Moracizine (mean dose 792 +/- 84mg, range 600 to 900 mg/day) was evalu
ated in 18 patients aged 62 +/- 7 years for spontaneous nonsustained (
n = 3) or sustained monomorphic (n = 12) ventricular tachycardia, card
iac arrest (n = 1) or syncope (n = 2). All patients had spontaneous or
induced sustained monomorphic ventricular tachycardia. Diagnoses incl
uded coronary artery disease (n = 7) and dilated cardiomyopathy (n = 4
), valvular heart disease (n = 2), myocarditis (n = 1), or a combinati
on of these (n = 4). The mean left ventricular ejection fraction was 3
2 +/- 9% (range 15 to 52%). Prior to moracizine, antiarrhythmic drug a
dministration included a mean of 2 +/- 1 trials with class IA (n = 17)
, IB or IA + IB (n = 6) or IC (n = 5) antiarrhythmic drugs, or amiodar
one (n = 3). Prior antiarrhythmic drugs were discontinued for either t
he occurrence of noncardiac side effects or lack of efficacy. On morac
izine, new sustained monomorphic ventricular tachycardia occurred in 3
patients with previous nonsustained ventricular tachycardia; spontane
ous sustained monomorphic ventricular tachycardia recurred in 5 (and a
ppeared to be worse in at least 2) patients with previous sustained mo
nomorphic ventricular tachycardia; sustained monomorphic ventricular t
achycardia was induced in all 11 patients undergoing repeat electrophy
siology testing and was more difficult to terminate in 2 patients; 1 p
atient with an implantable defibrillator died suddenly after receiving
multiple implantable defibrillator shocks while on moracizine despite
recent electrophysiology testing demonstrating satisfactory defibrill
ation thresholds. Serious arrhythmic events occurred in 7 patients wit
hin 7 days of therapy with the drug. In this patient population with i
nducible or spontaneous sustained monomorphic ventricular tachycardia,
moracizine was not effective and caused frequent, serious (usually ea
rly) proarrhythmic effects.