Abstract 4142080: Bridge from Arrest to Recovery: Sudden Cardiac Arrest in a Young Patient with Concomitant Myocardial Bridge and Hypertrophic Cardiomyopathy

Case Presentation: A 27-year-old-male without any known medical history presented after witnessed sudden cardiac arrest. Initial rhythm in the field was ventricular fibrillation. He underwent CPR with three rounds of external defibrillation with 200 J and after return of spontaneous circulation (ROSC) was transferred to our facility. He was initially normotensive, bradycardic, hypothermic to 35.6°C and hypoxic requiring non-rebreather mask. He was intubated for airway protection. Post ROSC 12-lead surface ECG revealed sinus rhythm with a prolonged QT interval and left ventricular hypertrophy. Initial high-sensitivity Troponin I was elevated to 83 pg/ml that peaked to 4631 pg/m. On transthoracic echocardiogram, ejection fraction was 55-60% with moderate concentric left ventricular hypertrophy and an interventricular septum end diastolic thickness of 1.3 cm as well as normal left ventricular outflow tract pressure gradient. Coronary angiogram was notable for prominent myocardial bridge (MB) of the middle left anterior descending (LAD) artery without any evidence of atherosclerotic disease. Cardiac magnetic resonance imaging (CMR) showed asymmetric left ventricular hypertrophy with reverse septal curvature variant and evidence of patchy late gadolinium enhancement. A dual-chamber implantable cardioverter defibrillator was placed for secondary prevention of ventricular arrhythmias and sudden cardiac death. Metoprolol tartrate was started for management of hypertrophic cardiomyopathy (HCM) and MB. At follow-up visit he was asymptomatic and genetic testing was positive for heterozygous gene mutation in MYBPC3. Discussion: MBs have been recognized as a common congenital anomaly of the epicardial coronary arteries, with a higher prevalence reported in patients with HCM. We present a unique clinical scenario of a young patient with asymmetric HCM, patchy late gadolinium enhancement on CMR and evidence of prominent MB of the LAD artery. Hemodynamically significant MBs have been implicated in the degree of fibrosis in HCM which is significant due to the correlation between extent of fibrosis and adverse cardiac remodeling, and the consequent predisposition to arrhythmogenesis. However, the existing literature is inconclusive regarding the exact association between MBs and cardiovascular mortality in HCM. Here, we highlight the potentially increased risk of sudden cardiac arrest conferred by MB in HCM and the need for further studies to delineate this association.