Abstract
Intravenous administration of procainamide is widely used for the management of ventricular tachycardia (VT). Although its efficacy has been clinically established,’ the precise mechanism by which the drug interrupts VT still remains unclear. An experimental study on VT induced in the canine myocardial infarction model has suggested that a class I antiarrhythmic drug (lidocaine) causes conduction block preferentially within the reentry circuit and this interrupts the tachycardia.2 We recently suggested3 that transient entrainment of a tachycardia allows a selective examination of antiarrhythmic drug effect on the area of slow conduction within the reentry circuit of VT. This report presents data that suggest the possible mechanism of action of procainamide in its slowing and interruption of VT in man.
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