Abstract

Electrophysiological mechanisms which underlie the ectopic ventricular beats occurring 1 day after occlusion of the anterior descending coronary artery of dogs were explored. In intact dogs, bipolar electrograms were recorded in the infarcted and normal zones. Both Purkinje and ordinary myocardial potentials were recorded from the endocardial surface of the normal zone, but only Purkinje potentials were recorded from the infarcted zone. The Purkinje potentials in the infarcted zone were diminished in amplitude and rapidity. The threshold for endocardial pacing was higher in the infarcted zone than it was in the normal zone. The refractory periods of Purkinje cells were longer in the infarcted zone than they were in the normal zone. Excised specimens of endocardial surface containing the infarcted zone were superfused with Tyrode's solution. No ordinary myocardial cells were electrically active at the endocardial surface of the infarcted zone. Purkinje cells showed diminished resting and action potentials, reduced upstroke velocity, enhanced automaticity and phase 4 depolarization, and long action potentials with prolonged phase 3. Excitability was depressed within the infarcted zone. During superfusion, even with Tyrode's solution poor in oxygen and free of dextrose, Purkinje cells recovered toward normal with respect to amplitude of resting and action potentials, upstroke velocity, automaticity, and excitability. The prolonged action potentials persisted. Repetitive firing was easily elicited within the infarcted zone. Various types of pacemaker activity were detected within the infarcted zone. Thus Purkinje cells in the infarcted zone showed distinctive alterations in electrophysiological properties which were probably related to deleterious factors that accumulated in that zone. It is likely that the arrhythmia which occurred in the intact dogs at this time originated within the altered Purkinje cells of the infarcted zone.

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