key: cord-0043652-tk7o7snp authors: nan title: Full Issue PDF date: 2020-05-20 journal: JACC Case Rep DOI: 10.1016/s2666-0849(20)30423-x sha: c0bb0dd7d476d4888d87e3b3e44496cb3ca97ade doc_id: 43652 cord_uid: tk7o7snp nan To highlight the role of multidisciplinary management of fungal endocarditis. and right quadrantanopia. Laboratory examination was significant for leukocytosis (white blood count: 13.85 Â 10 cells/mm 3 ) with eosinophilia (eosinophils: 25.41%). The presentation of infective endocarditis is often variable and requires a high index of suspicion. The Duke criteria, which incorporate serological, physical, and imaging findings, is recommended to risk stratify patients into 3 categories of definite, possible, and rejected diagnosis (1) . A minimum of 3 sets of blood cultures obtained from different sites with an interval of at least 1 hour between the first and last set is recommended (1) . Echocardiography plays a crucial role in the diagnosis and must be performed expeditiously, ideally within 12 h of initial evaluation (1) . If the clinical suspicion of endocarditis is high and the initial transthoracic echocardiogram (TTE) findings are negative, a repeat TTE or a TEE should be performed. The use of other imaging modalities such as computed tomography and cardiac magnetic resonance imaging (MRI) may also play an important role (1) . Intraoperatively, immediate identification of the pathogen using polymerase chain reaction has also proven useful (1) . Figures 1A to 1E show the various manifestations of endocarditis in our patient. MRI of the brain showed multiple embolic lesions in the right occipital and left parietal lobes with hemorrhagic transformation (Figures 1D and 1E) . The patient was restarted on vancomycin, gentamicin, and rifampin while further work-up was conducted. Findings on an initial TEE were negative. However, computed tomography of the chest demonstrated a lesion above the prosthetic aortic valve. A repeat TEE 2 days following admission showed large vegetations on the anterior wall of the aorta, and this finding was confirmed with MRI of the chest. The patient was subsequently taken to surgery for treatment of infective endocarditis. Following surgery, intravenous amphotericin was started. Our patient received an EPIC bioprosthetic valve, which was chosen on the basis of on patient and family preference. The patient was reluctant to take warfarin, and there was concern for the risk of hemorrhagic conversion with anticoagulation. Selection of a replacement valve is based on consideration of life expectancy, patient preference, compliance with anticoagulant agents, lifestyle, risk of bleeding, and risk of recurrent surgery (2) . The patient's age alone should not be the determining factor. Structural valve dysfunction over time, leading to regurgitation or stenosis, is the major disadvantage of bioprosthetic valves and the major reason for repeat intervention. The management of complications of infective endocarditis or neurological sequelae is controversial. Cerebrovascular complications secondary to embolization from endocardial vegetations have a 20% to 40% incidence and are associated with an increased risk of post-operative morbidity and mortality (1, 3) . Guidelines from the American Heart Association and the European Society of Cardiology recommend delaying surgery for at least 4 weeks following intracranial hemorrhage (1, 3, 4) . Results of a previous retrospective study demonstrated higher mortality when valve replacement was performed within 7 days of intracranial hemorrhage (5) . Our patient's brain lesions were embolic with hemorrhagic transformation, which raised concern regarding the use of high-dose heparin during the surgical procedure. Following extensive discussions with the patient, family members, and the multidisciplinary care team, the decision was made that the benefit of surgery outweighed the risks. The patient tolerated the surgery without complications, and MRI performed following surgery showed no evidence of hemorrhage or enlargement of prior lesions. Intraoperatively, a vegetation measuring 10 mm was discovered on the anterior wall of the aorta, and a perforation was noted on 1 leaflet of the EPIC valve. The valve was replaced, and the anterior wall was patched with bovine pericardium. A wet mount of the vegetation showed numerous hyphae, and the final pathology examination that showed positive results for Trichosporon asahii yielded the diagnosis of fungal endocarditis ( Figure 1B ). The etiologic agents most frequently isolated are Candida and Aspergillus (6) . The genus Trichosporon currently contains 37 recognized species, of which 8 are associated with infection or allergy: T. asahii, T. asteroides, T. cutaneum, T. inkin, T. mucoides, T. ovoides, T. domesticum, and T. montevideense (6, 7) . Fungal endocarditis is a rare clinical entity that has been associated with prior drug use, indwelling catheters, prosthetic valves, or immunocompromised states (1, 6) . Trichosporon infection can lead to disseminated fungal infection in immunocompromised individuals, particularly in patients with malignant disease (8) . Fungal infection with T. asahii carries a grave prognosis with a high mortality rate (1, 8) . Invasive Trichosporon infections have been associated with prior antibiotic therapy, a history of central catheter use, malignant disease, and hospitalization in intensive care units (8) . The route by which T. asahii invades the human body remains unknown, however (8, 9) . One prior study of Trichosporon infections determined that blood, urine, and surgical wounds were the most common sites of infection, and T. asahii was the most frequently isolated species (8) . This study also identified neutropenia, central venous catheters, The past medical history included hypertension, chronic kidney disease, and multivessel TA. The differential diagnosis included acute ischemic stroke, central nervous system infection, vasculitis, carotid artery stenosis, and coronary artery disease. To recognize the spectrum of findings of Takayasu arteritis for prompt diagnosis and treatment. To highlight the incidence of coronary artery involvement in Takayasu arteritis and how this presents a therapeutic challenge. Elevated erythrocyte sedimentation rate and C-reactive protein may support the diagnosis; however, one study of 60 TA patients found erythrocyte The primary treatment for active disease is highdose glucocorticoids, while maintenance therapy involves tapering of steroids in combination with immunomodulatory and biologic agents, such as methotrexate or azathioprine (6) . Many patients experience relapse or disease progression despite treatment, with estimated relapse rates of w40% (6) . A recent randomized controlled trial of 36 TA patients in remission assigned to placebo or the novel interleukin-6 receptor antagonist tocilizumab showed a trend toward increased time to relapse without reaching significance (p ¼ 0.0596) (7) . Surgical options for those with vascular complications include stenting or bypass grafting, although restenosis in areas of active tissue inflammation poses significant concern. One study reports restenosis in 31.7% of surgical interventions, with decreased incidence when performed after medical therapy or during a quiescent stage of disease (8) . The patient's multiorgan involvement presented a unique diagnostic and therapeutic challenge. Coronary artery involvement is seen in only 7% to 9% of cases and typically results in ostial occlusion, unlike the diffuse triple-vessel stenosis seen in this case (1, 9) . Treatment can be challenging, as coronary artery revascularization in TA is often unsuccessful due to ostial involvement, active inflammation, and high rates of restenosis (10, 11) . Although