Ventricular scars and ventricular tachycardia

Abstract

Ventricular tachycardia (VT) is a life-threatening arrhythmia that is common to all forms of heart disease and an important cause of sudden death. Ventricular scars from infarction or replacement fibrosis provide a substrate for reentry that is a common cause. Understanding the pathophysiologic link between ventricular scars and ventricular tachycardia informs approaches to identify patients at risk, has led to development of methods to ablate the arrhythmia substrate that can be applied even in severe heart disease, and suggests future diagnostic and therapeutic strategies.

Fig. 1

Polymorphic VT is shown in Panel A. Monomorphic VT is shown in Panel B. A schematic for reentry in a region of scar is shown in Panel C. Reentry wavefronts are indicated by black arrows. Fibrosis creates a channel for conduction through the scar. A gray scale rendition of a voltage map of the left ventricle as viewed from the right oblique projection is shown in Panel D. This map was created by moving a mapping catheter over the endocardial surface of the left ventricle and plotting the peak to peak electrogram amplitude. An extensive anterior wall infarct is present, indicated by low voltage (lighter shades of gray). The basal portion of the ventricle has normal amplitude (darker shade of gray). Exit regions for VT were identified along the border zones (interface between low voltage and normal voltage regions) in this patient.