Remodeled left ventricular myocardium remote to infarction sites is the arrhythmogenic substrate for sudden cardiac death.

Ventricular tachyarrhythmias are life threatening cardiac arrhythmias and are the most common causes of sudden cardiac death. Greater post-infarction left ventricular remodeling has been shown to have a greater preponderance of ventricular arrhythmias. The hypothesis herein is that adverse structural and electrophysiological remodeling at non-infarcted regions after myocardial infarction constitutes the arrhythmogenic substrate responsible for clinically occurring ventricular arrhythmias leading to sudden cardiac death. Post-infarction patients with more severe left ventricular remodeling (regional hypertrophy) at sites remote to infarction scar might have the highest risk for sudden cardiac death due to lethal ventricular arrhythmias. In the hypertrophic non-infarcted zone, larger action potential duration and repolarization heterogeneity is not in self arrhythmogenic, but can predispose towards arrhythmia development under certain condition, such as transient myocardial ischemia. We should draw more attention to apparently "normal" non-infarction region for further understanding the mechanism of sudden cardiac death. Copyright 2010 Elsevier Ltd. All rights reserved.