Method for evaluating the effects of antiarrhythmic drugs on ventricular tachycardias with different electrophysiologic characteristics and different mechanisms in the infarcted canine heart.

In a canine model of myocardial infarction caused by coronary occlusion and reperfusion, ventricular tachycardia occurs spontaneously at 24 hours and has many of the characteristics of an accelerated idioventricular rhythm. It cannot be induced by premature or rapid stimulation of the ventricles; overdrive pacing during this tachycardia usually causes some transient overdrive suppression but occasionally there is overdrive acceleration. We suggest that this arrhythmia is caused mainly by enhanced automaticity. Ventricular tachycardia also can be induced by premature or rapid ventricular pacing 3 to 5 days after infarction, but it does not occur spontaneously. It can be stopped by overdrive pacing, suggesting that it is caused by reentry. Electrocardiographic features are identical to chronic, recurrent sustained ventricular tachycardia in human patients. Because the arrhythmias occurring at different times probably result from different mechanisms this canine model is useful for comparing the actions of drugs on different kinds of arrhythmias. Lidocaine and procainamide generally abolished tachycardia 24 hours after infarction, but only procainamide abolished tachycardia 3 to 5 days after infarction. Isoproterenol accelerated tachycardia at both times. Verapamil did not abolish tachycardia 3 to 5 days after infarction.