The importance of the electrophysiologic substrates in the development of ventricular tachyarrhythmias.

Our electrophysiologic findings are summarized in Table 3. In our animal model of chronic myocardial infarction, induced sustained ventricular tachyarrhythmias occur from 3 days to months following the infarction procedure. Isolated tissues removed from the infarcted region in these animals and studied (table: see text) in vitro reveal regions of slow conduction and local conduction block. These characteristics also persist over this time period and appear to be the substrate responsible for the reentrant excitation at the basis of the ventricular tachyarrhythmias. Our cellular electrophysiologic studies indicate the mechanisms responsible for the abnormal conduction change with time. Up to approximately 2 weeks following the infarction procedure, cellular membrane depolarization is depressed and cell-to-cell electrical continuity is decreased. Both of these factors probably contribute to the slow conduction. Depression in membrane excitability does not seem to play a role. Although an increased dispersion in refractoriness probably contributes to the inducibility of ventricular reentry due to an enhanced propensity for a premature impulse to undergo functional block in one region while continuing to conduct in another region. At two weeks and beyond, action potential depolarization has returned to normal. At this time the sole contributor to the abnormal conduction appears to be cellular electrical uncoupling. Two possibilities for the cause of this cellular uncoupling are as follows: First, the low resistance gap junctions between cells may be modified in the infarcted region causing an increase in internal axial resistance. Another possibility is that the fibrotic matrix in which the surviving cells in the mottled infarct are distributed may contribute to an increase in extracellular resistance as compared to normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Critical appraisal of programmed electrical stimulation for evaluating hearts prone to ventricular tachyarrhythmias.

Programmed electrical stimulation has provided a unique new opportunity to evaluate both mechanisms and treatment regimens aimed at preventing ventricular tachyarrhythmias. The variable results that have been reported from different laboratories, undoubtedly are due in part to the differences in programmed electrical stimulation protocols. Although it is unlikely that all laboratories will adapt the same programmed electrical stimulation protocol, it nevertheless is very important that the number of sites of stimulation, stimulus strength, stimulus duration, stimulus polarity, drive train length, and patient population all be listed in order for some comparison between laboratories to be made.

Use of signal averaging to identify low level late potentials in hearts prone to developing tachyarrhythmias.

Our studies have shown that infarcted dogs which exhibit inducible sustained ventricular tachycardia had late potentials and could be distinguished from those with no arrhythmias by the following QRS characteristics. A QRS duration greater than 63 msec and a duration of late activity below 30 microvolts greater than 18 msec. In addition, delayed and fractionated epicardial activation in the infarcted region correlates with late potentials on the body surface. Finally, induced ventricular fibrillation in this animal model appears to have mixed causes and is a non-specific end point.