anatomical data in this case are furnished through the courtesy of Dr. George 
 Burgess Magrath, Medical Examiner of Suffolk County, Massachusetts. 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 752 
 
 Dr. RICHARDSON: Except as mention of the vein is made. The 
 thrombosis is due to something. 
 
 Dr. Casort: It is hard to see how a skin-graft in the thigh could 
 do that. 
 
 Dr. RicHarpson: Unless. there was some infection. There | 
 certainly was infection higher up. 
 
 Dr. CHURCHILL: Is it possible that in a patient with a congenital 
 heart lesion there exists some mechanical] situation which would favor 
 thrombosis? 
 
 Dr. Casot: I do not know any reason to think so. 
 
 Necropsy 2753 
 
 An American of thirty, who had been working intermittently 
 as a salesman, entered December 22. His father died of kidney 
 trouble. Since infancy the patient had at times been blue, especially 
 when he was chilled, and had always had dyspnea on exertion. At 
 four he had measles followed by ‘‘dropsy.”’ Until the age of twenty- 
 one he had frequent mild nosebleeds. At twenty-three he was 
 confined to bed for seven months with rheumatism—fever and pain 
 in the joints. 
 
 For six months he thought his dyspnea on exertion had been worse. 
 He had had a slight cough. A month before admission he had a 
 cold for a week, with nasal discharge and chilly feelings. Four 
 days before entrance he had chills followed by severe headache and 
 pains all over the body, especially in the right chest upon deep inspira- 
 tion, with cough, and for three days a good deal of white frothy spu- 
 tum, now blood-tinged. Although feeling feverish and unwell he had 
 tried to do a little business. For a few nights he had urinated twice. 
 There had been some general pain low in the abdomen. At entrance 
 from the Accident Room his hands, face, and ears were very cyanotic, 
 the pulse only moderately rapid. He complained of being chilly. 
 
 Examination showed a fairly developed, poorly nourished man 
 with rapid breathing frequently interrupted by a short cough, and 
 with the cyanosis mentioned. The throat was very red. His 
 nervousness and garrulity suggested toxic delirium. The apex 
 impulse of the heart was seen and felt over the outer region of the 
 precordium and as far as 3 cm. outside the nipple line in the 5th 
 space, with a very slight suggestion of impulse in the sixth space, 
 nipple line. The upper border of dullness was at the 4th rib, the 
 lower in the sixth space. No enlargement to the right was made out. 
 
752 FACTS ON THE HEART 
 
 The action was somewhat rapid, occasionally intermittent, forceful. 
 The first sound at the apex was replaced by a low-pitched blowing 
 systolic murmur transmitted towards the axilla, heard best in the 
 ard and 4th left spaces. The second sound at the apex was rather 
 weak. At the base P. was indistinct, fairly forcible but’ not loud, 
 rather obscured by systolic murmurs (sic). A, wasnot heard. At the 
 aortic area was a higher-pitched systolic murmur transmitted to the 
 region of the arch, the subclavian and carotid arteries on both 
 sides. A systolic murmur was heard also in the axilla and back. 
 The pulses were of fair volume and tension, regular except for occa- 
 sional intermissions. The artery walls were palpable. Lungs: 
 There were sharp crackles and a few moist rales at the base of both 
 axillae, slightly exaggerated bronchovesicular breathing with increased 
 whisper and voice but no rales, at the anterior right upper lobe. The 
 voice from the posterior apex to the spine of the scapula was slightly 
 increased. Expansion was slightly restricted. The abdomen was 
 held rigid. The pupils and reflexes were normal. 
 
 Temperature 104104.5°, pulse 8g-101, respiration 22-25. 
 Systolic blood pressure 105-85, diastolic not recorded. Urine: 
 Amount and sp. gr. not recorded. Cloudy. A trace of albumin; 
 many brown granular casts with occasional red blood corpuscles 
 attached; a few free red blood corpuscles; leucocytes. Blood: Hgb. 
 90%. Leucocytes 17,700-20,300. Reds 5,800,000, slight achromia,, 
 considerable variation in size, slight.poikilocytosis. Sputum: Prune 
 juice; predominating organism pneumococcus in pairs and in chains, 
 occasionally intracellular. 
 
 The day of admission dullness, bronchial breathing, broncho- 
 phony and numerous coarse moist rales developed over the right upper 
 and middle lobes. The heart remained as at admission except for a 
 sharp and reduplicated first sound at the apex suggesting a presys- 
 tolic murmur. A fairly definite presystolic thrill was now felt at the 
 apex. At the base was a loud systolic murmur apparently of dif- 
 ferent pitch and quality from the apical one, heard equally well 
 over the aortic and pulmonic areas. During the day the patient 
 became very delirious, at six p.m. showed a pulse of poor quality, 
 and at eight p.m. began to hiccough spasmodically, the pulse becom- 
 ing very weak and intermittent during the attacks. The patient 
 grew steadily worse, the chief complaint being irregular and super- 
 ficial breathing. Next morning he died. 
 
 Clinical Diagnosis (from Hospital Record).—Lobar pneumonia. 
 
 Chronic mitral endocarditis. 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 753 
 
 Congenital heart disease. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Mitral stenosis. 
 
 Aortic stenosis. 
 
 Lobar pneumonia. 
 Hypertrophy and dilatation of the heart. 
 
 Possibly some congenital heart lesion. 
 
 General passive congestion. 
 
 Anatomical Diagnosis.— 
 (Lobar pneumonia, right lung. 
 Stenosis of the pulmonary 
 { valve, congenital (?). 
 
 | Fibrous endocarditis of the tri- 
 ' cuspid valve; slight stenosis. 
 Hypertrophy and dilatation 
 of the heart. 
 Chronic passive congestion, 
 | general. 
 | Chronic pleuritis, right. 
 3. Historical landmarks. Defective closure of the fora- 
 men ovale. 
 
 The heart weighed 430 grams. The myocardium on section was 
 of good consistence, firm and pale red. The wall of the right ventricle 
 generally was markedly thickened measuring from 10 to 15 mm. 
 The right auricular wall was thickened The left ventricle wall 
 was 14 mm. The columnae carneae were markedly thickened in 
 the right ventricle and fairly well marked in the left. The cavity 
 of the right auricle was enlarged. The other cavities of the heart 
 showed no definite enlargement. The mitral valve measured ro cm. 
 in circumference, not remarkable. The aortic valve measured 514 
 cm. The cusps were slightly thicker than usual but otherwise the 
 valve was not remarkable. The tricuspid valve measured 10 cm. 
 The circumference was decreased. The curtain showed a moderate 
 amount of diffuse fibrous thickening which in places was slightly 
 nodular. The pulmonary valve was about 514 cm. in diameter and 
 about 17 mm. in circumference. The orifice of this valve just about 
 admitted the passage of an ordinary lead pencil. There were three 
 cusps. The cusps were small but rather deep. The walls of the 
 cusps showed generally a moderate amount of diffuse fibrous thicken- 
 ing which was slightly nodular in places. There wassome fusion of the 
 contiguous cusp margins. The pulmonary artery and its primary 
 
 branches were small but the branches in the lung were of good size. 
 48 
 
 1. Primary fatal lesions. 
 
 ( 
 
 2. Secondary or terminal lesions. 
 
754 FACTS ON THE HEART 
 
 The coronary arteries were free. Each coronary was rather capa- 
 cious, the right showing more increase in size. The intima of the 
 coronary showed a few small plaques. The foramen ovale presented 
 an oval defective closure about 6 mm. in greatest diameter. The 
 aorta and its great branches were small. The intima of the aorta 
 showed a few yellowish fibrous plaques here and there. Vena cava 
 not remarkable. 
 
 Note by Dr. Oscar Richardson.—The stenosis of the pulmonary 
 valve in this case is regarded as being probably congenital. The 
 cusps were small and the character of the fibrosis present was not 
 definitely that of endocarditis. In support of the hypothesis that 
 the lesion was congenital are the facts that the pulmonary artery 
 and its primary branches were small and that there was an oval 
 defective closure of the foramen ovale 6 mm. in diameter. Against 
 this hypothesis is the mentioned fibrous endocarditis of the tricuspid 
 valve. This however was slight in amount and apparently bore no 
 relation to the process in the pulmonary cusps. 
 
 Necropsy 2997 
 
 First Eniry—An unmarried American working-girl of twenty-four 
 entered December 13. Her father had died of ‘‘heart trouble.”’ She 
 had had measles in infancy, “‘dropsy”’ at eight, and pneumonia at ten. 
 As a child she was never able to run and play because of dyspnea. 
 
 For the last four years she had been unable to do much work on 
 account of dyspnea and occasional edema of the legs. She had also 
 had a slight hacking cough with occasional white sputum. She slept 
 with three or four pillows. For six weeks she had been especially 
 dyspneic and orthopneic. 
 
 The physical examination was as at the second entry, except for a 
 less marked general anasarca. X-ray showed a mass which did not 
 pulsate at the right of the heart. The pulsations of the heart itself 
 were very indistinct. The outline of the heart shadow with the poor 
 pulsation suggested pericardial disease. There was extensive 
 mottling extending out from both lung roots. The apices were 
 slightly involved on the left. 
 
 Temperature, 96° to 100°. Pulsations, 61 to129. Respirations 
 23 to 33. Urine: Specific gravity. 1013-1010... Slight tracesmar 
 albumin at three of five examinations. Blood: Hemoglobin 95%. 
 Leucocytes 17,900 to gooo. Two Wassermanns positive, one 
 strongly. Gonococcus fixation test positive. 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 755 
 
 The patient improved in general condition. The heart condition 
 did not change. The vaginitis cleared up under douches and stock 
 vaccines. The sputum was negative for tubercle bacilli. January 
 10 she was discharged. | 
 
 Second Entry.—-February 3 she returned, having been in bed since 
 her discharge with much dyspnea, oliguria, orthopnea, increasing 
 edema of the legs and abdomen, and a troublesome cough. Her 
 physician reported that twice lately he had found her very cyanotic, 
 gasping for breath, frothing at the mouth, with relief from morphia 
 and nitroglycerin. 
 
 Physical examination showed a poorly nourished girl with yellow 
 and cyanosed skin, cyanotic mucosae and yellow sclerae, breathing 
 heavily. The lungs, and abdomen showed evidence of passive 
 
 Marked thrill over entire left precordia, 
 most marked over pulmonic region, 
 “also at apex. lst sound at 
 apex loud, snapping, pre- 
 ceded by roll, followed 
 by short rough systolic 
 murmur. Vany re 
 moist rales. 
 
