key: cord-0863841-t9knzadf authors: Khatri, Akshay; Wallach, Frances title: Coronavirus Disease 2019 (Covid-19) presenting as purulent fulminant myopericarditis and cardiac tamponade: a case report and literature review. date: 2020-06-09 journal: Heart Lung DOI: 10.1016/j.hrtlng.2020.06.003 sha: cca539123cadc19e236df775e22d916c23d54c66 doc_id: 863841 cord_uid: t9knzadf The vast majority of patients in the ongoing coronavirus Disease 2019 (Covid-19) pandemic primarily present with severe respiratory illness. We report a Covid-19 patient who presented with findings of acute coronary syndrome and was found to have purulent fulminant myopericarditis and cardiac tamponade. We compare our case to the previously reported instances of Covid-19-associated myocarditis. Through review of the available literature, we also highlight the potential mechanisms of cardiac injury in Covid-19. We hope to increase awareness amongst clinicians about this unusual presentation of Covid-19. In December 2019, the World Health Organization (WHO) was notified about multiple cases of pneumonia of unknown etiology originating in Wuhan city, Hubei province, China. The novel virus, named severe-acute-respiratory-syndrome-coronavirus-2 (SARS-Cov-2) was isolated on January 7 th , 2020 1 . The acute respiratory disease, renamed Coronavirus Disease 2019 (Covid- 19) , was declared a pandemic on March 11 th , 2020 2 . SARS-Cov-2 has been seen to produce primarily respiratory symptoms, with evidence of ground-glass opacities on chest imaging 3 . However, the cardiovascular effects of SARS-Cov-2 have not been fully characterized 4 . We report a patient with Covid-19 who presented with findings of acute coronary syndrome and was found to have purulent fulminant myopericarditis and cardiac tamponade, with subsequent circulatory shock. A 50-year-old gentleman presented to an outside hospital with fevers, chills, generalized malaise, non-productive cough, dyspnea for 3-4 days and an episode of near-syncope on the day of presentation. In the emergency department, he was intubated for acute hypoxemic respiratory failure and SARS-Cov-2 testing was positive. ST-segment changes were noted on the electrocardiogram (ECG), so he was transferred to our hospital for acute coronary syndrome (ACS) management. high sensitivity troponin 544ng/L, creatine kinase 2135 U/L, creatine kinase myocardial band 54.3ng/mL. Other inflammatory markers were also significantly elevated: erythrocyte sedimentation rate was 46mm/hr, d-dimer 1,068ng/mL d-dimer units, procalcitonin 8.16ng/mL, C-reactive protein 11.85mg/dL, ferritin 66,165ng/mL. T-cell subset analysis showed absolute CD4+ count 285/µL (26%) and CD8+ count 114/µL (10%). On arrival, he was immediately taken to the cardiac catheterization laboratory (CCL). Coronary 3 . Both SARS-Cov and MERS-Cov have been associated with myocardial injury, myocarditis, and heart failure [5] [6] [7] . Additionally, comorbidities like diabetes mellitus (DM) and hypertension in these patients were associated with increased mortality 8, 9 . A recent meta-analysis found that the prevalence of hypertension, cardiac/cerebrovascular disease and DM in Covid-19 patients was 17.1%, 16.4%, and 9.7%, respectively 10 . Patients needing ICU admission were also more likely to have these comorbidities 10 . Covid-19 patients with these comorbidities also had higher mortality rates 11 . A spectrum of cardiac complications [myocarditis, heart failure, cardiac arrhythmias, myocardial infarction (MI)] are being increasingly reported in Covid-19 patients 3,4,12,13 . A higher incidence of complications [acute respiratory distress syndrome (ARDS), malignant arrhythmias, AKI] and higher mortality rates were seen in Covid-19 patients with myocardial injury 13 . There have been few well-described case reports of SARS-Cov-2 causing focal myocardial and/or pericardial involvement [14] [15] [16] [17] [18] (Table 1) . Like our patient, they had elevated cardiac markers, with ECG changes and signs of ventricular dysfunction. Two patients had predominant symptoms of ACS without viral symptoms 15,17this correlates with reports of Covid-19 presenting with predominantly cardiovascular symptoms in some patients 19 . Despite their presentation, no significant findings were noted in those who underwent cardiac catheterization. Different treatment regimens were institutedhowever, apart from our case, one other patient expired 14 . Our patient, like other cases 14, 17 , met several criteria for fulminant myocarditis. These include acuity of onset; premonitory symptoms of viral infection; rapidly developing severe hemodynamic dysfunction; evidence of severe myocardial injury & diffuse decreased ventricular wall movement; and symptoms of injury to other organs 20 . The reported mortality rate of this rare syndrome is between 40-70% 21 . The current management of