enhanced atherosclerosis has been reported with TA, this was not seen in this patient (10) . Autopsy revealed chronic inflammatory changes in the coronary arteries, suggesting that earlier immunosuppression or immunologic therapy may have slowed the progression of disease. The diagnosis of TA remains challenging, owing to its indolent nature and nonspecific symptoms, which may belie significant underlying vascular damage. Early diagnosis is essential as immunosuppression may slow disease progression. A 62-year-old man presented to an outside hospital with complaints of resting and exertional interscapular back pain over the past few weeks that had progressed. These complaints were consistent with prior stable anginal-equivalent pain but were no longer responsive to nitroglycerin therapy. The patient had a blood pressure 109/70 mm Hg, and he was bradycardic with heart rate 47 beats/min and saturations 97% in room air. dose inotropic support that was rapidly tapered. He was discharged 3 days later and was able to walk hundreds of feet without any chest discomfort. There are increased risks of ventricular decompensation and eventual failure when myocardial territories have decreased perfusion during percutaneous interventions. The larger the at-risk area becomes, the less favorable the risk:benefit ratio for intervention becomes. Many nonsurgical patients have anatomy that is considered too high risk for attempting intervention, as operators may feel that there is no reasonable expectation against mortality with the risks of intervention in these patients. Looking at the role of MCS in shock lends some hope for future developments that will improve that risk:benefit ratio. ECMO, for example, has shown a life-saving role in the treatment of some patients with cardiogenic shock (1) . The American College of Cardiology/American Heart Association's ST-segment elevation However, there are no current guideline recommendations for or against MCS in hemodynamically stable patients. FOLLOW-UP. After his initial recovery period, the patient went home in good condition and has continued to follow-up with his medical team outside of the authors' healthcare system. As with other forms of MCS, ECMO support for nonshock, high-risk PCI is terrain still being charted in the modern era. The practice is increasingly substantiated by case reports and case series. years ago. The in-stent dissection was now more pronounced compared with observations made at the index PCI. No other dissections in the mid-LAD between the 2 stents were detected, which could have been the trigger for the intramural hematoma. These findings suggest that the in-stent dissection extended to the stent distal and caused intramural hematoma, leading to coronary artery occlusion. The coronary flow was completely restored after implantation of an additional drug-eluting stent (2. 75 Â 48 mm) overlapping the 2 previously implanted stents in the proximal and distal LADs (Video 6). Although in-stent dissection is generally considered a benign complication after PCI (1, 2) , operators should note that in-stent dissection can extend to the distal segment and cause intramural hematoma in a subacute setting, resulting in coronary artery occlusion (3) . Nevertheless, it is challenging to associate in-stent dissection with hematoma at the time of PCI if no hematoma can be identified. High-pressure post-dilatation aiming to compress the in-stent dissection should be considered. Further investigations are needed to better understand the mechanism and management of this rare but critical condition. We performed orbital atherectomy in the left circumflex artery through a stent that jailed the circumflex artery ostium. The orbital atherectomy catheter was entrapped within the stent and the stent was avulsed during catheter withdrawal. We should consider this potential complication when performing orbital atherectomy in a jailed side branch. Percutaneous coronary intervention was performed with a Diamondback 360 Coronary Orbital Atherectomy System (CSI, St. Paul, Minnesota). The lesion was crossed with the assistance of a 7-F Guidezilla extension catheter (Boston Scientific, Marlborough, Massachusetts). First, the lesion was ablated at 80,000 rpm. Then, the speed was increased to 120,000 rpm. Suddenly, the catheter became entrapped within the LM stent struts (Video 2). The double guiding catheter technique was performed. Another wire was advanced across the stent and a 2.25-mm balloon was inflated. However, the catheter still could not be withdrawn. Intravascular ultrasonography was performed using the parallel wire and revealed that the stent had been avulsed and was wrapped around the catheter ( Figure 1C, Video 3) . Finally, we exchanged the Guidezilla for a Guideplus (Nipro, Osaka, Japan) and pulled and pushed the Guideplus, which succeeded in withdrawing the Orbital Atherectomy catheter ( Figure 1D ). We implanted 3 drug eluting stents, which resulted in sufficient lesion dilatation by angiography with TIMI (Thrombolysis In Myocardial Infarction) flow grade 3. A similar complication with a cutting balloon catheter was previously reported (1) . This potential complication should be considered when evaluating whether to perform orbital atherectomy in a jailed side branch, especially when the side branch has an obtuse angle. A 65-year-old woman presented to the hospital with dyspnea and demonstrated New York Heart Association functional class III symptoms of congestive heart failure. The patient has a history of hypertension, hyperlipidemia, diabetes mellitus, and obesity. Computed tomography scan revealed a large adnexal mass measuring 36.2 Â 24.7 Â 33.6 cm, and occupying To understand the role of TAVR as a minimally invasive method of treating low-risk patients with severe symptomatic AS who require noncardiac surgeries. To understand that in patients with large intra-abdominal or adnexal masses careful planning and attention to modification of routine TAVR technique is essential for adequate access and groin management and to facilitate valve passage. most of the pelvis and lower abdomen ( Figure 1 ). The mass was deemed likely a benign ovarian serous or mucinous tumor. The primary consequence was the mass effect, which was elevating both hemidiaphragms and compressing both lungs. Furthermore, echocardiography revealed severe bicuspid AS with a mean gradient of 66 mm Hg, peak velocity of 5.4 m/s, and a calculated aortic valve area of 0.6 cm 2 in the setting of normal ejection fraction (60% to 65%) and mild-to-moderate aortic insufficiency (AI) (Supplemental Figure 1, Videos 1 and 2). The patient was referred for consideration of aortic valve replacement before adnexal mass resection. The patient was deemed intermediate risk for surgical aortic valve replacement (SAVR) because of the risk of prolonged intubation and respiratory failure related to the mass effect of the growth. The multidisciplinary heart team did not want to delay the patient's progress toward mass resection by subjecting the patient to a more prolonged recovery post-SAVR. Simultaneous mass resection and SAVR as combined procedure was considered but deemed high risk. Balloon aortic valvuloplasty (BAV) as a bridge to NCS was not an option given the baseline AI and the bicuspid valve. The gynecologic oncology team deemed her to have well over a 1-year life expectancy. Hence, TAVR was chosen as the optimal treatment strategy. Balloon-expandable prosthesis was chosen over a self-expandable prosthesis for the following reasons. The angle of entry from aorta into the left ventricle measured 62 ( Figure 2 ) making it more difficult to seal with a self-expanding prosthesis (2) . A balloon expandable SAPIEN 3 prosthesis was used for its greater radial force ( This