 Occasional 
 dry squeak 
 
 SY 
 O55 
 
 Dulness, diminished SSN y | Many fine moist 
 Liver edge breathing and fremitus. SSYY) rales. Slight — 
 amooth, farm, Numerous coarse moist rales dulness with dim- 
 slightly tender] SJ ,,-7>. : ; inf'shed breathing. 
 5 cm. below Cetaie dulness, Lungs— poor expansion, 
 
 costal margin. fluid wave. move about equally. 
 
 ~——-—- — -, 
 '. 
 
 Fic. 160.—Necropsy 2997. Clinical signs in a case of mitral stenosis, congenital 
 defect in the interauricular septum, defective closure of the foramen ovale. hypertrophy 
 and dilatation of the heart. 
 
 congestion. Marked systolic thrill over the precordia, most marked 
 over pulmonic region, also at apex. 1st sound at apex loud, snap- 
 ping, preceded by a roll, and followed by short rough systolic murmur. 
 The pulses were of fair volume and tension. The artery walls were not 
 felt. There was marked edema of the legs and ankles, and some 
 over the sacrum. The fingers and toes were clubbed. The pupils 
 and reflexes were normal. 
 
 Temperature 96.4° to 97.8°. Pulse, 120° to° 125. Respirations, 
 30 to 44. Systolic blood pressure 100. Urine not recorded. Blood: 
 hemoglobin 90%. Leucocytes 11,000, polynuclears 77%. 
 
 The day after entrance the patient was more cyanotic and 
 complained of more precordial distress. The right border of the 
 heart had moved out slightly. The heart sounds were very irregular 
 and poor in quality. After digipuratum gr. iss had been given 
 intravenously and again six hours later intramuscularly, there was 
 
756 FACTS ON THE HEART 
 
 some improvement in the character of the sounds. That night 
 4 vi of blood were withdrawn. After this the sounds became more 
 regular and better in quality, and the right border came in a little. 
 That night the patient died. 
 
 The heart weighed 665 grams, enlarged. On section the myo- 
 cardium was of good consistence and pale brown red. The right 
 ventricle wall measured 6 mm., the left ventricle wall 9 mm. The 
 columnae carneae, the papillary muscles and the pectinati on the 
 right side were enormously thickened. The columnae carneae on 
 the left side were fairly well marked. The cavities of the right side 
 were enormously enlarged. The cavities of the left side were only 
 slightly enlarged. The mitral valve circumference was 7 cm. The 
 curtain showed much diffuse fibrous thickening with irregular ridge- 
 like thickening of its free margin which was somewhat nodular in 
 places and showed small areas of roughening and minute to small 
 projecting fibrous tags. The chordae tendineae showed much 
 shortening, thickening and fusion. All of these changes deformed 
 the valve and decreased its circumference. The aortic valve meas- 
 ured 5 cm. The cusps were slightly thickened but otherwise were 
 not remarkable. The tricuspid valve measured 18 cm. The valve 
 showed some thickening and the circumference was very greatly 
 increased. The pulmonary valve measured 10 cm. The cusps 
 were greatly enlarged and showed some thickening. The circum- 
 ference was increased. The foramen ovale presented an oval shaped 
 defective closure 1 cm. in greatest diameter. The upper border of 
 the foramen ovale appeared as a strongly-marked, smooth-surfaced, 
 rounded ridge above which there was a defect in the interauricular 
 septum which easily admitted the passage of the middle finger. The 
 endocardium in the region of the defect was perfectly smooth and 
 shining. The superior and inferior cavae were as usual, but only 
 two pulmonary veins were made out and they were much larger than 
 usual. One of the veins emptied into the left auricle near the region 
 of the defect in the interauricular septum. The auricular appendices 
 were not remarkable. ‘The right side of the heart was engorged 
 with current jelly-like blood clot. The coronary arteries were free 
 and the intima was smooth. The aorta was rather small but other- 
 wise not remarkable. The great branches were not remarkable. 
 The venae cavae were not remarkable. 
 
 The other features of the necropsy beside the mitral stenosis and 
 the defect in the interauricular septum were: 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 757 
 
 Chronic passive congestion, general. 
 
 Infarct of the left lung. 
 
 Hydropericardium. 
 
 Hydrothorax. 
 
 Ascites. 
 
 Anasarca. 
 
 Slight acute glomerulo-nephritis. 
 
 Scoliosis. 
 
 Old infarct in one kidney. | 
 
 Note by Dr. Oscar Richardson.—In this case there was a defective 
 closure of the foramen ovale 1 cm. in greatest diameter and just above 
 the foramen border there was a defect in the interauricular septum 
 which easily admitted the passage of the middle finger. The 
 margins of the defect were smooth and shining. Taking the open 
 foramen ovale and the defect in the auricular septum together there 
 was a rather large channel of communication between the two 
 auricles, sufficient to interfere with the circulation. 
 
 Case LXIX 
 
 An unoccupied Bavarian-American of twenty-one entered 
 September 2 for study. His mother had one child stillborn. An 
 uncle died of tuberculosis. The patient had measles and pertussis 
 in childhood. For six years he had had regularly intermittent periods 
 of coughing. The present one was of two months’ duration. He 
 raised sputum, occasionally slightly bloody, chiefly on getting up. 
 Two years before admission he had tonsillitis. The spring before 
 admission he had severe nosebleeds lasting three or four hours. Alto- 
 gether he bled about three glassfuls. He had had two or three 
 heartburns and occasional indigestion and headaches. He was deaf 
 in the left ear. He sometimes urinated once at night. Three years 
 before admission he weighed 138 pounds, his best weight. His 
 usual weight was 130. He had not worked for two years and a half, 
 but had lived quietly out-of-doors all day. 
 
 His mother said that except for slight dyspnea on exertion 
 he seemed normal in every way until he had pertussis at four years. 
 Then for the first time after an attack of coughing he became cya- 
 notic. The cyanosis had persisted, with remissions of a few hours. 
 It became more marked on exertion or excitement, and sometimes 
 when he was quiet, usually in such cases after meals. He had 
 dyspnea on slight exertion. Medicine never helped him. His 
 condition was about the same as it always had been. 
 
758 FACTS ON THE HEART 
 
 Examination showed a well-nourished man with dusky, moist 
 skin and prominent veins. The mucous membranes were very 
 cyanotic, the sclerae injected. The chest showed an anomaly of the 
 fourth and fifth ribs in the left nipple line. The apex impulse of the 
 heart was not found. The percussion borders were 9 cm. to the left 
 of midsternum, 3 cm. to the right, the supracardiac dullness 5.5 
 cm. The sounds, action, and pulses were normal. A roughsystolic 
 murmur was heard over the whole precordia, loudest at the pulmonic 
 area. Electrocardiogram showed marked right ventricular prepon- 
 
 Fic. 161.—Cardiac shadow in Case LXIX. (Roentgenological Department, 
 Massachusetts General Hospital.) 
 
 derance. The blood pressure was 118/80 to 105/75. Thelungs were 
 negative. The liver edge was just palpable on inspiration. There 
 was marked clubbing of the fingers and toes. The genitals, pupils 
 and reflexes were normal. 
 
 The temperature was 96.2° to 99.6°, below 98° every morning 
 but three. The pulse was 63 to 105, usually 80 to 1oo. The 
 respirations were normal except for two rises to 29-31. The venous 
 pressure was 21cm. water. ‘The amount of urine was 27 to 63 ounces, 
 the specific gravity 1.010 to 1.020. There was a slight trace of 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 759 
 
 2 
 
 albumin at three of four examinations occasional leucocytes at one. 
 Tests for urine albumin before 8 a.m. on two days showed 0; between 
 Io a.m.and 1 p.m., two tests on two days, the slightest possible trace; 
 
 Stic caebinicaailalinavenii a 
 
 | 
 
 { 
 
 BSc i ai ai ti ied bn ot fon Se I WONT Te ST Cn SOOO Ie ae RE ae ces NYS OR Swe ae e a a iLs NS Oe eee scald 
 
 Fic. 162.—1. Shin in Case LXIX. 2 and 3. Shins of syphilitic patients. 4. 
 Normal shin.—No. 1 shows distinct thickening of the cortex of the bone (c). There 
 is also some waviness of outline (a), and a periosteal proliferation (b) at the lower end 
 of the tibia, signs seen also in syphilis, as in No. 3 (e, f; the spot near the middle e, 
 however, is a defect in the plate). No.1 differs from No. 2 in that the thickening of the 
 cortex in No. 1 is equally distributed over both the posterior and anterior surfaces, 
 (c, c) while No. 2 shows marked thickening in the anterior surface only (d). The 
 thickening in No. 2, as in No. 1, is at the expense of the marrow cavity. This equal 
 distribution of thickening on both anterior and posterior surfaces has been observed 
 at the Massachusetts General Hospital in only four cases out of about 100 syphilitic 
 tibiae. (Dr. G. W. Holmes.) 
 
 Dr. Edwin A. Locke, whose studies of pulmonary osteoarthropathy have made him 
 an authority on the subject,* agrees that it is not possible at present to say that equal 
 distribution of the thickening of the cortex is indicative of this condition. In his 
 opinion it would be impossible from the X-ray alone to distinguish No. 1 from a syphil- 
 itic bone. (Roentgenological Department, Massachusetts General Hospital.) 
 
 at 3.30 p.m.o. Ona fourth day the morning urine hada shade less 
 than the evening. The renal function was 40 per cent. The hemo- 
 
 *See his article, Secondary hypertrophic osteoarthropathy, etc. Arch. Int. Med., 
 May, 1916, Vol. XV, Part 1, p. 659. 
 