viral myocarditis involves use of immunomodulatory therapy (steroids, IVIG); supportive therapy (including mechanical ventilation); and circulatory assist devices (Impella heart pump, intra-aortic balloon pump) to reduced wall stress and inflammation 20, 22 . The role of ECMO and continuous renal replacement therapy (CRRT) in Covid-19 is unclear. It may help remove circulating cytokines and increase blood oxygen saturation, reducing the immune response and further reducing myocardial damage 14 . ECMO therapy has been useful in some Covid-19 patients with cardiogenic shock 15 , but more data is needed. It is unclear at this time what factors contribute to increased mortality in Covid-19 patients with myocarditis. Worse outcomes have been noted in those with coinfections 12 . In one case, worsening of certain hemodynamic parameters (such as pulmonary artery systolic pressure) indicate functional decline and may help as markers of mortality 14 . The exact mechanism of SARS-Cov-2-induced cardiac injury is not yet known. There are different theories: (a) Direct injury by viral replication. SARS-Cov has been detected in the heart on autopsy 23 (c) Hypoxia (due to SARS-Cov-2-induced ARDS) can lead to inflammation, cell injury and subsequent cardiac damage 28 . It can also lead to increased intracellular calcium deposition and apoptosis 19 . (d) Systemic inflammation potentiating localized inflammation in advanced atherosclerotic coronary vessels has been seen in other viral illnesses 29 . Lymphopenia 3, 27 has been noted in Covid-19 patients and has previously been linked to the development of atherosclerosis 30 . (e) Direct myocardial involvement mediated via Angiotensin-converting-enzyme-2 (ACE2). ACE2 is an endothelium-bound enzyme that converts angiotensin I & II to inactive metabolites 31 . Its expression was necessary for pulmonary infection by SARS-Cov 32 . In murine models, SARS-Cov precipitated an ACE2-dependent MI after pulmonary infection 23 . Our patient was diagnosed with a purulent myopericarditis and tamponade, causing circulatory shock with fatal multi-organ failure. His clinical picture, radiographic and laboratory findings fit the diagnosis of Covid-19. There were no other identified causes of myopericarditis. The rapidity of disease progression, combined with findings of purulent myopericarditis (previously unreported in the literature) contributes to the unique presentation of our case. In the current pandemic scenario, clinicians must keep SARS-Cov-2 infection in the differential of patients presenting with acute coronary syndromes and findings of purulent myopericarditis, cardiac tamponade and circulatory shock. Further research is needed to define the optimal management of such complex clinical scenarios. None Both authors declare that they have no pertinent conflicts of interest. Emergency preparedness, response: Disease outbreak news: Update -12 th World Health Organization. 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Lancet. 2020 Intermittent Hypoxia Causes Inflammation and Injury to Human Adult Cardiac Myocytes Role of acute infection in triggering acute coronary syndromes Relationship between low lymphocyte count and major cardiac events in patients with acute chest pain, a non-diagnostic electrocardiogram and normal troponin levels The role of ACE2 in cardiovascular physiology A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury Picture 1: Portable chest radiograph (Antero-posterior view) showing presence of diffuse bilateral patchy opacities within lung parenchyma. The cardiac silhouette appears normal in size with the tip above the carina. An enteric tube is noted (yellow arrow), with its distal end coursing below the diaphragm. A femoral approach Swan-Ganz catheter is noted (green arrow) Echocardiographic image (subcostal view) showing large pericardial effusion (red arrow) producing cardiac tamponade and collapse of right ventricle Key: AKI: acute kidney injury; ALC: absolute lymphocyte count; ALT: alanine transaminase BALF: bronchoalveolar lavage fluid; BNP: brain natriuretic peptide; CRP: C-reactive protein CRRT: continuous renal replacement therapy; CVA: cerebrovascular accident; DDU: D-dimer unit; DOHS: day of hospital stay; ECMO: extracorporeal membrane oxygenation; ESR: erythrocyte sedimentation rate; HCQ: hydroxychloroquine; hsT: high sensitivity troponin; HTN: Hypertension; IABP: intra-aortic balloon pump LV: left ventricle; LVEF: left ventricular ejection fraction; MP: methylprednisolone; MV: mechanical ventilator support; NP-PCR: nasopharyngeal polymerase chain reaction; ntBNP: nterminal brain natriuretic peptide; PCR: polymerase chain reaction; RV: right ventricle The authors gratefully acknowledge Sonia Henry, MD, FACC for her assistance in interpretation of the echocardiographic images.This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.