case serves as a reference for patients needing prompt NCS in the setting of severe AS. Although an enormous adnexal mass needing prompt resection is somewhat rare, more commonly patients present with AS-related syncope complicated by orthopedic injuries, such as hip fracture, and are in need of prompt valve intervention before definitive correction of the orthopedic injury. Although the mass presented a technical challenge, the case illustrates the advantages of performing TAVR on low-risk patients. Recent publications of the low-risk TAVR trials demonstrate that in low surgical risk patients, TAVR is at least as good if not superior to SAVR (5, 6) . Recent data have suggested that elimination of routine BAV during TAVR may be beneficial (7); however, cases such as ours raise the question as to when it is necessary. Certainly the presence of An electrophysiology study the next day demonstrated infrahisian and intrahisian disease resulting in placement of a permanent pacemaker. The patient did well subsequently and was discharged home with a plan for adnexal mass resection in the near future as an outpatient. To recognize that recipients with transplanted hearts are subject to a slew of complications which may include common valvular diseases. To understand the importance that a multidisciplinary heart team approach plays in management of complex structural heart patients. To illustrate the expanding role of transcatheter aortic valve replacement to serve complex patients. The differential diagnosis for shortness of breath in a patient with prior heart transplant is extensive but includes predominantly transplant rejection, which can be acute cellular rejection, humoral rejection, and coronary artery vasculopathy (CAV) (1, 2) . Lung infections can also present with shortness of breath, due to either community-acquired pneumonia or opportunistic infections by organisms such as cytomegalovirus, Epstein-Barr virus, Toxoplasma gondii, Aspergillus fumigatus, or Candida albicans. Lymphoproliferative disorder of the lung and lung cancer are also in the differential. Blood work showed normal white blood count and mild anemia. B-type natriuretic peptide was elevated (600 ng/l). Creatinine was 8 mg/dl with normal electrolytes. Chest radiographs showed no lung in- During that time, the patient was asymptomatic. Left heart catheterization revealed an 80% stenosis in the mid portion of the left anterior descending artery, which was treated with one drug-eluting stent. The lesion was focal, consistent with coronary artery disease, and lacked features concerning for CAV, but it was deemed significant enough and was fixed in preparation for valve intervention. For a heart to be considered for transplantation, donors must be younger than 55 years of age, although Continuous-wave Doppler using a Pedoff probe in the right upper sternal border, revealing a peak velocity of 4.7 m/s and a mean gradient of 52 mm Hg, consistent with severe aortic stenosis. Abbreviations are as in Figure 1 . Beale et al. Beale et al. A 32-year-old male with hypertension and hyperlipidemia presented to the hospital with complaints of central chest pain which was worse on exertion. Results of serum troponin analysis and resting electrocardiograms were normal. He underwent an exercise treadmill test which returned normal results. In view of the nature of his chest pain, he underwent a coronary angiogram. Coronary angiography ( Figure 1A , Video 1) in the anteroposterior cranial view (RAO 1 CRAN 39) revealed a single coronary artery arising from the right coronary sinus giving rise to the right coronary artery and a large branch that supplies the left anterior descending and left circumflex arteries. An aortogram did not reveal any other coronary origin. Computed tomography coronary angiography (CTCA) ( Figure 1B) 3-dimensional volume-rendered computed tomography heart image (LAO 7 CRAN 56) was obtained which showed a single coronary artery arising from the right coronary cusp bifurcating into the right coronary artery and an anomalous left main artery which coursed leftward anterior to the main pulmonary artery before dividing into the left anterior descending artery and the left circumflex artery. The Agatston coronary calcium score was 0. There was no coronary artery stenosis or other cardiac abnormality. He was treated with analgesia for presumed musculoskeletal chest pain, with resolution of his symptoms. There was no symptom recurrence during the subsequent 2 years of follow-up. Single-coronary artery is a rare congenital anomaly that is usually isolated but may be associated with other congenital heart anomalies such as tetralogy of Fallot and truncus arteriosus (1). CTCA is useful for delineating the coronary anatomy and exclude associated cardiac anomalies. It is important to identify the "malignant" interarterial course of the anomalous coronary artery between the main pulmonary artery and the aorta, which is associated with myocardial ischemia and sudden death. In the present patient, the anomalous left main artery assumed a "benign" course anterior to the main pulmonary artery and was not found to be the cause of his chest pain. ADDRESS FOR CORRESPONDENCE: Dr. Perryn Ng, National University Heart Centre, Singapore, National University Health System, 5 Lower Kent Ridge Road, Singapore 119074. E-mail: perryn_lf_ng@ nuhs.edu.sg. The proximal RCA bifurcates into an anterior branch (arrow) and the mid RCA. (A) AP cranial view (RAO 1 CRAN 39). The proximal RCA bifurcates into an anterior branch (arrow) and the mid RCA. (B) 3D VR CT heart image (LAO 7 CRAN 56) which shows a single coronary artery (asterisk) arising from the right coronary cusp (D) which bifurcates into the RCA (single arrow) and an anterior branch (double arrows) which courses leftward and further bifurcates anteriorly to the main pulmonary artery into anterior (single arrowhead) and posterolateral (double arrowheads) branches. The anterior branch courses along the anterior interventricular grove to supply the LAD territory and the posterolateral branch courses along the left atrioventricular groove to supply the LCX territory. AP ¼ anteroposterior; CT ¼ computed tomography; LAD ¼ left anterior descending artery; LCX ¼ left circumflex artery; RCA ¼ right coronary artery; VR ¼ volume rendered. A 52-year-old male was diagnosed with severe Rafiq et al. Failure to pass a nasogastric tube in the intensive care unit raised the suspicion of esophageal atresia with TEF, confirmed by full body X-ray ( Figure 1 ). After consulting general pediatric surgery, gastrostomy tube placement occurred on day of life 5. We held feeds and did not extubate prior to esophageal repair. Despite the posterior TAPVC repair's relationship to the TEF, the proximal and distal esophageal pouches were anastomosed without tension. A male infant, born at 38 weeks to a gravida 2 para 1 to Although rare, AVT is a serious cause of abnormal blood flow from the aorta to the ventricle in infancy. Echocardiography is the diagnostic investigation of choice and must be used to distinguish AVT from other lesions that cause rapid runoff of blood from the aorta. Optimal management of patients with AVT includes prompt surgical repair to prevent progression into heart failure. There was no evidence of aortic stenosis nor worsening of mild aortic regurgitation. AVT is a paravalvular connection between the aorta above the sinotubular junction and the ventricle. It was first reported in 1963 by Levy et al. (1) and continues to be a rare defect that only accounts for 0.1% to 0.5% of all congenital cardiac defects. AVT is a rare cardiac malformation that may cause progressive postnatal heart failure and is often associated with other cardiac lesions. In utero diagnosis currently improves