760 FACTS ON THE HEART 
 
 globin was 150 to 145% (Sahli). There were 10,000 to 8000 leuco- 
 cytes, 70 to 58% polynuclears, 30 to 42%, mononuclears, 9,390,000 to 
 8,688,000 reds, appearing normal at two examinations, universally 
 large and massed at the third. The blood nitrogen was 61 mg. 
 per 100 gm. blood. The coagulation time was 84 minutes. A 
 Wassermann was negative. A stool was negative. The sputum 
 showed no tubercle bacilli at two examinations. Examination of the 
 fundi showed the retinal veins extremely dilated, tortuous, and 
 cyanotic, the arteries somewhat so, the discs very red. X-ray of the 
 tibiae (see Fig. 162) showed notable thickening of the cortex at the 
 
 Fic. 163.—Case LXIX. P.—Projection often seen in congenital heart disease. S— 
 Thickened interlobar septum. (Roentgenological Department, Massachusetts General 
 Hospital. ) 
 
 expense of the medullary portion, and well-marked periosteal 
 proliferation. The skull, hands, and feet were not remarkable. 
 The lungs (see Fig. 163) showed an area of mottled opacity between 
 the fourth and fifth right ribs in the nipple line. The shadow of the 
 lung root was much thickened on this side. There was also evidence 
 of thickening of the interlobar septum. 
 
 The patient was kept in bed, with the usual house diet and no 
 medicine. He showed no change during his stay. ‘The visiting 
 physician noted a systolic thrill, felt with difficulty, and found the 
 
 7 
 
CONGENITAL HEART DISEASE—ILLUSTRATIVE CASES 7601 
 
 murmur late systolic and the pulmonic second sound diminished. 
 September 16 the patient was discharged relieved. 
 
 Dr. Richard C. Cabot’s Diagnosis.—Congenital deformity of the 
 heart. (Probably pulmonary stenosis and interventricular septum 
 defect.) 
 
 Polycythemia (symptomatic). 
 
 Osteoarthropathy affecting the long bones. 
 
 Interpretations of X-rays—Tibiae: The process is quite definitely 
 specific. 
 
 Lung: Lesion is pneumonic in type; may be a localized infection. 
 Syphilis should be considered. 
 
 Heart: Slight enlargement of the left side of the heart; some bulg- 
 ing in the region of the left auricle. 
 
SUMMARY OF THE BOOK 
 I 
 
 AS REGARDS HEART DISEASE AS A WHOLE 
 
 1. Over ninety per cent of all cases of genuine* heart disease fall 
 under one of the three types here called “rheumatic,” syphilitic, 
 and hypertensive. This knowledge is of value because by narrowing 
 the field, it focusses our attention. 
 
 2. The only other type occurring with any considerable frequency 
 is acute and subacute endocarditis ordinarily due to a streptococcus. 
 This made up a little less than 10% of the present series, if one 
 includes the terminal and probably insignificant cases and those quite 
 overshadowed by a primary septic malady, such as perforating appen- 
 dicitis with peritonitis. Without these, the primary and recurrent 
 types of the disease amount only to 102 cases in 1906 or 5%. 
 
 3. Of the three main types of heart disease, the ‘‘rheumatic” 
 usually begins in early youth, and the hypertensive after the fiftieth 
 year, while syphilitic heart is commonest between thirty-five and 
 forty-five. Heart disease in a young woman is almost always rheu- 
 matic (mitral stenosis). In a middle-aged man without rheumatic 
 history a valvular lesion is apt to be due to syphilitic aortitis, producing 
 regurgitation at the aortic valve. In an elderly man previously free 
 from heart trouble, circulatory disease is usually of the hypertensive 
 type. 
 
 4. Each of these three diseases has not only its own characteristic 
 time of life, but attacks a particular part of the heart. 
 
 (a) Rheumatism usually affects the mitral valve. 
 
 (b) Syphilis falls upon the aortic arch (aneurism, angina pectoris) 
 or the aortic valve. 
 
 (c) Hypertensive disease enlarges the whole heart, leaving the 
 valves intact. 
 
 Thus one gets from the physical examination hints as to the type 
 of disease and from the type of disease, as revealed in the history, 
 hints as to what physical examination will show. But the history is 
 of value chiefly in this way and not by delineating a characteristic 
 
 * Most diagnoses of heart disease, whether made by physicians or suspected by the 
 patient, are in my experience wrong. In such cases the heart is usually sound. 
 762 
 
HEART DISEASE AS A WHOLE 763 
 
 symptomatology. ‘‘Heart symptoms” are mostly those of passive 
 congestion (lungs, legs, liver especially), whatever type of heart 
 disease produces it. Only the age, the sex, and the negative or posi- 
 tive history of rheumatism or syphilis give us much help. 
 
 5. Affections of the aortic valve are usually in males. ‘This applies 
 to syphilitic aortitis, to rheumatic aortic stenosis and regurgitation 
 (with or without mitral trouble as well), to acute and subacute endo- 
 carditis, and to the non-deforming aortic scars. 
 
 6. Within the field of the three main types in which our diagnostic 
 inquiries move, hypertensive heart disease occupies by far the largest 
 area. It is so much commoner than any other type that if we know 
 that we have a case of heart disease to study, we know at the same 
 time that it is probably of the hypertensive type, that we shall prob- 
 ably find a chronic elevation of blood pressure and that there will be 
 nothing else very notable in our cardiovascular examination. 
 
 This relative predominance of hypertensive trouble will presumably 
 increase in proportion as the measurably preventable types—rheu- 
 matic and syphilitic—are diminished by public or by private effort. 
 
 7. Most of the other types of heart trouble (acute endocarditis, 
 acute and chronic pericarditis, congenital defects, thyrotoxic disease) 
 are for one reason or another practically unimportant as well as relatively 
 rare. The congenital effects are almost never seen beyond childhood; 
 in childhood they are usually obvious (‘‘blue baby”) or very difficult 
 to identify. Pericarditis in either of its forms we usually cannot 
 diagnose and its effect in weakening the heart is in most cases slight. 
 The remaining deleterious and occasionally diagnosable cases can 
 probably be classed as rheumatic. 
 
 Non-deforming chronic endocarditis does not produce symptoms 
 or signs and has therefore no clinical significance. 
 
 Acute and subacute endocarditis is by no means unimportant but 
 runs most of its course with infectious rather than with cardio-vascular 
 symptoms. Its unsusceptibility to treatment is notorious, so that 
 its recognition is important mainly for prognostic ends. 
 
 8. The focussing of attention on three main types of heart trouble 
 is aided both by realizing the rarity of the remaining types and by 
 clearing the ground of lesions not clinically recognizable, such as myo- 
 carditis and mitral regurgitation. This is especially important with 
 fashionable diagnoses which, like the two last mentioned, do much to 
 blur our knowledge. 
 
 There is no justification for making these diagnoses any longer. 
 
 9. Each of the three types—rheumatic, syphilitic, hypertensive 
 
764 FACTS ON THE HEART 
 
 usually occurs alone. Rheumatism and syphilis almost never affect 
 the same heart and a combination of hypertensive disease with 
 
 either of these infections is rare. The practical importance of this 
 
 fact is that if we have satisfactorily identified one of them—e.g. 
 syphilitic aortitis, with aortic regurgitation—we can be practically 
 certain that the others are absent and the other valves sound. 
 
 II 
 AS REGARDS RHEUMATIC VALVULAR DISEASE 
 
 t. Rheumatic fever (with Sydenham’s chorea and tonsillitis) is 
 the only infection clearly related to deforming lesions of the mitral 
 valve. When the aortic is diseased, syphilis is the only other cause 
 to be considered. (I am excluding here the cases of acute and sub- 
 acute endocarditis.) Our series contains no good evidence that 
 scarlet fever, pneumonia, tuberculosis, typhoid, influenza, gonorrhea 
 or any other infection, except rheumatism and syphilis, can deform 
 the heart valves. 
 
 2. The non-deforming scars or scleroses—often called “chronic 
 endocarditis’? in necropsy protocols—are harmless landmarks and 
 should not be confused with the deforming lesions. | 
 
 3. Rheumatic disease affecting the mitral valve alone (almost 
 invariably stenosis) is commoner in women than in men, 64 to 5o. 
 But when the aortic and the mitral are both affected, males strongly 
 predominate and when the disease is confined to the aortic, not women 
 but elderly men are the sufferers in eight-ninths of the cases. . 
 
 4. Rheumatic heart disease is predominantly a malady of young 
 girls and young women. Somewhere between three-fourths and nine- 
 tenths of all cases begin before the thirtieth year. 
 
 5. Mitral stenosis is the usual rheumatic lesion. In over one-half 
 the cases it occurs without any other valve lesion. On the other 
 hand no other valve is often affected alone. Not once in our whole 
 experience has the pulmonary or the tricuspid been affected alone by a 
 clearly rheumatic endocarditis and the aortic alone has been the seat 
 of rheumatic disease only 28 times as compared with 107 solitary 
 lesions of the mitral. 25 of these 28 cases occurred in men. 
 
 6. The only notable peculiarity in the symptomatology of mitral 
 rheumatic disease is the relative frequency of an early and prolonged 
 palpitation, corresponding presumably to auricular fibrillation. This 
 type of arrhythmia seems to be twice as common in solitary stenosis 
 of the mitral as in cases complicated by aortic disease and shows a 
 tendency to appear “‘early or never,” i.e. the patients who are aware 
 
 Aw Te - _ 
 
RHEUMATIC VALVULAR DISEASE 765 
 
 of any palpitation at all have usually been aware of it among their 
 earliest and most constant symptoms. 
 
 7. Possibly the greater frequency of palpitation in “‘pure” mitral 
 disease may be connected with another peculiarity of that affection, 
 namely, that zm the ‘‘ pure”’ cases uncomplicated by any other valve 
 lesion, the stenosis is ordinarily of greater duration and of greater degree 
 than in the cases with aortic or other valve lesions in addition to the 
 mitral lesion. The more prolonged and more stenosing endocarditis 
 perhaps involves the auricular walls more extensively and thus sets up 
 the fibrillation which thereafter is usually constant because it does not 
 stop without treatment. 
 
 8. But it is notable that the degree of narrowing at the mitral 
 orifice bears no other relation to the kind or severity of the complaints 
 or to the physical signs. The most extreme stenoses are not corre- 
 lated with the severest symptoms of passive congestion. 
 
