Inducible sustained ventricular tachycardia 4 years after experimental canine myocardial infarction: electrophysiologic and anatomic comparisons with early healed infarcts.

Abstract

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< .001) and shorter electrogram duration (p< .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 <.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.

Standards for analysis of ventricular late potentials using high resolution or signal-averaged electrocardiography

“…Results of laboratory (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and clinical (31)(32)(33)(34)(35)(36)(37) studies implicate reentrant mechanisms, at least in part, in the genesis of sustained ventricular tachycardia complicating ischemic heart disease. Abnormal ventricular conduction during sinus rhythm has been observed in regions bordering the infarct (31,32,(38)(39)(40)(41)(42)(43) and appears temporally related to the development of ventricular tachycardia (20)(21)(22)(39)(40)(41)(42)(43).…”

“…Myocardial activation may be delayed because the pathway of excitation is lengthened, conduction velocity is slowed, or both. Structural features may be critical determinants of delayed activation (40,41). Clinically, most myocardial infarcts do not result in complete transmural necrosis (42).…”

“…Islands of fibrosis create barriers that lengthen the excitation pathway. The increased separation of myocardial bundles and disruption of their parallel orientation by fibrosis distort ventricular activation (40,41). However, the action potentials of surviving myocardial cells may appear relatively normal (40).…”

Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context

“…Patchy myocardial scars with surviving islands of myocytes characterize human infarcts (10,17). Heterogeneous intramyocardial sympathetic nerve sprouting at scar border zones leads to labile repolarization, increased peak Ca 2ϩ current, and susceptibility to ventricular fibrillation in hypercholesterolemic rabbits (15).…”

Detection and localization of prolonged epicardial electrograms with 64-lead body surface signal-averaged electrocardiography.

“…(Circulation 1991;84:871-883) P rolongation of electrograms recorded directly from ventricular myocardium can frequently be detected after experimental and clinical myocardial infarctions.1-10 Prolonged, fractionated electrograms are thought to be generated by slow and inhomogeneous activation of adjacent muscle fibers, resulting from impairment of cell-to-cell coupling by graphic potentials at the end of the QRS complex that are not detectable by standard electrocardiography (ECG).12-16 These electrocardiographic "late potentials" are commonly seen in patients with sustained ventricular tachycardia16-18; in canine infarct models, they are associated with inducible ventricular arrhythmias. [19][20][21][22] Late potentials are thought to arise from tissue that generates prolonged, fractionated electrograms. Studies in humans and canine infarct models have shown an association between the presence of late potentials and the presence of prolonged electrograms.121519,2123,24 For example, Spear et al19 showed in a canine infarct model that dogs with inducible ventricular tachycardia generally had both electrocardiographic QRS late potentials and prolonged ventricular epicardial electrograms and that dogs without inducible arrhythmias generally had neither.…”