The proarrhythmic effects of class IA
antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular
premature beats whose baseline study, performed while no
antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained
ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of
procainamide,
quinidine and
disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic
ventricular tachycardia; sustained polymorphic
ventricular tachycardia;
ventricular fibrillation; reproducibly inducible nonsustained monomorphic
ventricular tachycardia. During 55
antiarrhythmic drug trials (24 of
procainamide, 21 of
quinidine, 10 of
disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic
ventricular tachycardia in 3,
ventricular fibrillation in 2, nonsustained monomorphic
ventricular tachycardia in 1. Thus, 11% of
drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one
drug did not predict a similar response to another
drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying
heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of
digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during
antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)