 9g. When fever and leucocytosis occur they are usually due either 
 to a complicating acute endocarditis or to an auricular thrombus. 
 
 to. Over half the cases of mitral disease do not die of passive conges- 
 tion, but of some intercurrent infections, of trauma, operation, etc. 
 This is especially true of the patients who get by the second decade. 
 In them the disease remains latent for many years and is compatible 
 with long life. 
 
 tt. In the minority of cases when death zs due indirectly to the 
 valvular disease itself, it may be produced not by heart failure (pas- 
 sive congestion) but by an implanted acute endocarditis with septi- 
 cemia or by an embolism of leg, arm or brain from a loosened bit of 
 auricular thrombus which our statistics show is present in a quarter 
 of the decompensated fibrillating cases. Hence the clinical picture of 
 the final illness may be not at all that of heart disease, but rather of 
 a peripheral gangrene, a hemiplegia or a septicemia. In such cases 
 heart disease may be never suspected and the heart never carefully 
 examined. , 
 
 12. These facts and also the fact that death may be very sudden 
 account, in part, for the small number of correct diagnoses made 
 before death in the cases of this series. Over half the cases of mitral 
 disease were not recognized in life. I doubt if the percentage of success 
 is any greater in other institutions or in private practice. 
 
 13. Recognition would be more frequent if physicians realized 
 that the characteristic mid-diastolic or presystolic murmur is not 
 always to be heard unless one takes special measures (exercise, amyl- 
 nitrite inhalation, special positions of the body, auscultation at differ- 
 
766 FACTS ON THE HEART 
 
 ent times of day) which may bring out the important evidence. Well 
 directed search for mitral stenosis will be undertaken oftener if we 
 remember that it is a latent possibility, especially under the following 
 conditions: 
 
 (a) In cases of cerebral or peripheral embolism occurring in rela- 
 tively young persons and so presumably not due to arteriosclerosis. 
 
 (b) In arrhythmic decompensating heart disease without evidence 
 of syphilis or hypertensive cardiovascular trouble, and especially if 
 there is a rheumatic history. 
 
 (c) With evidence of an acute endocarditis (since a chronic endo- 
 carditis usually underlies this lesion). 
 
 (d) In the presence of a sharp first sound and a dull or feeble 
 second sound at the apex; of a doubling of the second sound (or a 
 third heart sound) along the left sternal margin; of absolute arrhy- 
 thmia without known cause in a young person. 
 
 14. Mitral regurgitation without stenosis was apparently present 
 in seven out of the 19c6 necropsies of this series, three of them doubt- 
 ful. It is obviously, therefore, one of the rarest of lesions 
 discoverable post-mortem. During life there are no signs by which 
 it can be recognized. Itis nota clinical entity. 
 
 III. AORTIC STENOSIS 
 
 1. On the whole it seems most probable that our twenty-eight 
 cases of solitary aortic stenosis belong with the rheumatic group. 
 Their history and the post-mortem findings incline us to this belief. 
 
 On the other hand the age and sex distribution is a strange one if 
 the lesion is a rheumatic one, for whereas in most rheumatic heart 
 disease the typical patient is a girl or a young woman, in aortic stenosis 
 it is an elderly man. These facts make us think first of that disease 
 most characteristic of elderly men—arteriosclerosis; but there is 
 strong evidence against this in the pathological anatomy. Only in 
 one doubtful case out of this whole series did arteriosclerosis appear 
 to the pathologist to have produced an aortic lesion. 
 
 Some stray considerations make me consider the question whether 
 the cases of ‘‘pure” aortic stenosis (the other valves remaining 
 untouchea) may represent healed cases of subacute streptococcic 
 endocarditis. These considerations are: 
 
 (a) The presence in the necropsies on cases of aortic stenosis of 
 an unusual number of o/d renal infarcts, possibly thrown off during 
 an earlier attack of vegetative endocarditis. 
 
AORTIC STENOSIS 707 
 
 (b) The fact that while in most rheumatic lesions an old complica- 
 ting pericarditis is often shown by the presence of pericardial adhesions, 
 these adhesions are rarely found in aortic stenosis (one case in twenty- 
 eight) or in subacute endocarditis. 
 
 (c) The fact that the male sex is the commoner in both these 
 diseases. 
 
 Admittedly these stray facts are not important evidence; they 
 only suggest a possibility which is not negatived by the excessively 
 fatal nature of acute and subacute endocarditis, since it is demon- 
 strable that some of these attacks do get well. 
 
 2. In its clinical picture aortic stenosis is peculiar not only in its 
 proneness to occur in elderly men, but also in the frequency of pre- 
 cordial pain, of faintness on exertion, and of angina pectoris. 
 
 3. The contour of the rigid valves, fixed in a position neither open 
 nor shut, seems to compel us to believe that there is regurgitation as 
 well as obstruction of the blood stream. Yet in nearly half the cases 
 no diastolic murmur is detected. 
 
 4. Another strange fact is that even in a case with rigid and 
 immovable valves the aortic second may be not only audible but may be 
 actually accentuated and the systolic blood pressure high. How 
 physiologists would account for this I do not know. 
 
 5. The classical quartette of signs (systolic murmur and thrill 
 in the second right interspace, with a diminished or absent aortic 
 second sound and a flat-topped pulse wave) were not often present 
 as a complete group in this series. Indeed Corrigan’s pulse, the oppo- 
 site of which we expect, is recorded in six out of twenty-eight cases, 
 and a characteristic thrill is often wanting. Yet it can be said that 
 it is still by these four signs (some or all of them) that we can recognize 
 the lesion if we recognize it by any physical signs at all. 
 
 But reasoning helps. When a diastolic murmur and other evi- 
 dence of regurgitation are found in a case with a rheumatic history, 
 it is safe to assume the presence of aortic stenosis also, since only in 
 rare cases does rheumatic disease produce regurgitation, alone and 
 with stenosis. In this way we can often reason ourselves to a correct 
 (though not very important) diagnosis, which direct observation could 
 not make. 
 
 6. The average amount of cardiac hypertrophy is greater in 
 aortic stenosis than in any other valve lesion except syphilitic aortitis 
 with aortic regurgitation. 
 
 7. Even when the aortic orifice is reduced to a mere slit, an abnor- 
 mally high systolic and diastolic blood pressure may in rare cases 
 
768 FACTS ON THE HEART 
 
 be maintained in connection with the complicating nephritis such as 
 was present in over one-third of the cases of this series. 
 
 8. If the disease is rheumatic and begins like most rheumatic heart 
 disease in youth, the advanced age attained by most patients would 
 imply that they live longer than in any other type of heart disease. 
 
 9. Death in six out of twenty-eight cases was notably sudden. - In 
 most, however, it was due to chronic passive congestion. 
 
 IV 
 SYPHILITIC HEART DISEASE 
 
 1. Aside from a single case of myocardial gumma, the lesions 
 here studied were all in the aorta. 
 
 2. Here manifest syphilitic aortitis shows itself clinically as aneu- 
 rism, as aortic regurgitation, as angina pectoris or as some combination 
 of these three troubles. The manifest and harmful cases number 
 about one-fifth as many as those of rheumatic valvular disease and 
 about one-ninth as many as those of hypertensive heart disease (see 
 page 419). : 
 
 3. So far as the aorta is concerned, the disease probably remains 
 latent and harmless for fifteen to twenty years after the original 
 syphilitic infection. In many, perhaps most, cases it is merely a 
 historical landmark in the post-mortem examination. 
 
 4. It is six times as common in men as in women and usually 
 makes itself felt between the thirty-fifth and the fiftieth year, a little 
 later than most rheumatic and a little earlier than most hypertensive 
 cases. An isolated aortic-regurgitant lesion in a man under forty- 
 five is Usually syphilitic. 
 
 5. Though it may be latent and symptomless for many years, it 
 usually leads to death within two years of its first clinical manifesta- 
 tion. 
 
 6. There is no evidence that the disease attacks any valve but the 
 aortic. There it produces in about one-half the cases a regurgitation. 
 The larger portion of the valve remains flexible and capable of good 
 function, but at the contiguous margins where two valves touch 
 each other, a fibrous process binds them back against the aortic wall 
 so that they cannot spread out to support the column of blood during 
 diastole. Hence the regurgitation. 
 
 The heart walls, especially the left ventricle, undergo so great an 
 hypertrophy that the heart’s weight is greater in this type of disease 
 than in any other except in adhesive pericarditis with mediastinitis. 
 
HYPERTENSIVE HEART DISEASE. 769 
 
 7. When the syphilitic process attacks the aorta higher up, above 
 the valves, and leaves the latter normal, no hypertrophy and ordinarily 
 no weakening of the heart occurs even though the aortic wall may 
 be weakened so that aneurism results. Aneurism does not produce 
 cardiac hypertrophy. 
 
 8. Angina pectoris is a common feature of the disease. It may 
 occur (a) in association either with narrowing of the coronary orifices 
 by the syphilitic process in the aorta, or () without any change either 
 in these orifices or in any part of the coronary artery. Angina pectoris 
 before the forty-fifth years should arouse a suspicion of syphilitic 
 aortitis. 
 
 g. The diagnosis of syphilitic aortitis should be relatively easy when 
 angina pectoris or an isolated aortic-regurgitant lesion appears in 
 a young or middle-aged man with a history of syphilitic infection 
 fifteen to twenty years earlier and without any rheumatic history. 
 The Wasserman reaction—which is positive in at least 80% of cases— 
 may assist the diagnosis. 
 
 to. When the disease produces aneurism without angina or aortic 
 regurgitation, it may not be discovered or suspected for a good while 
 unless accidentally shown up by an X-ray taken for some other 
 purpose. For it is only when symptoms of pressure on adjacent 
 structures, (symptoms such as pain, hoarseness, abnormal pulsation 
 of the chest wall) happen to occur that the patient is led to seek an 
 examination. Allsuch pressure symptoms may be absent. 
 
 tr. On the other hand when definite evidence of an aneurismal 
 tumor is obtained, it may be safely assumed to be of syphilitic origin. 
 There is no good evidence that aneurismal tumors are due to any other 
 cause. The so-called “dissecting aneurisms”’ and “‘mycotic aneur- 
 isms” do not produce a tumor or any other recognizable signs. Clini- 
 cally they are negligible. Arteriosclerosis often enlarges the whole 
 aortic arch but does not weaken it, does not produce a tumor, and 
 does no harm of any sort, so far as our cases show. 
 
 V 
 HYPERTENSIVE HEART DISEASE 
 
 t. The commonest of all types of heart disease with decompensa- 
 tion is that here called hypertensive. In fact it is commoner than all 
 the other types put together. 
 
 2. Under this heading are grouped in the present study all cases 
 of enlarged heart* without valve lesions or chronic pericarditis, even 
 
 * (But see no. 12, page 771.) 
 49 
 
77° . FACTS ON THE HEART 
 
 though the proof of hypertension was not always obtained, the 
 cases being studied only at the end of life. 
 