the neonatal management of AVT through assessment of its prognosis and programmed assisted delivery. High suspicion is To make a differential diagnoses in the evaluation of abnormal cardiac size and function in a D-transposition of great arteries post-ASO patient. To understand the role of different imaging modalities, and in particular, the role of CMR in the workup of patients with surgically corrected transposition of the great arteries. To recognize features of athlete's heart and its overlap with ischemic and dilated cardiomyopathy. anteroseptal segments and normal diastolic function (Table 1) . There was also a prolapsed anterior mitral leaflet with moderate mitral regurgitation (vena an appropriate hyperdynamic cardiac response to exercise in athlete's heart, which patients with DCM are rarely able to achieve (3, 4) . Stress-imaging modalities like echocardiography and myocardial perfusion imaging would be able to assess for these features. Although echocardiography is the standard modality to assess diastolic function, this can also be assessed via CMR. CMR, however, may have a growing role as the imaging modality of choice for patients. CMR has the added benefit of LGE assessing for fibrosis, a feature that may be present in DCM but not seen in athlete's heart. T1 and ECV mapping may also have an additional role, especially in cases where the diagnosis is uncertain. Higher native T1, ECV, and T2 relaxation times have also been reported in patients with DCM compared with controls and athletes, with native T1 showing to be the best discriminator for both conditions (3). In our case, the patient had no increased uptake on LGE. Additionally, he showed a hyperdynamic response to exercise with no wall motion abnormalities, and T1 and ECV mapping values were normal. This rules out ischemic cardiomyopathy and DCM, giving the diagnosis of athlete's heart. The effects of detraining in our patient (i.e., reduction in LV mass with no change in LVEF) were also consistent with findings in another study (6) . After detraining, a repeat echocardiogram showed a normal LV systolic function with a reduction in LV size. Because of considerations mentioned previously, a strategy of watchful waiting with advice of strictly avoiding vigorous physical activities has been used. The multiple diagnostic considerations in this case highlight the advantages of ergometer stress CMR as a safe and comprehensive imaging modality in the assessment of a patient with complex congenital heart disease. With a noninvasive test without and <17 cm/s for CB (8, 9) . As shown in the right panel of Figure 1 , local endo- Now it has been demonstrated that a considerable degree of EEA can occur in both the RA and the LA. It can be assumed that EEA can occur anywhere in both atria. This is in line with prior epicardial mapping studies demonstrating that focal waves, which may arise due to EEA, occurred throughout both atria without predilection sites (10 their great clinical outcome and by the beautifully descriptive iconography provided in their case report. In this "Da Vinci" corner, we sought to review the anatomical determinants necessary to understand LBB pacing and the normal anatomy (and its variants) of the left bundle branch in the human heart. Figure 1F) , and 40 mm in the right CIA ( Figure 1H , Table 1 ). The patient has been followed on aspirin with close monitoring until the present time. Coronary artery aneurysm (CAA) is classically defined as a focal dilatation of more than 1.5 times the diameter of an adjacent artery (1) Kang et al. Coronary artery was diffusely dilated without aneurysm and that the wall of an abdominal aorta was thickened without aneurysm. Diagnosis of CAEBV After prednisolone was administered, the wall thickness of an abdominal aorta was decreased. 2 yrs after the diagnosis (allogenic bone marrow transplantation) An abdominal aortic aneurysm and CIA aneurysm with maximum diameter of 34 mm in the abdominal aorta, and that of 26 mm in the right CIA. A coronary artery aneurysm from LMT through left anterior descending and RCA with maximum diameter of 7 mm in the LMT, and that of 6 mm in the RCA. The EBV-DNA level in peripheral blood decreased to beneath the detection limit. international coronary artery aneurysm registry (CAAR). Int J Cardiol 2020;299:49-55. He had no formal medical history nor any family history. His parents were first cousins of South Asian origin. There was a pansystolic murmur in the mitral region with no signs of fluid overload. Cranial nerve examination was normal. There was wasting of the upper limb muscles with proximally distributed weakness. The lower limb weakness was distally distributed. All reflexes were absent but with normal plantar reflexes. Sensation was normal. Multisystem involvement and parental consanguinity raised the suspicion of a recessively inherited myopathic disorder. Electrocardiogram showed poor R wave progression and Troponin I was mildly elevated. Echocardiogram To be aware that lipid storage diseases, such as ATGL deficiency, can cause heart failure. To appreciate that heart transplantation is an effective cure for triglyceride cardiomyovasculopathy. He was treated with optimal guideline directed medical therapy and cardiac resynchronization therapy-defibrillator. He remained stable for 18 months. In the following 12 months, he was hospitalized 4 times with decompensated heart failure. Heart Association functional class I to IV. He was hospitalized again due to repeated Figure 2A) . This confirmed the diagnosis of triglyceride deposit cardiomyovasculopathy (2) and helped to exclude other causes of heart failure. His case was discussed at the transplant multidisciplinary meeting. Besides his mild neuromuscular weakness, he had no other comorbidities and thus he was placed on the urgent waiting list for a heart transplant. However, despite being on inotropic support, his condition deteriorated rapidly and he developed cardiogenic shock. Therefore, a biventricular assist device was implanted to maintain end-organ perfusion and bridge him to heart transplantation. Some go on to have distal limb involvement (9) . Serum CK levels remain elevated throughout (6, 8, 9) . Approximately 40% of patients exhibit cardiac dysfunction which appears to be affected later in the course of the disease, usually after the age of 20 (2,3,5-9). The extent of cardiac involvement is influenced by many factors as evidenced by siblings who carry the same ATGL mutation (3, (5) (6) (7) (8) (9) . Estrogen appears to have a protective effect demonstrated by the higher incidence of cardiac damage in male patients (3, 8) . A complex venous graft angioplasty was performed and a drug-eluting stent was implanted. Initially, the most frequent causes of fever in hospitalized patients, such as urinary or respiratory To use PET/CT as a diagnosis and follow-up technique in an infected aneurysm. To consider conservative treatment in patients with infected graft aneurysm and high surgical risk. Once an SVG aneurysm is detected, a chest CT should be performed to determine graft patency, as well as the exact location of the aneurysm within the mediastinum to guide the surgical approach. Cardiac catheterization should also be done to assess coronary anatomy and potential distal targets for revascularization. There is no consensus on the optimal management of SVG aneurysms. Treatment options include surgical repair and percutaneous closure with Amplatzer devices, covered stents, and arterial coiling (1). In In our center, daptomycin is the first-line therapy for methicillin-resistant S. aureus bacteremia (6). Rifampin is bactericidal against S. aureus, achieves A 77-year-old man was referred to our hospital for the evaluation of a suspected mediastinal mass that was