Mechanisms, Prediction and Treatment of Ventricular Tachyarrhythmias Occurring Late After Myocardial Infarction

Abstract

Studies from the 1980s, refined in the intervening years, have examined the milieu for ventricular tachycardia (VT) and ventricular fibrillation (VF) occurring late after acute myocardial infarction (AMI). The arrhythmogenic substrate appears to be patchy areas of fibrous tissue interdigitating with viable bundles of myocardium which have distorted orientation and tortuous interconnections. These promote conduction delay in sinus rhythm. Factors found to promote induction of VT rather than VF are longer conduction delay in sinus rhythm, larger infarct size, a more ragged infarct edge and longer ventricular extrastimulus coupling intervals. Predictors of spontaneous VT and VF late after AMI include inducible VT at electrophysiological studies (EPS), delayed conduction in sinus rhythm detected as late potentials on signal-averaged surface electrocardiogram (ECG), and low left ventricular ejection fraction (LVEF). Treatments of propensity for VT or VF after AMI include insertion of a defibrillator (ICD), which has the best track record, antiarrhythmic medication (less reliable), and ablation or excision of arrhythmogenic substrate (for refractory VT and VF).