 3. Whether nephritis and arteriosclerosis are to be regarded as 
 causes, as results, or as diseases independent of hypertension, is not 
 clear. ‘The impressions derived from the cases studied in this book are 
 (a) that arteriosclerosis has little or no tendency to enlarge the heart, 
 (b) that nephritis does exert such a tendency, but (c) that hypertension 
 (with its results in cardiac enlargement and final cardiac failure) is a 
 common disease independent of any nephritis or arteriosclerosis. 
 
 4. Hypertension and the associated cardiac hypertrophy last in 
 many cases for years without producing any considerable discomforts 
 or limitations in the individual’s activity. It is discovered ordinarily 
 in the course of a physical examination undertaken for some other 
 purpose (e.g. life insurance). High blood pressure is then the sub- 
 stance of the finding, for the cardiac enlargement is often difficult 
 to make out unless with the aid of the X-ray, and murmurs and 
 arrhythmias are usually absent at this relatively early stage of the 
 disease. 
 
 5. In many, perhaps most, cases, cardiac failure never occurs at 
 all and the patient dies of some other disease or of some extra-cardiac 
 manifestation of hypertension, such as cerebral hemorrhage. 
 
 6. As the disease progresses it may show itself in slight dyspnea 
 on exertion, in a “‘pounding”’ of the arteries of the neck and head and 
 in an awareness of the cardiac impulse. Still, it bothers the patient 
 little unless he is alarmed by what he is told about the disease. 
 
 7. At this latent stage it may, nevertheless, contribute to death 
 in case the patient is prostrated by infection, trauma, toxemia or 
 surgical operation. 
 
 8. Less often—in about one-third of our cases—the heart itself 
 weakens and death occurs from passive congestion. In such cases 
 the hypertension may continue to the end or may disappear. 
 
 9. In these cases death usually follows within a year from the 
 first serious evidences of stasis, shown as in other types of heart trouble 
 by arrhythmia, tachycardia, pulse-deficit and passive congestion. 
 Systolic (and occasionally diastolic) murmurs may be present at the 
 base or at the apex of the heart, but are of no diagnostic value; the 
 same is true of an accented aortic second sound. 
 
 Diagnosis rests on the presence or history of a chronic hypertension, 
 on the cardiac enlargement, and on the lack of evidence pointing to 
 valvular disease, chronic pericarditis or thyrotoxicosis. Hypertensive 
 
ACUTE AND SUBACUTE ENDOCARDITIS Tia 
 
 disease is often wrongly diagnosed as myocarditis, mitral regurgita- 
 tion, “‘cardiorenal disease” or ‘‘the senile heart.” 
 
 to. The degree of cardiac enlargement discoverable post-mortem 
 is usually moderate; the extreme hypertrophies resulting from chronic 
 pericarditis or from disease of the aortic valve were not seen in hyper- 
 tensive cases of this series. gro grams was the weight of the largest 
 heart. 
 
 t1. The disease is more than twice as common in men as in women 
 and appears usually about the fiftieth year, though no decade of life, 
 except the first, is exempt from it. 
 
 12. The disease is to be distinguished from the cardiac hyper- 
 trophies which occur almost constantly in pernicious anemia and 
 in leukemia. These diseases are associated with low or normal blood 
 pressure. 
 
 VI. MYOCARDITIS 
 
 1. Fibrous myocarditis is an item of post-mortem anatomy usually 
 associated with other and more important cardio-vascular lesions, 
 such as arteriosclerosis, nephritis and hypertension in elderly men.. 
 
 2. It is not recognizable clinically and should be left out of diag- 
 nostic terminology, although its pressure may be vaguely suspected 
 when evidence of cardiac infarction Is present. 
 
 VII. ACUTE AND SUBACUTE ENDOCARDITIS 
 
 1. The labors of Libman and others have gone far to separate out 
 a recognizable group of cases to which the name of “‘subacute bacterial 
 endocarditis” is given. Very possibly this is a separable disease 
 entity. In our series, however, its distinction from rheumatic, septic 
 and terminal cases of endocarditis is not clear. It has seemed better, 
 therefore, to group together here all cases showing soft vegetations on 
 the valves and then to attempt clinical-pathological sub-groupings 
 as follows: 
 
 (a) Those in which the soft endocarditis and its results constituted 
 apparently the whole of the disease, before and after death (the so- 
 called ‘‘ primary” cases, 36 out of 180). 
 
 (b) Those identical with the above except that an old hard endo- 
 carditis accompanies the soft acute process (“recurrent primary”’ 
 cases, 66 in 180). 
 
 (c) Those in which a septic process (such as purulent peritonitis) 
 outside the circulatory system seemed at necropsy to be the starting 
 
1/12 FACTS ON THE HEART 
 
 point and main body of the disease (pyemic cases with or without an 
 old endocarditis, 44 in 180). 
 
 (d) Those in which some non-septic disease—such as cancer or 
 nephritis appeared to be the main cause of death, (‘terminal endo- 
 carditis,” 34 in 180). 
 
 In each of these groups there have been cases with bacteria found 
 in the circulation (usually some type of streptococcus) and cases in 
 which none were found. In each there have been cases clinically 
 acute and others clinically subacute. On a histological basis alone, it is 
 doubtful whether one has a right to make time-distinctions. 
 
 The relation of the soft endocarditis to the hard valve lesions which 
 were also present in 102 of 180 cases is problematic. Are we correct in 
 speaking of the soft process here as recurrent, i.e., a return of the 
 same disease which produced the hard lesions? Or is it another 
 disease which has supervened, as pneumonia may invade a previously 
 tuberculous lung? I do not see how an answer can as yet be given. 
 In the “primary” groups of cases (a and 0 above) the coincidence of 
 hard and soft lesions attains 64%. 
 
 2. It is a disease prone to attack both sexes equally and especially 
 young adults (twentieth to fortieth year). But possibly in children 
 it gets well or becomes arrested and so is not reckoned with in statistics 
 which like these deal only with fatal cases. 
 
 3. The mitral valve is affected in over three-fourths of the cases. 
 It is the only valve attacked in nearly one-half. In general the fre- 
 quency with which the different valves are attacked is about the same 
 as in chronic (‘“‘rheumatic”) endocarditis with deformity. The tri- 
 cuspid is rarely attacked (13 in 180). 
 
 4. We have never found the gonococcus or the influenza bacillus 
 in the blood or in the lesions. 
 
 5. Clinically the disease is recognized when symptoms of sepsis 
 (fever, leucocytosis, chills, anemia, jaundice, bacteriemia) are com- 
 bined with evidence of a valve lesion and of embolism. But the 
 latter is discovered clinically in only one-third of the cases, though 
 at necropsy embolism is shown in two-thirds of the primary cases 
 (a and 6 above). The skin, spleen, kidneys, brain and lungs are 
 oftenest hit by emboli. 
 
 6. A palpable thrill and an increasing anemia have been to me 
 the most helpful diagnostic signals. 
 
 7. Nephritis occurred in thirty to fourty per cent of the cases, but 
 acute pericarditis, which one would suppose would be a common com- 
 plication, was found here in only nine cases out of 180 or five per cent. 
 
ACUTE PERICARDITIS PES 
 
 8. In many instances the diagnosis is masked by evidences of 
 passive congestion, associated in nearly 40% of our cases with cardiac 
 enlargement. This enlargement is usually explainable by chronic 
 lesions (valve deformities or hypertension), but occasionally seems 
 to be produced by the acute endocarditis itself. 
 
 g. The duration is usually weeks or months, sometimes years. 
 
 to. Evidence of a healed (perforating) lesion is sometimes found. 
 
 VIII. ACUTE PERICARDITIS 
 
 t. As already said, we can recognize this disease in only one-fifth 
 of the cases and then can usually do nothing to cure it. Its clinical 
 importance is therefore small. 
 
 2. This clinical insignificance is the more striking if we realize that 
 it is the main cause of death in less than 5% of the cases in 
 which it occurs. Usually it is only one localization of a general 
 septicemia, or is a terminal event in nephritis, neoplastic disease, etc. 
 
 3. Other cardiovascular lesions (except hypertension and its 
 results) are rarely found with an acute pericarditis. Hence if we are 
 sure of that lesion, we can usually exclude endocarditis, acute or 
 chronic. 
 
 4. Organisms of the streptococcus-pneumococcus group can usually 
 be found in the blood or in the pericardial exudate; in children the 
 staphylococcus once freed from a local lesion, such as osteomyelitis, 
 is prone to attack the pericardium as well as to produce myocardial 
 abscess. | 
 
 5. Enlargement of the heart is present in two-thirds of the cases 
 and passive congestion in one-third. Over one-half of the enlarge- 
 ments are not explained post-mortem and while a previous hyperten- 
 sion probably accounts for some, it seems possible that an acute or 
 subacute pericarditis can itself produce cardiac enlargement. 
 
 6. Effusion in considerable amount is found in about one-third 
 of the cases, only 13% of which were recognized in life either by 
 the X-ray or by the presence of an extraordinarily wide percussion 
 area. 
 
 7. Like chronic pericarditis, the acute form is “a diagnostic mar- 
 plot” in that it produces sounds indistinguishable from intracardiac 
 murmurs. But since (as above said) endocarditis and pericarditis 
 seldom occur together, the former should usually be excluded if we 
 are sure of the latter. 
 
 ¢ 
 
774 FACTS ON THE HEART 
 
 IX. CHRONIC PERICARDITIS 
 
 1. When extensive and associated with mediastinitis in young 
 rheumatic subjects, this disease produces the largest hearts known 
 (1328, 1158, 1150 grams in uncomplicated cases) and leads to death 
 from passive congestion (28 cases out of 112). 
 
 2. In only 20 cases of 112 was the disease associated with a chronic 
 endocarditis. Most cases are “vestigial,” that is, are evidence of a 
 previous acute pericarditis but produce no passive congestion; the 
 patients (mostly elderly men) die of some non-circulatory disease. 
 
 3. As in acute pericarditis males overwhelmingly preponderate. 
 
 4. Diagnosis is rarely possible (6 of 112). Thus far X-ray has 
 given us no help. 
 
 5. Diastolic and presystolic murmurs are often heard, especially 
 in cases with large hearts, and lead to false diagnoses of endocarditis. 
 
