Abstract
The effect of verapamil cardioplegia on atrioventricular conduction was examined in 19 dogs. During 90 minutes of ischemic arrest, five dogs received multidose potassium cardioplegia, containing 1.2 mg/L of verapamil (group 1), five received potassium cardioplegia containing 600 micrograms/L of verapamil (group 2) and nine animals received cardioplegia containing 300 micrograms/L of verapamil (group 3). Atrioventricular conduction was measured in all groups before bypass, after 90 minutes of ischemia and after 45 minutes of reperfusion. Specially designed plunge electrodes were used to monitor the electrical status of the heart during arrest in group 3 and, in addition, left ventricular function and concentration of high-energy phosphates were determined before and after ischemic arrest. Conduction was prolonged in four group 1 dogs and in two group 2. Atrioventricular conduction was measured in six group 3 dogs; five had prolonged conduction and one experienced second-degree heart block. Small-amplitude electrical potentials were recorded from the myocardium in two of nine dogs in group 3. Persistent electrical activity was associated with continued use of high-energy phosphates and resulted in decreased left ventricular function after 90 minutes of ischemic arrest. Our data indicate that small doses of verapamil will delay atrioventricular conduction and will not prevent small-amplitude electrical activity.