The authors studied the effects of lidocaine in 18 consecutive dogs with myocardial infarction 1 to 4 days after two-stage left anterior descending coronary artery ligation. Electrophysiologic testing was performed in anesthetized dogs after infarction with single-, double-, or triple-programmed extrastimuli or rapid bursts (3 beats at 240 to 420 beats/min) delivered to the right ventricular outflow tract. Inducibility of sustained monomorphic ventricular tachycardia after an intravenous bolus of lidocaine (3 to 6 mg/kg) was compared in the same animal to the premedicated state. In the control state, sustained monomorphic ventricular tachycardia was inducible in 6 of 18 dogs. After administration of lidocaine, electrically induced sustained monomorphic ventricular tachycardia was initiated in an additional nine dogs (which were previously noninducible; after lidocaine administration vs control p < 0.02). The antiarrhythmic agent induced further rate-dependent slowing of conduction in the periinfarction subepicardium, which at a critical value of rate and amount of conduction delay resulted in sustained reentrant monomorphic tachycardia. These results show that lidocaine has marked proarrhythmic action in this canine model of myocardial infarction, probably because of its depressant effect on injured cardiac tissue.