LATE POTENTIALS ON THE SIGNAL-AVERAGED ELECTROCARDIOGRAM AFTER CANINE MYOCARDIAL-INFARCTION - CORRELATION WITH INDUCED VENTRICULAR ARRHYTHMIAS DURING THE HEALING PHASE

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 ± 5 versus 57 ± 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 ± 20 versus 46 ± 33 μV, p = 0.04) and a longer late potential duration (19 ± 4 versus 15 ± 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration >58 ms, a terminal QRS amplitude <20 μV and a late potential duration >18 ms. Using this definition, late potentials were seen in two distinct phases—immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG. This suggests that the propensity to ventricular arrhythmias after myocardial infarction is closely dependent on the development of slowed conduction. © 1990, American College of Cardiology Foundation. All rights reserved.