Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 + 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 + 2.0 1ag/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 30 to 352 46 msec (p < .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p < .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 + 10 months. By life table analysis, outcome did not differ between group 1 and group 2 patients with respect to either development of sudden death or syncope (four patients in group 1 vs five patients in group 2) or the development of any arrhythmia event or side effect that required withdrawal of antiarrhythmic therapy (nine patients in group 1 patients vs 12 patients in group 2). Forty percent of group 2 patients developed adverse effects necessitating withdrawal of drug. We conclude in patients in whom rapid ventricular tachycardia is induced on amiodarone (1) type IA agents increase the cycle length and result in improved hemodynamic tolerance but rarely prevent induction of ventricular tachycardia, and (2) outcome is not improved by the addition of a type IA agent to therapy.