Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: Evidence for distinct mechanisms

AbstractTo determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infuse ot a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia.The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 ± 4 vs. 7.4 ± 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 ± 78 vs. 450 ± 81 ms, p = NS) and QRS duration (184 ± 38 vs. 185 ± 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.In summary, infusion of procsinamide with use of the described dosing regimen terminated 93% of sustained, nemodynamically tolerated ventricular tachycardia episodes without causing hypotension. The ability to terminate ventricular tachycardia with an infusion of procainamide did not reliably predict subsequent success in preventing inducible ventricular tachycardia. Finally, the reinitiation of ventricular tachycardia with an identical configuration and similar cycle length and at constant serum procainamide concentrations suggests that, at least in some patients (7 of 13; 54%), the electrophysiologic mechanism of drug-induced ventricular tachycardia termination is different from that of arrhythmia prevention