incidentally detected on chest radiography ( Figure 1 ). His vital signs were stable. All physical and laboratory examination results and the electrocardiogram were unremarkable. The patient had a history of ischemic stroke, diabetes, hypertension, hyperlipidemia, and smoking. He underwent subtotal gastrectomy for a gastric ulcer at 45 years of age and coronary angiography for angina at 49 years of age. We initially suspected atherosclerotic-related CAAs, postintervention coronary pseudoaneurysms, or inflammatory and infectious diseases. Echocardiography revealed 2 huge masses around the heart ( Figure 2) . Contrast-enhanced computed tomography (CT) revealed multiple CAAs severely compressing the cardiac chambers ( Figure 3) . In addition to a left gastric artery aneurysm (LGAA), we To understand radiological findings in coronary and abdominal artery involvements associated with IgG4-RD. To review the causes of CAAs. To understand that genetic testing may be necessary for diagnostic accuracy when encountering patients with low levels of LDL-C. To understand the causes of low levels of LDL-C and how to manage patients with genetic conditions that cause low levels of LDL-C. The patient's childhood development was normal, with no reported history of failure to thrive; no symptoms of malabsorption; and no neurological, hepatic, or visual abnormalities. There was no history of chronic or acute infections, recent hospitalizations, or inflammatory disease. Causes of very low levels of LDL-C are listed in Table 1 . Based on the history and available data, the etiology of this patient's very low LDL-C was hy- Medication effects -- Cascade screening for low levels of LDL-C was performed for firstand second-degree relatives. Next, the index patient and 7 family members ( Figure 3 ). The index patient and affected cases were not clinically followed after the management plan was discussed due to the proximity of residence to clinic location. To make a differential diagnosis of causes of recurrent syncope episodes in a patient with paroxysmal atrial fibrillation started on amiodarone with background history of ischemic cardiomyopathy. To recognize one of the subacute amiodarone side effects affecting the cardiovascular system, which include complete heart block, prolonged QTc, and recurrent TdP. In this setting, ventricular pacing from conventional sites was arrhythmogenic whereas pacing at the His bundle region suppressed TdP. Each ventricular escape rhythm is followed by premature ventricular ectopic of varying morphology. In general, amiodarone has low proarrhythmic effect both in normal and heart failure patients despite QT prolongation due to its fast phase III repolarization, a low incidence on dispersion of repolarization, a lower potential to induce early after depolarization, and a weak effect on reverse frequency dependence (7, 8) . However, the proarrhythmic effect of amiodarone has been well described (7, 8) . In our case, the proarrhythmic effect of amiodarone was likely exacerbated by low repolarization reserve in this patient. However, the patient declined genetic testing for long QT syndrome. Conventional pacing at the RV apex and epicardial LV through the CS vasculature triggered TdP Table 1 . After temporary symptomatic relief with the introduction of guideline-directed drug therapy for heart failure, his dyspnea worsened, and approximately 1 year after symptom onset, the patient was once again in New York Heart Association functional class III. Coronary angiogram revealed nonobstructive coronary artery disease. Echocardiography showed To understand that SLONM is a rare, potentially treatable cause of heart failure. To know how to diagnose and treat SLONM associated with monoclonal gammopathy and heart failure. MANAGEMENT Approximately 2 years after first being diagnosed with heart failure, the patient was in New York Heart Association functional class IV with dyspnea at rest despite optimal pharmacological treatment for heart failure. His hemodynamics were severely compro- Table 1) . On physical testing, he had improved muscle strength, but persistent weakness of the proximal and axial muscles. He was deemed fit to tolerate highdose chemotherapy with autologous stem-cell support, which we recently performed without severe side effects. Nemaline myopathy is usually an early-onset, inherited disease caused by mutations in genes encoding myocyte structural proteins. The rare sporadic late-onset variety has been associated with MGUS. In a few cases, concomitant heart failure has been reported (4). In SLONM, the MGUS presumably causes myopathy through interaction between the monoclonal immunoglobulins and the sarcomeric proteins of the myocytes (4). Presumably, the same mechanism is responsible for the heart failure, but notably, we did not find nemaline bodies on endomyocardial biopsy. In case series, successful treatment of MGUS has led to recovery from the myopathy (4, 5) , and in 2 single cases, simultaneous recovery from heart failure has been reported (6, 7) . In the latter cases, SLONM with MGUS preceded the onset of heart failure. In our patient, on the other hand, heart failure preceded the onset of symptomatic myopathy by several months. SLONM with MGUS should therefore be considered in the diagnostic evaluation not only in progressive myopathy, but also in unexplained heart failure. Importantly, skeletal muscle, biopsy, but not endomyocardial biopsy, was diagnostic in our case. By the time treatment for MGUS was initiated, our patient had severe, end-stage heart failure, which nevertheless improved rapidly. Notably, the left ventricular function recovered more rapidly than skeletal muscle function, suggesting that the pathophysiologic mechanism of heart failure in SLONM with MGUS is different from that in the skeletal muscles. This is supported by the fact that nemaline bodies were not detected in 2 separate sets of endomyocardial biopsies in our patient. Progressive Heart Failure, Myopathy, and MGUS The patient had presented in a similar fashion to an outside facility in Georgia 5 months before this presentation. At that time, she reportedly underwent left-sided heart catheterization (LHC) that showed nonobstructive coronary artery disease (w30% left circumflex lesion). She subsequently moved to our city and started working in a plasma donor center. To recognize the spurious causes of hypertroponinemia. To incorporate the clinical context when analyzing diagnostic data. The patient ran out of her antihypertensive medications after moving to our area. Her presentation was concerning for several possibilities, including acute coronary syndrome (ACS), acute aortic dissection, and acute pulmonary embolism. ACS was initially thought to be the most likely cause because her chest pain occurred at rest and was associated with left arm numbness. The initial work-up in the emergency department included a 12-lead electrocardiogram (ECG) (Figure 1 Kassem et al. Notwithstanding the lack of evidence, we suspect that our patient's exposure to blood products in the plasma donor center may have led to the development of HAMA antibodies. In follow-up, the patient continued to report recurrent episodes of atypical left-sided chest and arm discomfort. She received a diagnosis of carpal tunnel syndrome and underwent tendon release surgery. On The initial broad differential diagnoses of syncope and chest pain included acute coronary syndrome, cardiac tachyarrhythmias or bradyarrhythmias, and pulmonary embolism. Cardioverter-Defibrillator Therapies Delivered After End of Service gency department with mild chest discomfort and constitutional symptoms (i.e., nausea, vomiting, and anorexia) for the past 5 days. His history was notable for mild persistent asthma, allergic