Ventricular fibrillation arrest with cardiomyopathy in the setting of exogenous T3 consumption in a previously healthy young male.

Ventricular fibrillation (VF) is an often-fatal cardiac arrhythmia with increased prevalence in those with structural heart disease, congestive heart failure, and history of myocardial infarction. Our case describes a young adult male who presented with VF arrest and new onset cardiomyopathy in the setting of exogenous testosterone and triiodothyronine supplementation. Comprehensive work-up demonstrated a severely reduced ejection fraction, no angiographically significant coronary artery disease on invasive coronary angiography, and evidence of right ventricular mid-lateral wall scarring on electrophysiology study and cardiac magnetic resonance imaging. Exogenous thyroid hormone and testosterone supplementation have been independently associated with development of dilated cardiomyopathy; however, VF arrest has rarely been described in otherwise previously healthy individuals with concomitant use of these substances. Optimal management, risk stratification, and prognosis in this population remains unknown. Our case identifies an at-risk population of sudden cardiac death where appropriate work-up and shared clinical decision-making is essential to improved patient outcomes and quality of life. Learning objective: Exogenous triiodothyronine (T3) intake may be a risk factor for the development of acute cardiomyopathy, as cardiac myocytes directly uptake T3 which can induce arrhythmias and cardiac arrest. This process may be separate from tachycardia-mediated cardiomyopathy. Prognosis of hyperthyroid induced ventricular fibrillation and cardiomyopathy is unclear. Reversing the hyperthyroid state may reduce the risk of repeat sudden cardiac death. The decision for secondary prevention should be a joint decision understanding patient-specific risk factors and goals.