 X. THYROCARDIAC DISEASE 
 
 1. In most thyroid intoxications the heart is noisy and demon- 
 strative; it is apparently but not actually enlarged and if death 
 occurs it is from the self-poisoning, not from passive congestion. 
 
 2. In old non-toxic goitres and in toxic adenomata, congestive 
 heart failure with fibrillation may after many years supervene. 
 Operation appears to be of benefit in some cases. 
 
 No constant cardiac lesions are found post-mortem. 
 
 XI. ANGINA PECTORIS AND CARDIAC INFARCT 
 
 1. Angina pectoris if distinguished from the symptoms accom- 
 panying cardiac infarct has no constant anatomical basis. 
 
 2. Coronary disease and macroscopic changes in the aortic arch 
 are often absent in cases of angina pectoris, and still more often pres- 
 ent without angina. 
 
 3. Angina may cease when passive congestion is established, but 
 in most of our cases this is not true. 
 
 4. When a coronary is blocked by clot or sclerotic changes, and 
 cardiac infarction follows, we may find a characteristic clinical 
 picture corresponding: intense, usually epigastric pain lasting for 
 hours, often with pulse failure and fainting. The symptoms are not 
 produced by exertion or emotion and are not relieved by rest or 
 nitrites. . 
 
 5. Coronary occlusion, acute or chronic, with or without cardiac 
 infarction, may be symptomless. 
 
INDEX 
 
 ABSCESS, myocardial, 527 
 
 Adams, Louis M., 343, 344, 457 
 
 Adrenalin, 89 
 
 Allbutt, Sir T. Clifford, 123, 418, 499, 550 
 
 Anemia in acute endocarditis, 572 
 
 Anemia, pernicious, see Pernicious. 
 
 Aneurism, 27; abnormal area of pulsation 
 in, 333; arteriosclerosis in, 336; 
 asthmatic type, 335; cardiac, 534, 
 537; illustrative cases, 537; complica- 
 tions in, 336; diagnosis of, 334; dis- 
 secting, 412; dysphagia in, 335; 
 edema in, 335; inequality of pupils in, 
 334; mycotic, 412; nephritis in, 336; 
 paralysis of recurrent laryngeal nerve 
 in, 334; physical signs of, 334; pres- 
 sure signs of, 335; ruptured, 399; 
 
 symptoms of, 333; systolic murmurs | 
 
 in, 334; systolic thrill in, 333; tracheal 
 tug in, 333, 334; valvular lesions in, 
 3360; with acute endocarditis, 336; 
 with non-deforming endocarditis, 
 
 336; with myocarditis, 336; with 
 pericarditis, 336; with rheumatic 
 valve lesions, 336; X-ray examina- 
 tion in, 334 
 
 Angina pectoris, 548, 774; and aortic 
 stenosis, 218, 554; and blood pressure, 
 555; and myocarditis, 554; and 
 syphilitic aortitis, 552; cessation of 
 with passive congestion, 555; with- 
 out coronary narrowing, 550; with 
 fibrous myocarditis, 552; with perni- 
 cious anemia, 554 
 
 Angina, Vincent’s, 96 
 
 Aorta, arteriosclerosis of, 434; gummatous 
 focus in, 372; hypoplasia of, 23, 26; 
 hypoplastic, with cardiac hyper- 
 trophy, 423; hypoplastic, with 
 chronic passive congestion, 23; mural 
 thrombus of, 487 
 
 Aortic disease, types of, 257; regurgita- 
 tion, see Regurgitation; stenosis, see 
 Stenosis; wall, spirochetes of syphilis 
 In, 373 
 
 Aortitis, see Syphilitic. 
 
 Apocynum, 106 
 
 Arrhythmia in acute endocarditis, 574; 
 in chronic pericarditis, 683; in mitral 
 stenosis, 47 
 
 Arsphenamin, 355 
 
 Arteriosclerosis, 23, 26, 416, 417; and 
 nephritis, heart weights in, 427; 
 degree of, 424; of aorta, 434; pul- 
 monary, 23; pulmonary with chronic 
 passive congestion, 23; with aneu- 
 rism, 336; with chronic passive con- 
 gestion, 23 
 
 Arteriosclerotic degeneration of kidney, 
 23, 20, 428; with chronic passive con- 
 gestion, 23 
 
 Arthritis, 31 
 
 Atropin, 89 
 
 Auricular fibrillation, 83, 101; flutter, 83, 
 109 
 
 Austin Flint murmur, 683 
 
 BACTERIOLOGY in aortic stenosis, 217; 
 in acute endocarditis, 578; in acute 
 pericarditis, 640 
 
 Barry, John W., 224, 225 
 
 Blood in aortic stenosis, 217 
 
 Blood pressure in angina pectoris, 555; 
 diastolic, in myocarditis, 500; sys- 
 tolic, in myocardial infarction, 515 
 
 Bock, Arlie, 142, 702 
 
 Breed and White, 294 
 
 Brown, Lewis S., 166, 167, 168, 180, 181, 
 250, 345, 377, 378, 591, 698, 699, 741, 
 746 
 
 Casot, Hugh, 194, 349, 464, 480, 518, 
 534, 671 
 
 Cactus, 107 
 
 Caffein, 89, 387, 539 
 
 Caffein sodium benzoate, 126 
 
 Cardiac abscess, 527; aneurism, 534; 
 aneurism, illustrative cases, 537; 
 disease, frequency of, 17; failure in 
 thyroid disease, 724; failure, septic, 
 
 775 
 
770 
 
 with dropsy, 637; hypertrophy, asso- 
 ciation with dilatation, 436, see 
 also Heart disease. 
 
 Cardiac hypertrophy and dilatation, 23, 
 25, 26, 52, 53; arrhythmia in, 449; 
 enlargement in, 449; cardiac failure 
 in, 436; casual lesions, 422; etiology 
 of, 421; chronic passive congestion 
 in, 449; correlation of, with various 
 diseases, 417; degrees of, in various 
 lesions, 432; heart sounds in, 449; 
 heart weight in, 449; in acute endo- 
 carditis;! 503,065 75;, 12 acute, -peri- 
 carditis, 643; in chronic non-deform- 
 ing endocarditis, 632; in myocardial 
 infarction, 515; in myocarditis, 497, 
 499; mode of death in, 437; murmurs 
 in, 449, 451, 452; palpitation in, 449; 
 relation of nephritis to, 416; type of 
 nephritis in, 449; with acute endo- 
 carditis, 423; with acute nephritis, 
 451, age in, 451, blood pressure in, 
 451, chronic passive congestion in, 
 451, duration of, 451, heart weight in, 
 451, Murmurs in, 451, 452, Sex IN, 451, 
 type of nephritis in, 451; with acute 
 pericarditis, 423; with arteriosclero- 
 sis, 23, 423, 424; with chronic pas- 
 sive congestion, 23; with chronic non- 
 deforming endocarditis, 423; with 
 chronic nephritis, blood pressure in, 
 448, sex in, 448; with chronic peri- 
 carditis, 423, 433; with hyperten- 
 sion, 423; with hypoplastic aorta, 
 423; with leukemia, 423; with myo- 
 carditis, 423; with nephritis, 423, 426; 
 with nephritis and arteriosclerosis, 
 427, age in, 446, blood pressure in, 
 448, chronic passive congestion in, 
 447, duration in, 446, heart weight in, 
 447, murmurs in, 447, sex in, 446, 
 type of arteriosclerosis in, 447, type 
 of death in, 448, type of nephritis in, 
 446; with pernicious anemia, 423; 
 with rheumatic valvular disease, 423; 
 with subacute nephritis, 450, chronic 
 passive congestion in, 450, duration 
 of, 450, heart weight in, 450, mur- 
 murs in, 450, sex in, 450, with syphi- 
 litic valvular disease, 423, without 
 nephritis or arteriosclerosis, 428 
 
 Cardiac infarction, diagnosis of, 516; 
 physical signs of, 515 
 
 INDEX 
 
 Cardiac murmurs, 17, 55, 59; in acute 
 endocarditis, 563, 575; in aortic 
 stenosis, 213; in acute pericarditis, 
 640, 641; in cardiac hypertrophy and 
 dilatation, 449; in chronic nonde- 
 forming endocarditis, 631; in chronic 
 pericarditis, 683; in hypertensive 
 heart disease, 443; mid-diastolic, 
 105; with subacute nephritis, 450 
 
 Cardiovascular lesions, 21, 24; manifest, 
 23; relative frequency of, 26 
 
 Chorea, 30, 41, 312; illustrative cases, 315 
 
 Christian, Henry A., 404 
 
 Chronic passive congestion, see Passive 
 congestion, chronic. 
 
 Coller, Frederick A’) 727, 728 
 
 Congenital heart disease, see Heart 
 disease, congenital. 
 
 Convallaria, 103, 106 
 
 Cor bovinum, 432 
 
 Coronary narrowing without angina 
 
 pectoris, 550; orifices, blocking of, 520; 
 sclerosis, without angina pectoris, 
 549; thrombosis, 556; thrombosis 
 with pain, 556; thrombosis without 
 pain, 556 
 
 Davis, Lincoln, 346 
 
 Death, cause of in acute pericarditis, 641; 
 congestive, 25; mode of, in aortic 
 stenosis, 219, in mitral and aortic 
 stenosis, 149, in mitral disease, 77; 
 in myocarditis, 502; toxic, in thyroid 
 disease, 725 
 
 Degenerations, 24 
 
 Diagnostic expectations, 
 682 
 
 Digifolin, 89, 175 
 
 Digipuratum, 282, 286, 466, 481 
 
 Digitalis, 106, 107, 108 
 
 Diuretin, 117 
 
 17; marplots, 
 
 EpsALL, David L., 705 
 
 Effort syndrome, 17, 723 
 
 Electrocardiogram, 83, 89, 101, 106, 109, 
 T15,° 132, 171, 188, 355, 405) 5005 
 523, 616, 691, 714, 758; in auricular 
 flutter, 186 
 
