Abstract

Sachin Kumar Amruthlal Jain1, Alehegn Gelaye2*, Timothy R. Larsen2and Shukri David1

Sudden cardiac death (SCD) is the leading cause of cardiovascular death in industrialized population and accounts for 300,000 to 400,000 deaths annually in the United States. It is estimated to account for up to 50% of all heart disease related deaths (Engelstein and Zipes, 1998). Despite advances in the treatment of acute coronary syndromes with early revascularization and effective secondary preventative therapies, the risk of sudden cardiac death remains high in the early period following myocardial infarction (MI). This is particularly true in the setting of severely reduced left ventricular function, reflected as a left ventricular ejection fraction (LVEF) less than 35% (Solomon et al., 2005; Klein et al., 2010). In majority of the cases, SCD results from a ventricular arrhythmia, typically ventricular tachycardia or fibrillation (Huikuri et al., 2001).