Abstract

Introduction: Sudden cardiac arrest has been documented in athletes, often secondary to left ventricular (LV) hypertrophy or previously undetected genetic conditions. Some athletes, however, experience these events without evidence of either LV or genetic disease. A hypothetical exercise-induced arrhythmogenic right ventricular cardiomyopathy (ARVC) has been previously described by La Gerche and colleagues, acquired through repeated, intense endurance exercise and associated cardiac remodeling rather than genetic inheritance. We present a case report of an endurance athlete presenting with ventricular tachycardia (VT), suspected to be secondary to exercise-induced ARVC. Results: A 40 year-old male endurance athlete was brought to the emergency department when he collapsed following a race in 2006. Upon arrival, he was in sustained wide-complex tachycardia at a rate of 200-220 BPM. Following conversion with IV amiodarone, left heart catheterization was performed, showing no significant coronary disease and LV ejection fraction (EF) measured 30-35%. He then underwent right ventricular outflow tract ablation. Cardiac MRI was inconclusive for ARVC. Biopsy was performed, negative for amyloidosis but with “focal mild to moderate chronic interstitial inflammatory infiltrates associated with focal muscle fiber necrosis.” Genetic testing was negative for pathologic variants or mutations associated with ARVC. Echocardiogram from 2020 showed EF 40-44% with significant RV enlargement and dysfunction. He required repeat VT ablation in 2010, 2014, and 2017. Arrhythmogenic scar was identified by electrophysiology mapping to be located at the sub-tricuspid RV. In combination with the prior RV outflow tract ablation, this is suggestive of the theoretical exercise-induced ARVC. Conclusions: There is still debate regarding right ventricular remodeling in endurance athletes. Increased volume and pressure in response to demand for cardiac output associated with this intense exercise has been proposed as a possible etiology of RV cardiomyopathy in athletes without identifiable genetic predisposition. Our case report supports this hypothesis.

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