Clinical, electrophysiologic and antiarrhythmic efficacy of moricizine HCl

The electrophysiologic effects and antiarrhythmic efficacy of moricizine HCl (1.5 to 2.0 mg/kg intravenously, and 600 to 800 mg orally/24 hours) were studied using electrophysiologic testing, ambulatory electrocardiographic monitoring, exercise stress testing and transesophageal stimulation of the left atrium. Moricizine HCl had no significant effects on the sinus node in patients with normal nodal function and did not depress sinoatrial conduction time even in patients with serious node dysfunction. Moricizine HCl significantly lengthened the following intervals: PA (32 +/- 5 to 40 +/- 5 ms), AH (82 +/- 13 to 92 +/- 12 ms), HV (45 +/- 12 to 50 +/- 12 ms), paced cycle length 1:1 atrioventricular node conduction (340 +/- 14 to 352 +/- 14 ms) and paced cycle length 1:1 ventriculoatrial conduction (300 +/- 14 to 400 +/- 13 ms). The refractory periods of atrium, atrioventricular node and ventricular myocardium did not change significantly, and there was no alteration of the QRS or QT intervals. The drug abolished anterograde and retrograde conduction over the accessory pathway and increased the refractory period of accessory pathway in all patients. Intravenous moricizine HCl terminated and prevented tachycardia in 72% and 68% of the patients, respectively. Oral moricizine HCl (600 to 800 mg/24 hours) prevented tachycardia in 40% of patients with a preexcitation syndrome. Intravenous moricizine HCl terminated atrioventricular nodal reentrant paroxysmal tachycardia in 66% of patients, whereas 40% responded to the oral drug. Moricizine HCl 600 to 800 mg/24 hours suppressed ventricular premature beats in 60% of patients. A similar drug, Ethacizine, had the same electrophysiologic effects as moricizine HCl but was more potent.(ABSTRACT TRUNCATED AT 250 WORDS)