Further electrophysiologic and anatomic correlates in a canine model of chronic myocardial infarction susceptible to the initiation of sustained ventricular tachyarrhythmias.

Abstract

A canine model of chronic myocardial infarction has been studied in which animals are susceptible to the initiation of sustained ventricular tachyarrhythmias using routine methods of programmed stimulation. The pacing-induced arrhythmias in this model are similar to those observed in man in their mode of initiation and termination, as well as in their response to both pacing and pharmacologic interventions. Indirect evidence has suggested a localized protected reentrant mechanism for these arrhythmias. The susceptibility to arrhythmia initiation in this model has been related to both electrophysiologic and histopathologic findings. Consistently, animals have demonstrated a marked heterogeneity of local properties of excitability and refractoriness at sites within areas of infarction. Correspondingly, animals have shown a marked inhomogeneity of histopathologic findings within areas of infarction, with close interspersing of normal and abnormal myocardium. Remarkably, even animals with small mottled infarctions, often less than 1 cm x 2 cm and electrocardiographically silent, were highly susceptible to the initiation of ventricular tachyarrhythmias, and especially fibrillation. Thus, initial provocative studies in this model have suggested its potential importance both in studying arrhythmia mechanisms and in evaluating the efficiency of potential antiarrhythmic interventions. In addition, this should be an ideal model in which to correlate pathophysiologic and morphologic alterations in the setting of chronic myocardial infarction.