Automatic and triggered impulse initiation in canine subepicardial ventricular muscle cells from border zones of 24-hour transmural infarcts. New mechanisms for malignant cardiac arrhythmias?

With standard microelectrode techniques, electrical activity of cells in the epicardial border zones of infarcts in the canine heart were studied. Either automaticity or triggered activity (or both) occurred in each of the 12 preparations studied from 24-hour infarcts. One 24-hour preparation had continuous activity indistinguishable from low-potential (abnormal) automaticity. This automaticity was not effected by flecainide 1-5 mg/l. Two other 24-hour subepicardial muscle preparations also were automatic. However, nine preparations from the subepicardium were not automatic during superfusion with standard Tyrode's solution. Delayed afterdepolarizations (DADs) and triggered activity could be induced in all of these preparations by treatment with catecholamines. The amplitude of these DADs was directly related to the stimulus rate of the train of impulses used to elicit them, and their coupling interval was inversely related to this rate of stimulation. Triggered activity occurred from maximal diastolic potentials of -58 to -88 mV in the 24-hour infarct zone preparations. In seven preparations from 72-96-hour infarct zones, the epicardial muscle cells did not show triggered activity after treatment with catecholamines. In one preparation from a 72-hour infarct, however, 3-5-mV DADs occurred. No DADs or triggered impulses occurred in subepicardial muscle from normal, noninfarcted hearts. Thus, triggered impulses and low-potential automaticity could contribute to arrhythmias occurring in the canine heart 24 hours after coronary ligation.