CARDIOVERSION, DEFIBRILLATION, AND OVERDRIVE PACING OF VENTRICULAR ARRHYTHMIAS - THE EFFECT OF MORICIZINE IN DOGS WITH SUSTAINED MONOMORPHIC VENTRICULAR-TACHYCARDIA

The purpose of this investigation is to define whether the antiarrhyth mic drug moricizine has beneficial or adverse effects on currently use d antitachycardia and antifibrillatory devices. These studies were per formed in a dog model of sustained monomorphic ventricular tachycardia (VT). In 11 dogs, the left anterior descending artery and all surroun ding epicardial collateral feeder vessels were ligated. Defibrillator patches were implanted and the dogs were allowed to recover. After a 7 -day recovery period, effective refractory period (ERP), end diastolic threshold (EDT), VT induction, and VT and ventricular fibrillation (V F) termination data were collected before and after moricizine infusio n (2 mg/kg). In this experimental model, moricizine caused the followi ng electrophysiological changes: a prolongation of the ERP from 173 +/ - 14 to 182 +/- 15 (P < 0.02) with no significant effect on the EDT fo r pacing; a prolongation of the VT cycle length from 175 +/- 18 to 201 +/- 23 msec (P < 0.003); an increased cycle length required for overd rive pacing from 136 +/- 20 to 157 +/- 22 msec (P < 0.01); no effect o n the energy required to cardiovert VT; an increase in the defibrillat ion threshold from 7.5 +/- 4 to 9.4 +/- 4 joules (P < 0.006) and; in 5 of the 8 dogs with VT, the VT could be initiated with somewhat less a ggressive stimulation. Significant beneficial electrophysiological eff ects were noted on the VT cycle length, including a proportionately pr olonged overdrive pacing cycle length for VT termination. These change s were contrasted by the significant increase in the VF conversion ene rgy required and the ease with which the VT could be induced postmoric izine. These findings suggest a possible proarrhythmic effect of moric izine.