Failure of antiarrhythmic drugs to affect epicardial delay during acute experimental coronary artery occlusion and reperfusion: correlation with lack of antiarrhythmic efficacy.

Five antiarrhythmic drug protocols were studied to evaluate their efficacy in reducing the incidence of coronary artery ligation and/or reperfusion ventricular arrhythmias and to determine whether their antiarrhythmic activity correlated with their effect on epicardial delay. Protocols were as follows: I) preligation lidocaine (N = 19); II) preligation amiodarone (N = 18); III) preligation procainamide (N = 19); IV) prereperfusion lidocaine (N = 19); V) prereperfusion verapamil (N = 18); and control (no drug, N = 61). A total of 50 (82%) of the 61 control animals developed ventricular arrhythmias during coronary artery ligation and 29 (68%) of the 53 control dogs that survived until reperfusion developed ventricular arrhythmias upon reperfusion. None of these treatment protocols had a significant effect in reducing the incidence of either ventricular arrhythmias or ventricular fibrillation during coronary artery ligation or reperfusion compared with the control animals (P greater than .05). Correspondingly, the mean maximal epicardial delay during coronary artery ligation was also unchanged by each of these drug treatment protocols compared with the control group. Similarly, none of these treatment protocols demonstrated significant effect in preventing reperfusion ventricular arrhythmias or a consistent effect on the degree of mean maximal epicardial delay during reperfusion. Although the lack of antiarrhythmic efficacy of these agents precludes further speculation, further study is warranted to determine whether changes in epicardial delay can be used as markers for antiarrhythmic activity.