Heart failure is associated with an increased risk of sudden death caused by ventricular tachyarrhythmias. The role of altered repolarization in the formation of arrhythmogenic substrates and triggers has been studied at multiple levels of integration, including molecular, cellular, tissue, and organ levels. Numerous studies have focused on conduction abnormalities in the context of ischemic heart disease and left ventricular dysfunction after myocardial infarction. However, ischemia alone, independent of left ventricular dysfunction, alters conduction by depressing membrane excitability and increasing tissue resistivity. In this review, we focus on the role of conduction abnormalities in the genesis of arrhythmias in nonischemic dilated cardiomyopathy and discuss their underlying cellular and molecular mechanisms, including changes in myocyte excitability, the extracellular matrix, and cell-to-cell coupling. We compare the nature of conduction slowing in ischemic and nonischemic heart failure and highlight the mechanistic differences between the two disease etiologies.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine