Electrophysiologic substrate for ventricular tachycardia: correlation of properties in vivo and in vitro

Cardiac electrophysiologic studies were performed in three control dogs and in nine dogs with previous (8 to 22 days) anterior myocardial infarction. During programmed stimulation, no control dog had more inducible ventricular fibrillation (VF) or tachycardia (VT), three dogs with infarcts had inducible VF and six had inducible VT. Recordings in vivo were made via a plaque electrode containing 10 bipolar electrodes (3.0 x 1.5 cm) placed on the epicardial surface of the anteroapical left ventricle. Subsequently, epicardial strips (2 mm thick) from beneath the plaque were prepared for studies in vitro. Electrogram durations were significantly greater in dogs with infarcts than in control dogs both in vivo (p less than .05) and in vitro (p less than .001). Electrogram amplitudes were significantly lower in dogs with VT in vivo (p less than .05) and in vitro (p less than .001). In control animals activation was continuous and most rapid in the direction of fiber orientation; there were areas of slow and/or discontinuous conduction in all dogs with infarcts. In one case, sustained reentrant beating in vitro was caused by functional unidirectional block and microreentry at a site of continuous electrical activity during VT in vivo. Reentrant beating in vitro persisted in 0.5 cc of isolated tissue. We conclude that broad low-amplitude electrograms in vivo and in vitro depict local areas of slow and/or discontinuous conduction, that the intrinsic asymmetry of cardiac activation due to fiber orientation is accentuated by infarction and may predispose to intraventricular reentry, and that intraventricular reentrant circuits that may be present on the epicardial surface may persist in a volume of myocardial tissue as small as 0.5 cc.