Moricizine (
moracizine,
ethmozine) is an orally active
phenothiazine derivative with direct myocardial Class I antiarrhythmic activity and minimal CNS effects. Placebo-controlled studies have confirmed its efficacy in suppressing nonmalignant ventricular arrhythmias (premature ventricular complexes, couplets and runs of
nonsustained ventricular tachycardia), including those refractory to previous antiarrhythmic
therapy. Preliminary findings have indicated that
moricizine is also effective in suppressing atrial ectopic activity, atrioventricular nodal re-entry
tachycardia and Wolff-Parkinson-White
tachycardias involving accessory pathways. As with other oral antiarrhythmics, malignant ventricular arrhythmias (sustained
ventricular tachycardia and
ventricular fibrillation) have been shown, both on noninvasive monitoring and programmed electrical stimulation, to be less susceptible to suppression by
moricizine than nonmalignant ventricular arrhythmias. The therapeutic potential of
moricizine is enhanced by its relatively low incidence of extra-cardiac adverse effects (predominantly gastrointestinal and neurological) and its lack of significant cardiodepressant activity in patients with normal or mildly to moderality depressed left ventricular function.
Moricizine has proved to be more effective than
disopyramide and
propranolol in suppressing ventricular ectopic activity, of comparable efficacy to
quinidine, but less effective than
encainide and
flecainide. The
drug appears to be particularly suited to the suppression of ventricular ectopy in patients with preexisting
left ventricular dysfunction. Further studies are required to confirm its long term efficacy and effects on mortality when used prophylactically in patients at increased risk of
sudden cardiac death.