ACUTE MYOCARDITIS: SECONDARY TO VIRAL INFECTION OR PHEOCHROMOCYTOMA?
Recommended Citation
Ivers T, Albusoul L, and Tita C. ACUTE MYOCARDITIS: SECONDARY TO VIRAL INFECTION OR PHEOCHROMOCYTOMA? J Am Coll Cardiol 2023; 81(8):3829.
Document Type
Conference Proceeding
Publication Date
3-7-2023
Publication Title
J Am Coll Cardiol
Abstract
Background: In a young healthy patient, acute cardiogenic shock with a dilated, thickened left ventricle is strongly suggestive of acute myocarditis.
Case: SM is a 33 year-old healthy man who presented with decompensated heart failure with severe hypervolemia. Notably, he was exposed to Hand-Foot-Mouth disease (HFMD) two weeks prior. B-type natriuretic peptide was elevated at 3,417 pg/mL (normal range < 50 pg/mL), and troponin was elevated. Echocardiogram revealed dilated, severe systolic dysfunction with thickened left ventricular walls. He progressed to cardiogenic shock and multi-organ failure. Right heart catheterization revealed significantly reduced cardiac output and index of 2.36 and 1.2, respectively. His course was complicated by left ventricular thrombus and subacute embolic stroke, acute renal failure and liver failure. He was treated with afterload reduction, inotropes, and diuresis. His shock resolved, and he improved with medical therapy for cardiomyopathy.
Decision-making: The clinical course is consistent with acute myocarditis leading to cardiogenic shock with multi-organ failure. A broad differential was considered, including viral etiologies, autoimmune diseases, vasculitis, and toxin-mediated myocarditis. Viral labs including COVID-19 and influenza, as well as HIV, and hepatitis B and C viruses were negative. Coxsackie B2 antibody was positive at 1:80, which is consistent with past or current infection. Rheumatology evaluation was unrevealing, and vasculitis was deemed unlikely given normal inflammatory markers. Urine drug screen was unrevealing. However, adrenergic myocarditis remained on the differential given an adrenal nodule noted on imaging. Plasma free metanephrines were significantly elevated, consistent with pheochromocytoma.
Conclusion: This is a case of acute myocarditis with two likely etiologies. The patient’s presentation correlates temporally with exposure to HFMD, suggesting viral myocarditis. However, he had gross hypervolemia and diuresed 50 pounds, which suggests a more indolent course. We propose that he had adrenergic myocarditis and undetected cardiomyopathy which was exacerbated by a second insult, the Coxsackie virus.
Volume
81
Issue
8
First Page
3829