Z Vera1, H P Pride, D P Zipes. 1. Division of Cardiology, University of California, Davis School of Medicine, USA.
Abstract
INTRODUCTION: The precise mechanism of reperfusion arrhythmias is not established. The role of early afterdepolarizations (EADs) and triggered activity in the genesis of reperfusion ventricular arrhythmia was investigated. METHODS AND RESULTS: Monophasic action potentials (MAPs) were recorded in the canine heart using Ag-AgCl contact electrodes from the left and right ventricular endocardium and the left ventricular epicardial border zone during 10 minutes of occlusion of the proximal left anterior descending coronary artery followed by 2 minutes of reperfusion. Ventricular arrhythmias during ischemia and reperfusion were studied in three autonomically varied groups. Group 1 (n = 8) had intact autonomic neural innervation; group 2 (n = 8) had bilateral transection of ansae subclavii and vagi; and group 3 (n = 8) underwent bilateral transection of ansae subclavii and vagi with bilateral ansae subclavii stimulation during reperfusion. Ventricular fibrillation (VF) on reperfusion occurred in 2, 3, and 5 animals in the innervated, denervated, and sympathetically stimulated groups, respectively. Rapid ventricular tachycardia during ansae subclavii stimulation, antecedent to VF, occurred in 4 of 5 episodes in the sympathetically stimulated group. The frequency of premature ventricular complexes, couplets, and triplets on reperfusion was not significantly different among the three groups. Phase 2 or phase 3 EADs were noted during the acute ischemic phase in 6 of 8, 7 of 8, and 7 of 8 animals in the three groups, respectively (and persisted during reperfusion in the majority). Thus, these EADs were not a de novo phenomenon during reperfusion. Of the 72 MAP recording sites, only one demonstrated de novo phase 2 EADs during reperfusion. EADs disappeared during reperfusion in 6 animals (prior to the onset of VF in 4), and 5 dogs developed reperfusion VF without EADs being recorded. There was no direct correlation between the presence of EADs during reperfusion and the development of VF. The prevalence and onset of reperfusion VF was not significantly different in the presence of sympathetic stimulation. CONCLUSION: This study demonstrates that EADs can be recorded in the majority of dogs during both ischemia and reperfusion and do not appear to be a major mechanism responsible for reperfusion ventricular tachycardia and VF.
INTRODUCTION: The precise mechanism of reperfusion arrhythmias is not established. The role of early afterdepolarizations (EADs) and triggered activity in the genesis of reperfusion ventricular arrhythmia was investigated. METHODS AND RESULTS: Monophasic action potentials (MAPs) were recorded in the canine heart using Ag-AgCl contact electrodes from the left and right ventricular endocardium and the left ventricular epicardial border zone during 10 minutes of occlusion of the proximal left anterior descending coronary artery followed by 2 minutes of reperfusion. Ventricular arrhythmias during ischemia and reperfusion were studied in three autonomically varied groups. Group 1 (n = 8) had intact autonomic neural innervation; group 2 (n = 8) had bilateral transection of ansae subclavii and vagi; and group 3 (n = 8) underwent bilateral transection of ansae subclavii and vagi with bilateral ansae subclavii stimulation during reperfusion. Ventricular fibrillation (VF) on reperfusion occurred in 2, 3, and 5 animals in the innervated, denervated, and sympathetically stimulated groups, respectively. Rapid ventricular tachycardia during ansae subclavii stimulation, antecedent to VF, occurred in 4 of 5 episodes in the sympathetically stimulated group. The frequency of premature ventricular complexes, couplets, and triplets on reperfusion was not significantly different among the three groups. Phase 2 or phase 3 EADs were noted during the acute ischemic phase in 6 of 8, 7 of 8, and 7 of 8 animals in the three groups, respectively (and persisted during reperfusion in the majority). Thus, these EADs were not a de novo phenomenon during reperfusion. Of the 72 MAP recording sites, only one demonstrated de novo phase 2 EADs during reperfusion. EADs disappeared during reperfusion in 6 animals (prior to the onset of VF in 4), and 5 dogs developed reperfusion VF without EADs being recorded. There was no direct correlation between the presence of EADs during reperfusion and the development of VF. The prevalence and onset of reperfusion VF was not significantly different in the presence of sympathetic stimulation. CONCLUSION: This study demonstrates that EADs can be recorded in the majority of dogs during both ischemia and reperfusion and do not appear to be a major mechanism responsible for reperfusion ventricular tachycardia and VF.