Why the study?
Does the electrophysiologic and anatomic substrate for ventricular tachycardia evolve between early (2-24 weeks) and late (4-6 years) healed myocardial infarction in a canine model?
Does the electrophysiologic and anatomic substrate for ventricular tachycardia evolve between early (2-24 weeks) and late (4-6 years) healed myocardial infarction in a canine model?
A substrate for reentrant tachycardia persists 4 to 6 years after reperfused infarction in dogs, but conduction characteristics are less abnormal and associated with shorter VT cycle lengths compared to early infarcts.
VT substrate persists years post-MI in dogs with shorter inducible CL; extends early animal models but leaves open human relevance.
We studied a group of 17 dogs 4 to 6 years after infarction produced by 2 hr occlusion of the anterior descending coronary artery followed by reperfusion. Dogs in this "late" infarct group were compared with a group of 24 dogs with "early" healed infarcts (2 to 24 weeks old). With signal-averaging techniques body surface potentials were recorded during sinus rhythm. After thoracotomy epicardial electrograms were recorded from 45 standardized sites within the infarcted region and characteristics of selected electrograms were compared with anatomic features of underlying myocardium. Epicardial recordings from the late infarct group demonstrated earlier local activation (p less than .001) and shorter electrogram duration (p less than .001) when compared with recordings from the early infarct group. There was less temporal dispersion of activation and electrogram duration among the 45 sites in dogs with late infarcts as measured by respective coefficients of variance (p = .007 and less than .001). With programmed stimulation six dogs in the late and eight in the early infarct group exhibited inducible sustained ventricular tachycardia. Mean cycle length of the tachycardia in dogs with late infarcts was significantly shorter (p = .035). Late potentials were notably less prominent in dogs in the late infarct group with ventricular tachycardia than in dogs in the early infarct group. Fewer abnormal electrophysiologic characteristics of late infarcts coincided with relatively less scar in the underlying myocardium. Moreover, the strength of electrophysiologic-anatomic correlations differed in late as opposed to early infarcts. The latter findings suggest long-term evolution of infarct anatomy. We conclude that a substrate for reentrant tachycardia is present in dogs 4 to 6 years after reperfused infarction. Conduction characteristics are less abnormal in these late healed infarcts and are associated with a shorter ventricular tachycardia cycle length and less pronounced late potentials on the body surface.
No takes yet. Share an insight, caveat, or question.
Hanich et al. (1988) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:
More from Circulation