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)