To characterize the electrophysiologic properties of the ventricular arrhythmias occurring during reperfusion after acute coronary artery ligation, a study was undertaken to correlate the time course of appearance of such arrhythmias with specific electrophysiologic mechanisms. Thirty-seven dogs survived 30minute ligations of the left descending coronary artery, and all had either instantaneous (onset at 0-1 minute) or delayed (onset at 2-7 minutes) ventricular arrhythmias on reperfusion. Local

more »

... electrograms recorded from ischemic myocardium were markedly abnormal after 30 minutes of coronary artery ligation, but rapidly returned to approximately normal within 1-2 minutes after reperfusion. Instantaneous reperfusion ventricular arrhythmias occurred in the midst of the recovery process when fragmented activity was recorded on electrograms from the ischemic area. This activity increased in amplitude, was of long duration (i.e., spanning diastole) and was associated with the occurrence of ventricular fibrillation in 24 of 37 dogs. By 3 minutes after reperfusion, all electrical activity was again synchronous and inscribed completely within the QRS complex. However, in eight of 19 dogs that survived the initial reperfusion period, including six resuscitated from ventricular fibrillation, there was a second surge of ventricular arrhythmias that was independent of diastolic or asynchronous electrical activity. In contrast to the instantaneous reperfusion ventricular arrhythmias, the delayed arrhythmias (2-7 minutes after reperfusion) were associated with electrophysiologic properties characteristic of enhanced automaticity and only infrequently (one of eight dogs) degenerated to ventricular fibrillation. Although the incidence of ventricular arrhythmias during the antecedent period of coronary artery ligation and the occurrence of instantaneous reperfusion arrhythmias were closely correlated, the delayed ventricular arrhythmias of reperfusion and those occurring during the antecedent coronary artery ligation period were not correlated. Distinct electrophysiologic mechanisms are apparently associated with a specific time course of appearance and with the severity of ventricular arrhythmias that occur when blood flow is suddenly restored to acutely ischemic myocardium. THE SUDDEN ONSET of ventricular tachycardia and fibrillation upon the release of a coronary artery occlusion in the experimental animal was observed as early. as the 19th century.1 A wealth of experimental data has subsequently confirmed this phenomenon.28 While new information identifying the mechanisms of the arrhythmias induced by coronary ligation has been described,9-13 the precise mechanism of the rhythm disorders observed upon reperfusion remains unclear. '4 Differences between the ventricular arrhythmias of ligation and those of reperfusion suggest that multiple mechanisms may account for the rhythm disorders attendant upon ligation and reperfusion.7 8, 14, 15 Reperfusion arrhythmias are usually sudden in onset and deteriorate to ventricular fibrillation within 5-30 seconds. Arrhythmias due to coronary ligation, however, are gradual in onset and develop over a period of several minutes.2 8 13, 14 Several therapeutic maneuvers that are generally successful in preventing From the ligation arrhythmias are ineffective in the presence of reperfusion arrhythmias,1 16 which appear to be more malignant because the incidence of ventricular fibrillation after reperfusion exceeds that after ligation.'8 Myocardial vulnerability to ventricular fibrillation and to repetitive ventricular responses has been found to be transiently increased after both ligation and reperfusion.' 8f, 17 Although the increase and subsequent decrease in vulnerability after ligation are gradual and occur over many minutes, the changes after reperfusion are more immediate and shortlived.6' 8, 17, 18 The present study was designed to characterize the electrophysiologic properties of ventricular arrhythmias occurring immediately after reperfusion of acutely ischemic myocardium and to correlate the time course of their appearance with specific electrophysiologic mechanisms. A 30-minute coronary artery ligation model was chosen to include dogs with both "immediate" and "delayed" ventricular arrhythmias of the acute ligation period.13 Materials and Methods This study was performed on 37 of 53 mongrel dogs (weight 18-30 kg) that survived 30 minutes of coronary artery ligation. Dogs were anesthetized with pentobarbital (30 mg/kg). Hearts were exposed via the fourth left intercostal space and suspended in a pericardial cradle. Ventilation was maintained by a Harvard room air respirator by means of a cuffed en-333 by guest on July 19, 2018 http://circ.ahajournals.org/ Downloaded from