Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction.

Abstract

This study examined electrophysiological and anatomic differences between dogs with ventricular tachycardia (VT) and fibrillation (VF) inducible by programmed ventricular stimulation 7-21 days after left anterior descending coronary artery ligation. Of 106 dogs studied, 40 had inducible VT, 19 had inducible VF, and 47 had no inducible arrhythmias. Differences between these three groups of animals were examined with cardiac mapping (to determine ventricular activation time in sinus rhythm) and post-mortem pathology (to measure infarct size and to reconstruct the anatomy at the infarct edge). Animals with inducible VT had longer maximal epicardial activation time (127 +/- 8 msec) than did animals with inducible VF (91 +/- 8 msec, p less than 0.05) or animals with no inducible arrhythmias (75 +/- 2 msec, p less than 0.001). Delayed epicardial activation occurred in 90% of animals with VT, 42% of animals with VF, and in only 6% of animals with no inducible arrhythmias. Endocardial and myocardial activation times were similar for the VT and VF groups. Infarct size was 18 +/- 2% of the ventricles for the VT group, much higher than for the VF group (11 +/- 2%, p less than 0.001) or for the group with no inducible arrhythmias (9 +/- 1%, p less than 0.001). The maximum diameter of viable muscle bundles interdigitating with scar tissue at the infarct edge was much larger in animals with VT (2.4 +/- 0.2 mm) than in animals with VF (1.8 +/- 0.2 mm, p less than 0.05) or animals with no inducible arrhythmias (1.7 +/- 0.1 mm, p less than 0.01). Thus, when compared with animals with inducible VF, animals with inducible VT had longer epicardial activation time, larger infarct size and viable muscle bundles of larger diameter at the infarct edge.