rhinitis, and previous smoking (5 pack-years). The patient denied any past or current history of drug use. Other than sinus tachycardia at 126 beats/min, the physical examination was unremarkable. He was afebrile, with a normal breathing rate, blood pressure of 100/79 mm Hg, clear chest sounds, nontender abdomen, and no peripheral edema. On laboratory work-up there was a normal hemoglobin level (14.5 g/dl), leukocytosis (24.0 Â 10 9 /l) with marked eosinophilia (11.7 Â 10 9 /l; i.e., 48%), and heightened C-reactive protein (19.9 mg/dl) and To identify eosinophilic granulomatosis with polyangiitis, a rare systemic necrotizing vasculitis, as a potential cause of fulminant life-threatening eosinophilic myocarditis. To recognize that mechanical circulatory support may be lifesaving in rapidly progressing eosinophilic myocarditis presenting as refractory cardiogenic shock. To recognize endomyocardial biopsy as a valuable diagnostic tool to establish diagnosis and define treatment decisions in fulminant myocarditis. erythrocyte sedimentation rate (28 mm/h). Liver enzymes, creatine kinase, and lactate dehydrogenase were elevated (aspartate aminotransferase: 119 IU/l; alanine aminotransferase: 50 IU/l; creatine kinase: 1042 IU/l; and lactate dehydrogenase: 986 IU/l), and mild acute kidney injury was present (serum creatinine, 1.45 mg/dl). Both high-sensitivity-cardiac troponin T and N-terminal pro-B-type natriuretic peptide were markedly increased (i.e., 2,500 ng/l and 18,795 pg/ml, respectively). A brief panel of autoantibodies was unremarkable. Electrocardiography ( Figure 1A) was notable for inferolateral ST-segment depression and chest radiography ( Figure 1B Hypersensitivity Antibiotics (mainly minocycline and beta-lactam antibiotics) Central nervous system acting agents (mainly clozapine followed by carbamazepine) Vaccines (e.g., tetanus toxoid, smallpox, and diphtheria/pertussis/ tetanus) Antitubercular agents (e.g., isoniazid) NSAIDs, ACE inhibitors, diuretics, digoxin, among others Lopes et al. Formerly known as Churg-Strauss syndrome, EGPA is a rare systemic necrotizing vasculitis involving small to medium-sized vessels and is associated with asthma and with blood and tissue eosinophilia. According to the American College of Rheumatology, the presence of 4 or more criteria ( Table 2 ) establishes the diagnosis with a sensitivity of 85% and a specificity of 99.7% (1). A 35-year-old African-American woman was admitted to the hospital with syncope. She was getting out of a car when she had an acute onset of palpitations and diaphoresis followed by loss of consciousness and implantable cardioverter-defibrillator (ICD) shock. She regained consciousness after a brief period of confusion and presented to the emergency department. On physical examination, the patient's temperature was 98.7 F, heart rate 97 beats/min, blood pressure 99/67 mm Hg, respirations 16 breaths/min, oxygen saturation 98% on room air, and body mass index 31 kg/m 2 . Cardiovascular physical examination revealed an irregularly irregular rhythm, no murmurs or gallops, jugular venous pulsation at 8 cm of water, and trace lower extremity edema. ICD pocket appearance was within normal limits. The patient's pertinent medical history included endstage renal disease due to pre-eclampsia, 2 failed renal allografts due to antibody-mediated rejection, anuria To create a differential diagnosis for restrictive cardiomyopathy using multimodality cardiac imaging. To recognize the clinical presentation of metastatic myocardial calcification. There was diffusely increased radiotracer uptake throughout the myocardium of the right and left ventricles, with no uptake in the apex. This corresponded to a visual score of 3, indicating myocardial uptake greater than bone. To appreciate that LAA-pulmonary artery fistula formation is a rare but potentially fatal complication of LAA closure. To better understand the anatomical relationship between the LAA and pulmonary artery utilizing multimodality imaging. effusion. Although she was at risk for bleeding, she was also at significantly increased risk for stroke. was concern that the placement of coils may increase the size of the peridevice leaks, prolonging her need for anticoagulation. The decision was made to continue with medical therapy and close observation. Apixaban (5 mg bid) was stopped and she was The patient remains hemodynamically stable. She completed 5 months of dual antiplatelet therapy and is now taking aspirin 81 mg daily. We plan to perform repeat TEE in 1 to 3 months. To our knowledge, this is the first case in which a LAA-PA fistula formed, tamponade did not ensue, surgical intervention was not performed, and followup TEE showed evidence of progressive tract closure. We felt that it was prudent to stop the anticoagulation after the initial recognition of the LAA-PA fistula, given the concern for possible hemopericardium and A pproximately 50% of patients presenting with ST-segment elevation myocardial infarction have residual lesions in nonculprit vessels after revascularization of the culprit artery (1). If left unattended, these nonculprit lesions confer unfavorable prognosis (2) . Several strategies are available for treatment of the nonculprit lesions. Among these strategies, staged revascularization supported by measurements of fractional flow reserve is a frequently used option. An alternative strategy for management of the nonculprit lesions is noninvasive detection of ischemia using cardiac magnetic resonance (CMR) imaging. We present the case of a 74-year-old male patient who presented with an inferior ST-segment elevation myocardial infarction. The patient was rushed to emergency angiography, which revealed a thrombotic occlusion of the right coronary artery ( Figure 1A , Video 1) and intermediate stenosis of the left anterior descending artery ( Figures 1B and 1C , Videos 2 and 3). The culprit was successfully treated through implantation of 2 drugeluting stents (Video 4). The patient returned to our clinic 1 month after discharge for follow-up of the lesion in the left anterior descending artery. Although the patient was asymptomatic, CMR revealed a transmural stress perfusion defect in 1 segment anterior mid ( Figure 1E , Video 5), with normokinesia on cine imaging ( Figure 1D , Video 6) and no contrast enhancement on the late gadolinium enhancement image ( Figure 1F ), opposite to an infarction of the inferior wall. Surprisingly, subsequent angiography did not reveal a significant nonculprit stenosis and fractional flow reserve in the left anterior descending artery was measured to be 0.94. However, after careful re-evaluation of the angiogram, we noted a chronic total occlusion of the second diagonal branch with a tapered proximal cap and anterograde filling of the distal segment through micro channels or bridging collaterals ( Figures 1B and 1C) . After discussion among our team, it was decided not to attempt revascularization because of the high lesion complexity and limited area of ischemia. A 54-year-old male was referred to the authors' institution with a 1-year history of worsening shortness of breath and lower limb swelling. His medical history was significant for recurrent episodes of idiopathic pericarditis that began 4 years previously and were treated with non steroidal antiinflammatory agents, colchicine, and prednisone. He showed no evidence of metastatic malignancy, uremia, tuberculosis, or chronic bacterial infection. On examination, the jugular venous pressure was elevated with a rapid "Y" descent, a pericardial knock, peripheral edema, and ascites. Chest radiography demonstrated cardiomegaly with prominence of the left cardiac border but no calcifications ( Figure 1A) . Transthoracic echocardiography showed ventricular