LAUSR

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The first case of SARS-CoV-2 (COVID-19) virus was reported in December, 2019 and is well known to cause febrile illness, gastrointestinal symptoms, respiratory disease, and coagulopathy. One of the less common sequelae of this illness is myocarditis. Here we present an interesting case of delayed onset myocarditis which occurred following COVID-19 infection. CASE PRESENTATION: A 32-year-old female with a past medical history significant for obesity presented with complaints of dull, left sided chest pain. She had associated symptoms of diaphoresis, lightheadedness, and nausea. Patient denied prior history of angina. Patient had a strong family history of coronary artery disease.Chest pain was reproducible with palpation to the chest. EKG showed T wave inversions in anterolateral and inferior leads. Troponin was elevated to 1.12 ng/mL (<0.05 ng/mL) and trended up to 9.57 ng/mL. NT proBNP was mildly elevated to 253 pg/mL (<126 pg/mL). Chest x-ray revealed no acute abnormalities. Patient tested positive for COVID-19 six months prior to admission. During the current admission patient's COVID-19 PCR was negative. Patient was given aspirin 324mg and started on heparin and nitroglycerin infusions.Echocardiography showed hypokinesis of apical myocardium and left ventricular (LV) ejection fraction of 60%. Patient was taken for coronary angiogram which revealed normal coronary arteries without evidence of stenosis or spasm. Cardiac magnetic resonance imaging (MRI) revealed increased signal in the mid-apical septum on short tau inversion recovery image (STIR) suggestive of edema or inflammation. LV systolic function was normal;however, hypokinesis of the apical septal wall was noted. These findings on MRI are highly suggestive of acute myocarditis. Endomyocardial biopsy was not performed as the patient was hemodynamically stable and showed no signs of heart failure or arrhythmia. DISCUSSION: A meta-analysis of 8971 hospitalized COVID-19 infected patients demonstrated that 20.0% of patient's had myocardial injury manifested by elevated troponin I levels [1]. Guo et al showed 28% of patients with COVID-19 had evidence of myocardial injury (elevated troponin T greater than 99th percentile upper limit) and Chen et al showed elevated BNP in 27.5% of patients. There have been reports of patients with myocarditis during active episodes of COVID-19 infection but limited published literature provides insight into patients who may develop myocardial injury in the time following the primary COVID-19 infection. CONCLUSIONS: This case represents an interesting presentation of delayed onset myocarditis following COVID-19 infection which must be considered in the differential for patients who present with NSTEMI. Delayed onset could be suggestive of prolonged systemic inflammatory response in the setting of COVID-19. It also displays a less frequently identified sequela of COVID-19 infection. REFERENCE #1: Prasitlumkum, N., Chokesuwattanaskul, R., Thongprayoon, C., Bathini, T., Vallabhajosyula, S., & Cheungpasitporn, W. (2020). Incidence of Myocardial Injury in COVID-19-Infected Patients: A Systematic Review and Meta-Analysis. Diseases, 8(4), 40. REFERENCE #2: Guo, T., Fan, Y., Chen, M., Wu, X., Zhang, L., He, T., … & Lu, Z. (2020). Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA cardiology, 5(7), 811-818. REFERENCE #3: Chen, C., Zhou, Y., & Wang, D. W. (2020). SARS-CoV-2: a potential novel etiology of fulminant myocarditis. Herz, 45(3), 230-232. DISCLOSURES: No relevant relationships by Joseph Adams, source=Web Response No relevant relationships by Sheraz Hussain, source=Web Response No relevant relationships by Ibrahim Kassas, source=Web Response No relevant relationships by Shermeen Memon, source=Web Response No relevant relationships by Mohammed Siddiqui, source=Web Response