 Embolic deaths in mitral stenosis, 78 
 
 Embolism in acute endocarditis, 563, 567, 
 568 
 
 Emerson, Haven, 26 
 
 Emphysema, 421 
 
INDEX 
 
 Endocarditis, acute, 23, 24, 26; acute and 
 subacute, 561; 775; age in; 563; 
 anemia in, 572; arrhythmia in, 574; 
 associated lesions in, 579; bacteri- 
 ology in, 578; cardiac enlargement in, 
 563, 575; cardiac murmurs in, 575; 
 constitutional sepsis in, 572; diagno- 
 sis of, 582; distribution of embolic 
 lesions in, 567; duration of, 580, 581; 
 embolism in, 563, 567; embolism 
 recognized in life in, 568; dyspnea in, 
 575; edema in, 575; foci of sepsis in, 
 570; heart weights in, 577; illustra- 
 
 _ tive cases, 583; initial, 565; leucocy- 
 tosis In} 573; mental state in, «572; 
 murmurs in, 563; nature of, 567; 
 nephritis in, 563, 569; primary, 562; 
 pyemic, 565; recurrent, 565; sex in, 
 563; skin hemorrhages in, 5609; 
 tenderness of fingers and toes in, 569; 
 terminal, 565; thrill in, 576; types of, 
 561; underlying disease in, 571; 
 valve affected in, 563; with aneurism, 
 336; with chronic passive congestion, 
 23; with meningitis, 570 
 
 Endocarditis, chronic non-deforming, 20, 
 23, 24, 26, 628; age in, 629; aneurism 
 in, 3363; associated lesions in, 631; 
 cardiac complaints in, 633; cardiac 
 hypertrophy in, 632; cardiac mur- 
 murs in, 631; etiology of, 629; sex in, 
 629; valves affected in, 632; with 
 chronic passive congestion, 23 
 
 Endocarditis, terminal, 571 
 
 Endocarditis, type of, 32, 309 
 
 Endocarditis, verrucose, 200 
 
 Error, probable, 20 
 
 FEVER in acute pericarditis, 636; in myo- 
 cardial infarction, 515 
 
 Fitz, Reginald F., 490 
 
 Fremont-Smith, Maurice, 142, 196, 197, 
 261, 265; 748 
 
 Frey, Max von, 108 
 
 GARLAND, Joseph, 63 
 Goiter, see Thyrocardiac diséase. 
 Gumma, cardiac, 322 
 
 HAMILTON, Burton E., 725, 727, 728 
 
 Hartwell, Harry F., 661 
 
 Heart defects, congenital, 23; 
 chronic passive congestion, 23 
 
 with 
 
 i id 
 
 Heart disease, congenital, 738; illustra- 
 tive cases, 739 
 
 Heart disease, hypertensive, 18, 416, 410, 
 769; age incidence in, 420; arterio- 
 sclerosis in, 440; blood pressure in, 
 440; cardiac enlargement in, 444; 
 cerebral symptoms in, 443; diagnosis 
 in, 443; duration of symptoms in, 
 439; false pericardial friction in, 443; 
 heart weight in, 421, 441; illustrative 
 cases, 454; latent, 420; murmurs in, 
 441, 443; nephritis in, 441; physical 
 signs in, 444; pulse pressure in, 441; 
 Sexi, 2426 
 
 Heart disease, imaginary, 17; latency of, 
 24; manifest, 24; manifest or latent, 
 419; predominating lesion in, 24; 
 pseudo, 17; rheumatic, see Rheumatic 
 heart disease; syphilitic, 322, 768; 
 valvular, 24 
 
 Heart, maximum weight of, 429; over- 
 demonstrative, 723; rupture of, 546 
 
 Heart muscle, gumma in, 375 
 
 Hemorrhages of skin in acute endocar- 
 ditis, 569 
 
 Hoffman, Frederick L., 403 
 
 Holmes, George W., 242, 389, 596, 663, 
 695, 759 
 
 Hypertensive cardiovascular disease, see 
 Heart disease, hypertensive. 
 
 ILLUSTRATIVE Cases: cardiac aneurism, 537; 
 chorea, 315; combined valve lesions, 
 160; endocarditis, acute, 563; hyper- 
 tensive heart disease, 454; myocardial 
 abscess, 529; myocardial infarction, 
 521; myocarditis, 454, 505; pericardi- 
 tis, acute, 647; pericarditis chronic, 
 685; regurgitation, aortic, 257; re- 
 gurgitation, mitral, 296; stenosis, 
 aortic, 221; ‘stenosis mitral,.080; 
 stenosis, mitral and aortic, 150; 
 syphilitic aortitis, 337; thyrocardiac 
 disease, 731 
 
 Infarction, myocardial, see Myocardial 
 infarction; splenic, 94 
 
 JAUNDICE, in aortic stenosis, 211, 218, 
 in mitral stenosis, 49; in rheumatic 
 heart disease, 63 
 
 KARELL diet, 156 
 Kidd, Frank, 532 
 
778 INDEX 
 
 Kidney, amyloid degeneration of, with 
 chronic passive congestion, 23; see 
 Arteriosclerotic degeneration and 
 Nephritis. 
 
 Kraus, F., 727 
 
 Lek, Roger I., 290 
 
 Lesions, combinations of, 25; multiple, 21; 
 single, 25, 26 
 
 Leucocytosis in acute endocarditis,. 573; 
 in acute pericarditis, 636 
 
 Leukemia, 23, 26; with chronic passive 
 congestion, 23 
 
 Lewis, Sir Thomas, 108 
 
 Locke, Edwin A, 759 
 
 Lung, gumma of (?), 405 
 
 Lymphoma, malignant, simulating aneu- 
 rism, 360 
 
 MACKENZIE, Sir James, 293 
 
 Magnesium sulphate, 227, 491 
 
 Magrath, George Burgess, 750 
 
 Means, James Howard, 398, 736 
 
 Mediastinitis, 432 
 
 Meningitis, and acute endocarditis, 570 
 
 Merrill, Adelbert S. 399, 410, 663, 708 
 
 Mitral disease, arrhythmia in, 47, 61; 
 auricular thrombi and arrhythmia in, 
 72; blood pressure in, 62; latent, 77; 
 nephritis and other complications in, 
 66, 72, sex in, 40; urinalysis in, 66; 
 See also Stenosis, mitral. 
 
 Mitral orifice, size of, 75, 76 
 
 Mitral regurgitation, see Regurgitation; 
 stenosis, see Sienosis; valve, fibro- 
 calcareous mass in, 204 
 
 Morphia, 234, 268, 286, 387, 410, 466, 493 
 
 Murmurs, see Cardiac murmurs. 
 
 Myocardial abscess, 527; coronary arteries 
 in, 529; embolism in, 528; illustrative 
 cases in, 529; local septic processes in, 
 528; physical signs of, 528; symptoms 
 of, 528 - 
 
 Myocardial infarction, 512, 515, 516; 
 cardiac hypertrophy in, 515; chronic 
 passive congestion in, 513; coronary 
 arteries in, 514; duration of attacks 
 of pain in, 514; epigastric localization 
 of, 514; fever in, 515; illustrative 
 cases, 521; intracardiac thrombi in, 
 515; pulse failure in, 514; recurrent 
 type, 520; site of pain in, 514; sudden 
 faintness in, 514; syphilitic aortitis 
 
 in, 515; systolic blood pressure in, 
 515; types of, 518; with symptoms in 
 life, 521 
 
 Myocarditis, fibrous, 23, 24, 26, 29, 494, 
 771; age in, 500; angina in, 490, 554; 
 arrhythmia in, 499; associated lesions 
 
 in, 497; blood pressure in, 499, 500; © 
 
 cardiac hypertrophy in, 497, 490; 
 chronic nephritis in, 503; coronary 
 sclerosis in, 497; diagnosis of, 498; 
 extreme diffuse, 501; good cardiac 
 function in, 501; illustrative cases, 
 454, 5053, infectious disease in, 497; 
 main factors in death, 503; mode of 
 death, 502; pulse pressure in, 500; 
 streptococcus sepsis in, 503; sex in, 
 500; slight cases, 502; syphilitic, 322, 
 496, 552; thrombi in, 500; with 
 aneurism, 336; with chronic passive 
 
 congestion, 23; without cardiac hyper- . 
 
 trophy, 497; with syphilitic aortitis, 
 552 | 
 
 NEOSALVARSAN, 383 
 
 Nephritis, 26; acute, 23; acute with 
 cardiac hypertrophy, 151; amyloid, 
 23; and arteriosclerosis, heart weights 
 in, 427; chronic, 23; chronic, in 
 myocarditis, 503; heart weights in, 
 426: in acute endocarditis, 563, 569; 
 in aortic stenosis, 218; in hypertensive 
 heart disease, 441; in mitral disease, 
 66; subacute, 23; subacute in cardiac 
 hypertrophy 450; type of in cardiac 
 hypertrophy, 449; with chronic pas- 
 sive congestion, 23; with aneurism, 
 336 
 
 Neurocirculatory asthenia, 723 
 
 Nitroglycerin, 289, 466, 524 
 
 OLIVER, E. Lawrence, 586 
 Ophuls, William, 417 
 Osler, Sir William, 292 
 Oxygen, 387 
 
 PALPITATION in mitral stenosis, 47 
 
 Passive congestion, chronic, 23, 24, 217, 
 637; with acute endocarditis, 23; 
 with acute pericarditis, 23; with 
 amyloid degeneration of kidney, 23; 
 with aortic regurgitation, 23; with 
 aortic stenosis, 23; with arteriosclero- 
 sis; 23; with arteriosclerotic degenera- 
 
 = 
 
INDEX 
 
 tion of kidney, 23; with cardiac 
 hypertrophy, 23; with chronic non- 
 deforming endocarditis, 23; with 
 chronic pericarditis, 23; with com- 
 bined valve lesions, 23; with congeni- 
 tal heart defects, 23; with hypoplasia 
 of aorta, 23; with leukemia, 23; with 
 mitral and aortic stenosis, 23; with 
 mitral regurgitation, 23; with mitral 
 stenosis, 23; with myocarditis, 23; 
 with nephritis, 23; with pernicious 
 anemia, 23; with pulmonary arterio- 
 sclerosis, 23; with syphilitic aortitis, 
 23; with toxic goitre, 23; with tuber- 
 culous pericarditis, 23 
 
 Pericardial effusion, 638 
 
 Pericarditis, acute, 23; 24, 26,'28; 635; 
 773; age in, 635; associated lesions 
 in, 636; bacteriology in, 640; cardiac 
 hypertrophy in, 643; diagnosis in, 
 636, 645; fever and leucocytosis in, 
 636; illustrative cases, 647; main 
 cause of death in, 641; murmurs in, 
 640, 641; sex in, 635; with aneurism, 
 336; with chronic passive congestion, 
 23; chronic, 23, 24, 26, 430, 672, 774; 
 age in, 675; arrhythmia in, 683; 
 ascites in, 684; diagnosis in, 676; 
 friction sounds in, 684; illustrative 
 
