Antiarrhythmic and myocardial metabolic effects of verapamil during coronary artery reperfusion.

Abstract

The accumulation of metabolic intermediates subsequent to impaired beta-oxidation of free fatty acids has been suggested to be a cause of cellular damage and ventricular arrhythmias in the ischemic heart. The effects of verapamil on ventricular arrhythmias and free fatty acids metabolism during coronary artery reperfusion in experimental dogs were evaluated over a period of 40 minutes and followed by reperfusion for 15 minutes. One tenth mg/kg/min of verapamil was administered for 5 minutes before occlusion and followed by an infusion of 0.01 mg/kg/min to the end of the experiment. Myocardial samples were obtained from both the non-ischemic and ischemic areas after coronary artery reperfusion and then ATP, free carnitine, long chain acyl carnitine and long chain acyl CoA were measured. In the control group, 3 dogs (27%) had ventricular fibrillation and 2 dogs (18%) had ventricular tachycardia during coronary occlusion. In addition, 2 dogs (25%) developed ventricular fibrillation after reperfusion. On the other hand, all 6 dogs treated with verapamil had neither ventricular fibrillation nor tachycardia during both coronary artery occlusion and reperfusion. ATP and free carnitine levels in the ischemic area were significantly higher in the verapamil group than in the control group (ATP: p less than 0.01, free carnitine: p less than 0.05), while long chain acyl carnitine levels in the ischemic area were significantly lower in the verapamil group than in the control group (p less than 0.01). However, there was no significant change in long chain acyl CoA levels between the control and verapamil groups.(ABSTRACT TRUNCATED AT 250 WORDS)