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TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Dilated cardiomyopathy is characterized by structural defects leading to impaired ventricular function. The etiology is often elusive. Viruses are some of the most common causes world-wide (1). Here we present a male with non-ischemic cardiomyopathy and heart failure due to Coxsackie B myocarditis. CASE PRESENTATION: A 36 year old male with history of heart failure with reduced ejection fraction (35%), non-ischemic cardiomyopathy, and ventricular tachycardia presented for syncope. He was found to be in cardiogenic shock. Work-up revealed an elevated troponin and NT-proBNP, 0.064 and 5570, acute kidney injury, creatinine 3.28, and congestive hepatopathy. Prior cardiac work-up consisted of a left and right heart catheterization which showed no atherosclerotic disease and elevated filling pressures (Pulmonary Capillary Wedge Pressure 16 and Pulmonary Artery Mean Pressure 33). Cardiac MRI showed global dilation of the cardiac chambers, global hypokinesis, and late gadolinium enhancement of the base and septum. This was suggestive of dilated cardiomyopathy and prior myocarditis. Echocardiogram revealed a severe decline in ejection fraction, < 15%, and EKG showed a widened QRS complex with left bundle branch block. Serologic tests were positive for Coxsackie B antibodies. Inotropic support was initiated. Bridge therapy and heart transplant were indicated. However, due to his uninsured status and COVID-19 restrictions, he was unable to be transferred to a heart transplant center. Cardiac Resynchronization Therapy was pursued instead. He was clinically stabilized, initiated on GDMT, and was discharged with close follow-up. Even though serologic antibodies lack specificity, given the history, cardiac MRI findings, and diagnosis of NICM, his clinical picture was presumed to be due to Coxsackie B. DISCUSSION: Myocarditis is an inflammatory condition of the myocardium. Viral is the most common cause in Western nations but Rheumatic and Chagas remain prevalent in the developing world. Diagnosis is confirmed with endomyocardial biopsy. This makes it difficult to ascertain the true incidence but there are approximately 1.5 million cases every year. COVID-19 has been frequently associated with myocardial injury and clinical myocarditis. In most cases, tissue diagnosis is lacking. Viral myocarditis can lead to dilated cardiomyopathy through a variety of mechanisms. It is hypothesized to be the result of direct toxicity via receptor mediated entry or an autoimmune response against viral fragments that are not cleared (2). CONCLUSIONS: Unfortunately, this case highlights the disparities of our healthcare system and how that can directly impact patient care. Viral myocarditis remains a difficult clinical scenario. Treatment is largely supportive but the sequelae of disease can be severe. Antivirals and interferon therapy are promising but further research is needed to explore more pharmacologic options (3). REFERENCE #1: Felker GM, Thompson RE, Hare JM, et al. Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. N Engl J Med 2000;342:1077. REFERENCE #2: Kang M, An J. Viral Myocarditis. [Updated 2021 May 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459259/ REFERENCE #3: Coletta AP, Clark AL, Cleland JG. Clinical trials update from the Heart Failure Society of America and the American Heart Association meetings in 2008: SADHART-CHF, COMPARE, MOMENTUM, thyroid hormone analogue study, HF-ACTION, I-PRESERVE, beta-interferon study, BACH, and ATHENA. Eur J Heart Fail 2009;11:214. DISCLOSURES: No relevant relationships by Adhish Singh, source=Web Response No relevant relationships by Michael Vu, source=Web Response