 779 
 
 Regurgitation, 31; aortic, 20; aortic, 
 
 illustrative cases, 257; aortic, pure, 
 23; aortic, rheumatic type, 252; 
 aortic, with chronic passive conges- 
 tion, 23; aortic with arteriosclerosis, 
 256; aortic without stenosis, 254; 
 mitral, 289; mitral, diagnosis in, 
 293; mitral illustrative cases, 2096; 
 mitral, pure, 23; mitral with chronic 
 passive congestion, 23 
 
 Rheumatic heart disease, 19, 28, 30, 746; 
 
 age at time of death, 38; anasarca in, 
 63; anginoid attacks in, 73; ascites 
 in, 63; blood cultures in, 75; cardiac 
 murmurs in, 55; cardiac hypertrophy 
 in, 50, §2; cyanosis in, 50, 63; dilata- 
 tion of cavities in, 53; duration of 
 life in, 35, 36; embolic and thrombotic 
 lesions.in,.70; fever in, 67; frequency 
 of certain symptoms in, 48; heart 
 sounds in, 56, 57, 58; hydropericar- 
 dium in, 63; hydrothorax in, 63; 
 infarcts in, 69; infections other than 
 rheumatism in, 43; jaundice in, 63; 
 leucocytosis in, 50, 68; liver in, 65; 
 positive post-mortem cultures in, 74; 
 pulse in, 61; spleen in, 65, 66; thrill 
 in, 60; thrombus feveri n, 67; tuber- 
 culosis in, 43; weight of heart in, 52 
 
 cases, 685; murmurs in, 683; primary | Rheumatism, 31, 41 
 rheumatic, 674; 680; secondary rheu- | Richardson, Maurice H., 518 
 matic, 675, 681; sex in, 675; vestigial, | Richardson, Oscar, 129, 137, 139, 140, 142, 
 
 673, 678; with aneurism, 336; with 
 cardiac hypertrophy, 433; with chronic 
 passive congestion, 23; tuberculous, 
 with chronic passive congestion, 23 
 
 153, 157, 100, 167, 168, 173, 176, 178, 
 180, 181, 189, 191, 196, 199, 223, 224, 
 225, 230, 241, 247, 250, 251, 261, 
 264, 271, 276, 279, 302, 315, 342, 343, 
 
 344, 345, 353s 357s 359, 304, 368, 377, 
 378, 387, 393, 397, 401, 406, 410, 415, 
 456, 457, 462, 470, 473, 477, 483, 493, 
 507, 512, 526, 530, 534, 540, 543, 587, 
 591, 601, 606, 619, 624, 662, 667, 671, 
 688, 693, 700, 708, 715, 721, 741, 742, 
 745, 746, 748, 750, 754, 757 
 
 Riesman, David, 563 
 
 Rupture of heart, 546 
 
 Pernicious anemia, 23, 26; with angina, 
 555; with chronic passive congestion, 
 23; with cardiac hypertrophy, 469 
 
 Pick’s syndrome, 682 
 
 Pneumonitis, chronic, 421 
 
 Polyarthritis, 31 
 
 Polygram, 113 
 
 Pratt, Joseph H., 585 
 
 Pulmonary arteriosclerosis, 23 
 
 Pulmonary artery, gummatous focus in, 
 374 SALICYLATES, 273 
 
 Putnam, James J., 546 Salt-free diet, 4091 
 
 Salvarsan, 301 
 
 Scudder, Charles L., 178 
 
 Sepsis, foci of in acute endocarditis, 570; 
 
 RECURRENT laryngeal nerve, paralysis of, pneumococcus, 197; streptococcus in 
 334 myocarditis, 503 
 
 QUINIDINE, sulphate, 83, 84, 108 
 
780 
 
 Septic deaths in mitral stenosis, 78 
 
 Septic heart failure and dropsy, 637 
 
 Shaw, H. Batty, 418 
 
 smith; “William: -H*1o% 5125)-5s0s 7 
 250, 286, 305, 364, 376, 380, 393, 473; 
 479, 506, 539, 590, 601, 698, 699, 719 
 
 Sodium nitrate, 524 
 
 Status lymphaticus in thyroid disease, 726 
 
 Stenosis and regurgitation, 31 
 
 Stenosis, aortic, 23, 147, 205, 766; age in, 
 206; angina pectoris in, 218, 555; 
 anginal pain in, 211 ; aortic second 
 sound in, 215; arterial walls in, 217; 
 bacteriology, 217; blood in, 217; 
 blood pressure in, 216; cardiac en- 
 largement in, 208, 212; cardiac mur- 
 murs in, 213; cardiac weights in, 
 213; with chronic passive congestion, 
 23, 217; complications in, 218; cough 
 in, 211; Cyanosis in, 211; dizziness in, 
 211; dyspnea in, 211; edema in, 211; 
 estimated duration of, 218; etiology 
 of, 205; fever in, 212; gastric symp- 
 toms in, 211; hydrothorax in, 211; 
 illustrative cases, 221; infarcts in, 
 210; jaundice in, 211; leucocytosis 
 in, 212; mode of death in, 219; mur- 
 murs in, 214, 215; nephritis in, 218; 
 nutrition in, 212; palpitation in, 211; 
 pulse in, 216; size of aortic aperture 
 in, 209; symptoms of, 210, 2117; thrill 
 in, 215; tightness across chest in, 211; 
 type of endocarditis in, 209; urine in, 
 217; weakness in, 211 
 
 Stenosis, mitral, 20, 23, 32; age of onset 
 in, 33; chronic passive congestion in, 
 23; Corrigan pulse in, 61; diagnostic 
 errors in, 79; diastolic murmurs in, 
 59; duration of life in, 34; earliest 
 cardiac symptoms, 45; embolic deaths 
 in, 78; etiology in, 41; hoarseness and 
 aphonia in, 63; illustrative cases, 80; 
 jaundice in, 49; mode of death in, 
 77, 78; nutrition in, 49; palpitation 
 in, 47; physical signs, 49; pulse in, 
 60, 61; septic deaths in, 78; sex in 
 relation to age of onset in, 33; sudden 
 death in, 78; symptoms, 44, 45 
 
 Stenosis, mitral and aortic, 23, 148; age in, 
 145; arrhythmia and palpitation in, 
 146; diagnosis in, 147; dilatation of 
 cavities in, 146; dyspnea in, 145; 
 fever and leucocytosis, 148; heart 
 
 INDEX 
 
 weights in, 146; illustrative cases, 
 150; infectious pulmonary complica- 
 tions in, 148; mode of death in, r4o; 
 nephritis in, 148; nutrition in, 146; 
 passive congestion in, 23, 148; 
 physical examination in, 146; posi- 
 tive cultures in, 148; rheumatism 
 in, 145; sex in, 145; symptomatology 
 of, 145; thrombi in, 148; with chronic 
 passive congestion, 23 
 
 Stenosis, mitral, aortic, and tricuspid, 
 159; mitral, aortic, tricuspid and 
 pulmonary, 159; mitral and tricuspid, 
 159; pulmonary and tricuspid, 159 
 
 Streptococcus sepsis in myocarditis, 503 
 
 Streptococcus viridans, 139, 185 
 
 Strophanthin, 199, 279, 286 
 
 Strychnia, 140 
 
 Syphilis, spirochetes of, in aortic wall, 373 
 
 Syphilitic aortitis, 19, 23, 26, 29, 422; 
 age of manifestation, 324; aneurismal 
 type, 323, 338; angina in, 332, 552; 
 arteriosclerotic lesions, in, 326; asth- 
 matic type, 331; cases with aortic 
 regurgitation, 323, 328; cases without 
 regurgitation, 323, 3293; cause of 
 death, 333; diagnosis in, 326; dysp- 
 nea in, 331; four types of, 323; general 
 cardiac symptoms of, 331; heart 
 weights in, 330; illustrative cases, 
 337; IM negroes, 325; latentjeaoa 
 occasions of discovery, 325; position 
 of disease in aorta, 326; sex in, 325; 
 Wassermann reaction in, 327; with 
 aortic stenosis, 323; with chronic 
 passive congestion, 23; with myocar- 
 dial infarction, 515; X-ray diagnosis 
 In, 327 
 
 Syphilitic heart disease, 322 
 
 TALBOT, Fritz Bi, 667 
 
 Tenderness of fingers and toes, 569 
 
 Terminology, 30 
 
 Thrill in acute endocarditis, 576 
 
 Thrombosis, coronary, 556; in myocardial 
 infarction, 515; in myocarditis, 500; 
 mural of aorta, 487 
 
 Thyrocardiac disease, 23, 26, 723, 774; 
 heart failure in, 724; illustrative 
 cases, 731; status lymphaticus in, 
 726; toxic death in, 725; with chronic 
 passive congestion, 23 
 
 Tileston, Wilder, 383 
 
INDEX 
 
 Tonsillitis, 41 
 
 Tracheotomy in aneurism, 363; in nephri- 
 tis, 482 
 
 Tuberculous pericarditis, 2 
 
 T-wave, inversion of, 115 
 
 URINE in aortic stenosis, 217; in mitral 
 disease, 66 
 
 VALVE measurements, 20 
 
 Valvular lesions, 26; combined, 23, 150; 
 diagnosis in, 159; etiology in, 150; 
 illustrative cases, 160; necropsies in, 
 159; symptomatology in, 159; with 
 chronic passive congestion, 23; de- 
 forming, 20; multiple, 145; with 
 aneurism, 336 
 
 781 
 
 Venesection, 481 
 
 Ventricular contractions, ectopic, ror, 
 106; escapes, 83 
 
 Vincent’s angina, 96 
 
 WartTain, A, S., 322 
 
 Wearn, Joseph T., 512 
 
 Welch, William H., 322 
 
 White; Paul-D.,/63, 71, 83, 105, .239, 479, 
 705, 712 : 
 
 Whittemore, Wyman, 652 
 
 Work-hypertrophy, 421 
 
 Wright, James Homer, 235, 370, 373, 375 
 
 Younc, Edward L., Jr., 180, 530, 546, 623 
 
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