Twenty patients with an average of more than 30
ventricular premature complexes (VPCs) per hour were treated with
ethmozine. Eighteen had either not responded or had adverse reactions to at least 1 other
antiarrhythmic drug. Patients were treated with 200 to 300 mg 3 times daily (8.25 to 11.7 mg/kg) and were followed for up to 6 months. Three patients were withdrawn from
ethmozine therapy because of unwanted effects before evaluation of efficacy. One of these patients had sustained
ventricular tachycardia (VT) after a loading dose of
ethmozine. Eleven of the remaining 17 patients (65%) experienced more than a 75% reduction in ventricular ectopic activity. Six patients had a smaller or no decrease in VPC frequency. Eleven of 16 patients (68%) with paired VPCs had a more than 90% reduction in paired VPC frequency. Eleven of 13 patients (84%) with VT events of 3 beats or more had more than a 90% reduction in VT events. Of the 11 patients in whom a more than 75% reduction in VPC frequency occurred, 1 patient died suddenly after 133 days of effective
drug therapy. Three patients discontinued
ethmozine therapy for reasons not related to the
drug. Of the 6 patients in whom there was less than a 75% reduction in VPC frequency, 2 patients discontinued treatment, 1 patient because of hyperanxiety and 1 because of
drug-related left anterior hemiblock.
Ethmozine lengthened PR and QRS intervals but not the JT interval. Thus,
ethmozine is effective and clinically useful for suppression of frequency VPCs in 50% (10 of 20 patients) of a selected population.