interdependence, respiratory variation of the mitral inflow, annulus reversus, and expiratory end-diastolic hepatic venous flow reversals, which was diagnostic for constrictive pericarditis (Supplemental Figure 1) . Cardiac magnetic resonance imaging demonstrated mild (3-mm) pericardial thickening anterior to the right ventricle ( Figure 1B , arrows) and no regional wall motion abnormalities. The patient was referred for pericardiectomy. Preoperative coronary angiography showed no atherosclerotic lesions, but there were discrete regions of diastolic compression of the mid left anterior descending artery; and diagonal, ramus, and distal left circumflex arteries ( Figures 1C and 1D , arrows, Video 1). During surgery, it was noted that the pericardium was thick, with transverse cylindrical cords of scar which compressed the underlying epicardium ( Figures 1E and 1F) . Surgical pathology revealed noncalcific fibrous thickening and minimal non-granulomatous lymphoplasmacytic infiltrate, consistent with constrictive pericarditis. The patient had an uneventful postoperative course. On 6-month follow-up, his symptoms of shortness of breath and edema had completely resolved, and repeated echocardiography showed no evidence of constrictive physiology. Diastolic coronary artery compression is a rare phenomenon (1-7), unlike systolic myocardial bridging of arteries with an intramural course. Diastolic external compression usually occurs from localized pericardial thickening during cardiac relaxation and enlargement. It has also been reported in association with left atrial enlargement and following coronary artery bypass grafting and heart transplantation (4-7). Myocardial ischemia is a theoretical concern which likely resolves after Figure) . One mass had a stalk originating from the lateral wall and the second mass had a separate stalk in the medial wall. Both masses, including the stalks and bases, were resected completely and sent to pathology for further evaluation (Supplemental Figure) . The patient recovered well. Histopathologic evaluation revealed low-grade leiomyosarcomas. She was referred to an oncologist and decision was made for surveillance given that further imaging did not show any residual lesion. She was contacted 4 months after surgery and has no evidence of recurrence. Primary cardiac leiomyosarcomas are rare and even fewer synchronous lesions have been reported. The incidence of primary cardiac tumors is 0.02%, and primary cardiac leiomyosarcomas represent <0.25% of all Figure 1A) . The posterior descending artery exhibited acute bacterial vasculitis and adjacent abscess ( Figure 1B) . Additional findings included microabscesses in the brain and spinal cord. Endocarditis is the most common cardiac manifestation of bacterial infection in developed countries. Perivalvular extension with abscess formation is a recognized complication, but isolated BM is exceptionally rare (1). A 24-year-old woman without relevant past medical history presented to the emergency room after 6 days of flu-like symptoms. In the last 24 h, she also presented dyspnea, hot flashes, and palpitations. The physical examination was relevant for hypertension and tachycardia. The electrocardiogram showed supraventricular tachycardia that was treated with adenosine and labetalol returning to sinus rhythm. Figures 1A and 1B) . The metaiodo-benzyl-guanidine scintigraphy showed signs of left adrenal gland neuroendocrine tumor (Figures 1C and 1D) Cardiomyopathy induced by pheochromocytoma represents a barely recognized entity. It has diverse clinical manifestations: Takotsubo syndrome, myocarditis, and dilated cardiomyopathy. The clinical presentation is variable: hypertension is the most frequent (65%), and the classical triad (headache, palpitations, and diaphoresis) is described in 4% (1). There are few reports of patients who present cardiogenic shock (2), but the predominance of multiorgan failure over catecholamine excess symptoms is frequently described (1) . In this case, dobutamine could contribute to the evolution because of its potential to induce shock in patients with pheochromocytoma (2) . The pheochromocytoma resection is associated with improvement of ventricular function in 96% of cases. The lack of intervention is related to an increase in mortality (33%), heart transplant (11%), and serious adverse events (44%) (1). (PA) and lateral chest radiographs can be used to evaluate lead position in relation to the cardiac silhouette and changes in lead position that may occur with somatic growth (2) . In patients with epicardial pacing leads, physicians should be alert to new clinical signs and symptoms, echocardiographic findings, and electrocardiographic changes. Echocardiography can help confirm the diagnosis in cases of valvular disturbance but is unlikely identify coronary compression. The purpose of this report is to highlight the importance of TTE as it provides aids to identifying and monitoring for dynamic compression. The first question that must be addressed is "Who is (6) . In a recent Twitter poll structured to attempt to gain a better understanding of use of the service, the majority of respondents (84%) claimed that <25% of their colleagues were on Twitter. Thus, although this sampling may be biased, it would suggest that only a minority of cardiologists are regular users of social media platforms such as Twitter. There are few robust data available that support the concept that the adoption of Twitter in cardiovascular medicine is widespread. A hashtag is a key word or phrase used to categorize one's tweet. Tweets that contain at least 1 hashtag can ISSN 2666-0849 https://doi.org/10.1016/j.jaccas.2020.03.008 users. During this timeframe, there were >120 million impressions, which seems to be a lot of impressions. How that relates to a growth of 7% in the use of radial artery access in percutaneous coronary interventions over the same timeframe is uncertain. An example of how impressions can be mis- beyond barriers, including geography, specialty, or practice setting (9) . This format is particularly useful in medical specialties with female underrepresentation. Women with limited access to mentors at their home institutions can harness the strength of social media to build mentorship networks that would otherwise be inaccessible (6, 9) . Early mentorship is essential to the successful recruitment of women trainees into cardiology. Mentorship paves the way for professional development, personal coaching, and, most importantly, The figure provides a framework for individual and systems-level initiatives that can be used to strengthen mentorship for female internal medicine residents. Interventions include direct guidance and counseling from fellows and faculty, creation of programs that allow residents to connect with faculty at the residency and fellowship levels, recruitment of residents to networking events by professional societies, and utilization of social media. Early introduction of these measures has the potential to change female residents' negative impression of cardiology and promote recruitment of women into cardiology. Single coronary artery in a young male with chest pain Solitary coronary ostium Single coronary artery: Pete Maravich anomaly revisited Congenital heart surgery nomenclature and database project: Ebstein's anomaly and tricuspid valve disease Ebstein's anomaly of the tricuspid valve: from fetus to adult Morphologic spectrum of Ebstein's anomaly of the heart: a review The spectrum of Ebstein's anomaly of the tricuspid valve Left heart lesions in patients with Ebstein anomaly Unusual combination: Ebstein's anomaly and hypertrophic obstructive cardiomyopathy Ebstein anomaly and hypertrophic cardiomyopathy Subaortic stenosis due to accessory tissue of