Moricizine (Ethmozine) is an antiarrhythmic used to treat documented life-threatening arrhythmias.
Moricizine exerts electrophysiological effects that are common to both class IA and IB agents. However, it does not belong in any of the existing drug classes.
No significant effect of moricizine is noted on the si-nus cycle length or on automaticity within the sinoatrial node.
Moricizine does not affect the atrial refractory pe-riod or conduction velocity within atrial muscle.
Moricizine depresses conduction and prolongs re-fractoriness in the atrioventricular node and in the in-franodal region. These changes are manifest in a pro-longation of the PR interval on the electrocardiogram.
The primary electrophysiological effects of mori-cizine relate to its inhibition of the fast inward sodium channel. Moricizine reduces the maximal upstroke of phase 0 and shortens the cardiac transmembrane action potential. The sodium channel blocking effect of mori-cizine is more significant at faster stimulation rates; an action referred to as use dependence. This phenomenon may explain the efficacy of moricizine in suppressing rapid ectopic activity. An interesting effect of moricizine is its depressant effect on automaticity in ischemic Purkinje tissue in contrast to its inability to alter the slope of phase 4 depolarization of spontaneous auto-matic Purkinje fibers.
The electrocardiographic effects of moricizine include alterations in conduction velocity without an effect on the refractoriness of heart tissue. Moricizine enhances sinus node automaticity and prolongs sinoatrial and His-Purkinje intervals and the QRS. Moricizine pro-longs ventricular conduction, thereby widening the QRS complex on the electrocardiogram. It has no sig-nificant effects on the QT interval.
The administration of moricizine is not associated with clinically significant hemodynamic effects.
The characteristics of moricizine:
Oral bioavailability : Not known
Onset of action : Within 2 hours
Peak response : 6 hours
Duration of action : 10–24 hours
Plasma half-life : 1.5–3.5 hours
Primary route of metabolism: Hepatic
Primary route of excretion : 56% biliary /fecal; 39% renal
Therapeutic serum concentration : Not established
Moricizine is indicated for the treatment of documented ventricular arrhythmias, particularly sustained ventricu-lar tachycardia. Moricizine was evaluated in the CAST clinical trial for the prevention of postinfarction ven-tricular premature complexes. It was ineffective and found to be proarrhythmic. Patients in the moricizine arm of the trial exhibited a greater incidence of sudden cardiac death than did controls.
The principal adverse gastrointestinal effect of mori-cizine is nausea (7%). Abdominal discomfort has also been reported. Dizziness (11%) is the most frequently reported CNS-related adverse effect. Such reactions increase in frequency with prolonged drug adminis-tration.
As with other antiarrhythmic drugs, moricizine has proarrhythmic activity, which may manifest as new ven-tricular ectopic beats or a worsening of preexisting ven-tricular arrhythmias. These effects are most common in patients with depressed left ventricular function and a history of congestive heart failure. Cardiovascular ef- fects requiring drug withdrawal include conduction de-fects, sinus pauses, junctional rhythm, and A-V block.
Patients with preexisting second- or third-degree A-V block, cardiogenic shock, or drug hypersensitivity should not be treated with moricizine.
Clinically significant interactions with moricizine do not appear to exist.
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