A Study of Ventricular Arrhythmias Associated with Acute Myocardial Infarction in the Canine Heart

Abstract

A study was designed to correlate changes in bipolar epicardial electrograms recorded from normal and acutely infarcted myocardium with the onset of ventricular arrhythmias. Electrodes were sewn to selected sites on the left ventricle, and after control electrograms and ECG's were recorded, the left anterior descending coronary artery was doubly ligated close to its origin. Electrograms recorded from within the infarct initially manifested diminished amplitude and increased duration of the deflection which reflected depolarization. The appearance of ventricular arrhythmias during phase 1 of Harris was associated with the appearance in electrograms recorded from within the infarct of continuous electrical activity which extended beyond the T wave of the preceding beat and preceded the onset of the arrhythmia. During the continuous electrical activity, it was not possible to delineate which deflections of the electrogram reflected depolarization or repolarization and it was suggested that the continuous electrical activity was localized fibrillation. For three experiments in which no arrhythmias occurred during phase 1 of Harris and for all animals which survived into phase 2 of Harris, the absence of ventricular arrhythmias was correlated with the absence of continuous electrical activity or locallized fibrillation recorded from within the area of the infarct.Additional Indexing Words: Acute myocardial infarction Ventricular electrograms Localized fibrillation Ventricular arrhythmias IT IS well known that ventricular arrhythmias are associated with myocardial infarction.' Wilson's group2 3 was the first to study experimentally produced myocardial infarction by recording epicardial electrograms and to correlate changes in the local electrogram with changes in the ECG which occurred during the experimentally produced infarction. Since then, there have been numerous studies which have contributed to the understanding of the nature of arrhythmias associated with myocardial infarction. In 1943, Harris and Rojas4 used a string galvonometer to record epicardial electrograms from ischemic areas of the canine heart following acute occlusion of the left anterior descending coronary artery. They reported that as the ischemia developed, electrograms recorded from within the area of the infarct demonstrated a progressive loss of amplitude and increase in duration, until in many cases, no electrogram could be recorded. Recent studies using more sophisticated electronic recording technics 7 have demonstrated that bipolar electrograms could be recorded from areas of ischemic myocardium. The present study was designed to reexamine the observations of Harris and Rojas by recording bipolar electrograms from acutely infarcted regions of the canine myocardium and correlating the electrical activity thereby recorded with the occurrence arrhythmias involving the remainder of the ventricles. From the Methods Twenty-five mongrel dogs weighing 15-25 kg were anesthetized with intravenously administered pentobarbital, 30 mg/kg. For each anim...

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

“…In addition to conduction delay, ischemia regularly produces a loss of electrogram amplitude (11)(12)(13)33). This phenomenon was also observed in the present study.…”

“…Indeed, it was their inability to record these conditions which prompted them to discount reentry as the mechanism for the early occlusive arrhythmias. However, subsequently several different groups of investigators have studied the effects of acute ischemia on local electrophysiology with the use of bipolar electrodes (11)(12)(13)(14)(15)(16)(17)33). (36).…”

“…The inability to demonstrate enhanced automaticity (14), the finding of delayed conduction (11)(12)(13)(14)(15)(16)(17)33), and the recording ~of continuous electrical activity between normal and premature beats (12,13,37) support reentry as the most plausible mechanism responsible for early ischemic arrhythmias. However, since a reentry pathway has never been mapped in its entirety in the intact heart, this mechanism remains an unproven theory and has not gone unchallenged.…”

“…Although there has been an extensive investigation of the mechanisms underlying the arrhythmias of acute myocardial ischemia (11)(12)(13)(14)(15)(16)(17)(18)(19)(20), until recently there has been relatively little attempt to understand the mechanism for reperfusion arrhythmias. This may be related to the specialized conditions necessary to produce reperfusion arrhythmiasnamelv temporary myocardial ischemia.…”

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

“…In this malignant model, we have focused on the lethal end point of ventricular fibrillation, rather than electrophysiologic markers such as ventricular ectopy or fractionation of local electrograms. [10][11][12] The design of this study allowed us to evaluate these agents with respect to their roles in both the primary (prophylactic, before an ischemic event) and secondary (postischemic, before reperfusion) prevention of ventricular fibrillation.…”