the mitral valve associated with Ebstein's anomaly in an adult Native mitral valve causing left ventricular outflow tract obstruction in an adult with Ebstein's anomaly An unusual cause of dynamic left ventricular outflow obstruction Case of Ebstein anomaly complicated by left ventricular outflow tract obstruction secondary to deformed basal septum attributable to atrialized right ventricle Pathologic anatomy of Ebstein's anomaly of the heart revisited Embryology and pathologic features of Ebstein's anomaly Left ventricular geometry and function in adults with Ebstein's anomaly of the tricuspid valve Aortic-left ventricular tunnel Aortoleft ventricular tunnel: an alternative surgical approach Aortico-left ventricular tunnel: a clinical review and new surgical classification Aortico-left ventricular tunnel and aortic insufficiency Aortico-left ventricular tunnel: 35-year experience Repair of aortico-left ventricular tunnel associated with sub-pulmonary obstruction Aorto-left ventricular communication after closure: later post-operative problems Aneurysmal aorto-left ventricular tunnel causing right ventricular outflow tract obstruction Saphenous venous graft pseudoaneurysm: a review of the literature Natural history and management of aortocoronary saphenous vein graft aneurysms: a systematic review of published cases Coronary stent infection successfully diagnosed with FDG-PET CT Clinical value of FDG-PET/CT in bacteremia of unknown origin with catalase-negative gram-positive cocci or Staphylococcus aureus New treatments for methicillin-resistant Staphylococcus aureus Daptomycin treatment in Gram-positive vascular graft infections Giant coronary artery aneurysms: review and update IgG4-related disease IgG4-related cardiovascular disease from the aorta to the coronary arteries: multidetector CT and PET/CT A suspected case of coronary periarteritis due to IgG4-related disease as a cause of ischemic heart disease Serum levels of IgG4 and soluble interleukin-2 receptor in patients with coronary artery disease Low LDL cholesterol-friend or foe? Hypobetalipoproteinemia: genetics, biochemistry, and clinical spectrum Abetalipoproteinemia and homozygous hypobetalipoproteinemia: a framework for diagnosis and management Clinical utility gene card for: Abetalipoproteinemia-update 2014 Variation across 141,456 human exomes and genomes reveals the spectrum of loss-of-function intolerance across human protein-coding genes A global reference for human genetic variation A novel APOB mutation identified by exome sequencing cosegregates with steatosis, liver cancer, and hypocholesterolemia Cohort profile: the HUNT study Early acute hepatitis with parenteral amiodarone: a toxic effect of the vehicle? Acute hepatitis after parenteral amiodarone administration Probable early acute hepatitis with parenteral amiodarone Acute hepatic dysfunction following parenteral amiodarone administration Amiodarone-induced third degree atrioventricular block and extreme qt prolongation generating torsade des pointes in paroxysmal atrial fibrillation Comparison of the in vitro electrophysiologic and proarrhythmic effects of amiodarone and sotalol in a rabbit model of acute atrioventricular block Influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and clinical outcome Predictive value of cardiac troponin I and T for subsequent death in end stage renal disease Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism It's time for a change to a troponin standard Fourth universal definition of myocardial infarction The antibody configurations of cardiac troponin I assays may determine their clinical performance Circulating antibodies to mouse monoclonal immunoglobulins in normal subjects-incidence, species specificity, and effects on a two-site assay for creatine kinase-MB isoenzyme Incidence and specificity of interference in two-site immunoassays Human anti-animal antibody interferences in immunological assays The American College of Rheumatology 1990 criteria for the classification of Churg-Strauss syndrome (allergic granulomatosis and angiitis) EULAR/ ERA-EDTA recommendations for the management of ANCA-associated vasculitis The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases Diagnosis and management of myocardial involvement in systemic immune-mediated diseases: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest Prognostic factors in polyarteritis nodosa and Churg-Strauss syndrome. A prospective study in 342 patients KEY WORDS acute heart failure, autoimmune, cardiac assist devices, Churg-Strauss syndrome Hypercalcemia and metastatic calcification Metastatic calcification of the cardiac conduction system with heart block: an underreported entity in chronic renal failure patients Myocardial calcification in a patient with end-stage renal disease A heart of stone: an autopsy case of massive myocardial calcification An autopsy case of sudden death in renal transplant recipient Metastatic calcification of Neglected tropical cardiomyopathies: II. Endomyocardial fibrosis: myocardial disease Current perspective on endomyocardial fibrosis Tropical Endomyocardial Fibrosis Clinical course of endomyocardial fibrosis Typical clinical aspect of endomyocardial fibrosis How to recognize endomyocardial fibrosis? Diagnosis and management of endomyocardial fibrosis An innovative technique for the relief of right ventricular trabecular cavity obliteration in endomyocardial fibrosis Long-term follow up of patients with endomyocardial fibrosis: effects of surgery KEY WORDS cardiac magnetic resonance, cardiomyopathy, fibrosis, restrictive, right ventricle APPENDIX For supplemental figures and videos, please see the online version of this paper Diastolic segmental coronary artery obliteration in constrictive pericarditis Segmental diastolic compression of circumflex coronary artery secondary to pericardial constriction: an uncommon cause of angina pectoris Atypical phasic coronary artery narrowing Diastolic compression of the left anterior descending artery Diastolic coronary artery compression in a cardiac transplant recipient: treatment with a stent Phasic compression of left circumflex coronary artery during atrial systole Diastolic segmental compression of saphenous vein bypass graft Department of Surgery Pheochromocytoma as a reversible cause of cardiomyopathy: analysis and review of the literature Unexpected triggers for pheochromocytomainduced recurrent heart failure Understanding social media opportunities for cardiovascular medicine Social media becomes a growing force in cardiology The British Cardiovascular Society 2014 Work Force Survey. A Report to the BCS CardioTweeters: an analysis of Twitter use by UK cardiologists Number of active physicians in the U.S. in 2019, by specialty area Cardiology in 280 characters: cardiologists use of Twitter in the United States Tweeting the meeting: rapid growth in the use of social media at major cardiovascular scientific sessions from 2014-to 2016 The Kardashian index of cardiologists: celebrities or experts? A perspective on the K-Index Social media and assessing the "impact" of medical publications KEY WORDS analytics, impressions, social media Physician Specialty Data Report: ACGME Residents and Fellows by Sex and Specialty Changes in the professional lives of cardiologists over 2 decades Perceptions of women medical students and their influence on career choice Defining surgical role models and their influence on career choice Social media in the mentorship and networking of physicians: important role for women in surgical specialties Sex differences in the pursuit of interventional cardiology as a subspecialty among cardiovascular fellows-in-training Association of Women Surgeons. The AWS Coaching Project Social media and advancement of women physicians