SummaryMoracizine (mean dose 792 ± 84mg, range 600 to 900 mgJday) was evaluated in 18 patients aged 62 ± 7 years for spontaneous nonsustained (n = 3) or sustained monomorphic (n = 12) ventricular tachycardia, cardiac arrest (n = 1) or syncope (n = 2). All patients had spontaneous or induced sustained monomorphic ventricular tachycardia. Diagnoses included coronary artery disease (n = 7) and dilated cardiomyopathy (n = 4), valvular heart disease (n = 2), myocarditis (n = 1), or a combination of these (n = 4). The mean left ventricular ejection fraction was 32 ± 9% (range 15 to 52%). Prior to moracizine, antiarrhythmic drug administration included a mean of 2 ± I trials with class IA (n = 17), IB or IA + IB (n = 6) or IC (n = 5) antiarrhythmic drugs, or amiodarone (n = 3). Prior antiarrhythmic drugs were discontinued for either the occurrence of noncardiac side effects or lack of efficacy.On moracizine, new sustained monomorphic ventricular tachycardia occurred in 3 patients with previous nonsustained ventricular tachycardia; spontaneous sustained monomorphic ventricular tachycardia recurred in 5 (and appeared to be worse in at least 2) patients with previous sustained monomorphic ventricular tachycardia; sustained monomorphic ventricular tachycardia was induced in all 11 patients undergoing repeat electrophysiology testing and was more difficult to terminate in 2 patients; 1 patient with an implantable defibrillator died suddenly after receiving multiple implantable defibrillator shocks while on moracizine despite recent electrophysiology testing demonstrating satisfactory defibrillation thresholds. Serious arrhythmic events occurred in 7 patients within 7 days of therapy with the drug.In this patient population with inducible or spontaneous sustained monomorphic ventricular tachycardia, moracizine was not effective and caused frequent, serious (usually early) proarrhythmic effects.
