Moricizine (Ethmozine) is an antiarrhythmic used to
treat documented life-threatening arrhythmias.
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
Moricizine does not affect
the atrial refractory pe-riod or conduction velocity within atrial muscle.
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.
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
Oral bioavailability : Not
Onset of action : Within 2
Peak response : 6 hours
Duration of action : 10â€“24
Plasma half-life : 1.5â€“3.5
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
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.
interactions with moricizine do not appear to exist.