Cardiac electrophysiologic effects of moricizine hydrochloride.
Moricizine is a class I antiarrhythmic drug. In preclinical studies, it produces a concentration-dependent decrease in the maximal rate of phase 0 depolarization, speeds repolarization of phases 2 and 3, and decreases the action potential duration and effective refractory period duration in cardiac Purkinje fibers. It has no effect on the slope of phase 4 depolarization, but suppresses normal automaticity in vitro and in vivo and suppresses abnormal automaticity in depolarized Purkinje fibers. Also, it suppresses early afterdepolarizations, delayed afterdepolarizations and triggered activity. In patients, moricizine has minimal effects on the normal sinus node, slows conduction in the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium and has little effect on the atrial and ventricular refractoriness. The intensity of moricizine action on the atrioventricular node, His-Purkinje system and JT interval are dose-related. Co-administration of digoxin and moricizine intensified the lengthening of the PR, AH and HV intervals, and produced more shortening of the JT interval. Patients in whom moricizine was efficacious had a significantly greater lengthening of the AH and QRS intervals than those in whom moricizine was not efficacious. In some patients with sinus node dysfunction, moricizine produced sinus bradycardia, increased sinus node recovery time, and produced second-degree or complete sinoatrial block.[1]References
- Cardiac electrophysiologic effects of moricizine hydrochloride. Bigger, J.T. Am. J. Cardiol. (1990) [Pubmed]
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