Abstract

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The cardiac implications of Covid-19 are variable. Here we describe a gentleman with Covid-19 induced myocarditis with resultant atrial fibrillation. CASE PRESENTATION: A 39 year-old male with no past medical history presented to the hospital with fevers and lower extremity swelling that started 7 days prior. In the ED an EKG revealed new-onset atrial fibrillation with RVR, while a TTE showed newly reduced EF of 10%. An infectious workup was conducted and positive for Covid-19. Inflammatory markers including ESR and CRP were found to be significantly elevated, along with mildly elevated troponin T which remained flat. Other etiologies of heart failure such as valvular disease, thyroid disorders, etc. were ruled out. Coronary angiography was deferred as suspicion for ACS remained low. It was noted that the patient's heart rate began to normalize as the fevers improved and the markers of inflammation decreased. Cardiac MRI was performed which revealed late gadolinium enhancement involving the subepicardium, consistent with myocardial injury and a diagnosis of myocarditis. Prior to discharge, the patient converted to normal sinus rhythm and repeat bedside echocardiogram suggested moderate improvement in ejection fraction. Patient was discharged medically stable with a repeat TTE scheduled to be performed in three months. DISCUSSION: The patient was suspected to have Covid-19 induced myocarditis leading to atrial fibrillation. Acute myocarditis is supported by new onset heart failure developing over the course of three months or less. It is further characterized by symptom onset following a GI or respiratory infection and/or dysrhythmias. This patient's cardiomyopathy occurred during the acute phase of a Covid-19 infection. Other typical etiologies of viral myocarditis such as coxsackie B were ruled out via negative respiratory viral panel and serologic titers. While there is limited knowledge on Covid-19 induced myocarditis, the presumed mechanism is thought to be secondary to direct viral damage and cytokine expression. Furthermore, these cytokines, including CRP and IL-6, produce oxidative stress and endothelial dysfunction that leads to cardiac remodeling precipitating atrial fibrillation. This patient's dysrhythmia was noted to improve as inflammatory markers improved. While myocarditis was considered to be the precipitant of this patient's cardiomyopathy-induced atrial fibrillation, the severely elevated inflammatory markers were presumed to play a secondary role. CONCLUSION(S): The importance of this case highlights the severe cardiac manifestations of the novel SARS-COV-2 virus. With continued research and awareness, it is reasonable for clinicians to include Covid-19 on the differential for viral myocarditis. Reference #1: Korantzopoulos P, Letsas KP, Tse G, Fragakis N, Goudis CA, Liu T. Inflammation and atrial fibrillation: A comprehensive review. J Arrhythm. 2018;34(4):394-401. Published 2018 Jun Reference #2: Caforio AL, Pankuweit S, Arbustini E, et al. 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. Eur Heart J 2013;34:2636. Reference #3: Carpenter A, Chambers OJ, El Harchi A, et al. COVID-19 Management and Arrhythmia: Risks and Challenges for Clinicians Treating Patients Affected by SARS-CoV-2. Front Cardiovasc Med. 2020;7:85. Published 2020 May 5. DISCLOSURES: No relevant relationships by Fadi Kandah, source=Web Response No relevant relationships by Andres Martinez, source=Web Response No relevant relationships by sebastian Mikulic, source=Web Response No relevant relationships by Pujan Patel, source=Web ResponseCopyright © 2020 American College of Chest Physicians

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