Cibenzoline, a new antiarrhythmic agent, was tested in 26 patients who had symptomatic ventricular tachycardia (24 patients) or premature ventricular complexes (2 patients) unresponsive to conventional drugs. Cibenzoline was given orally every 8 hours to maximal doses of 65 mg in 2 patients, 81.25 mg in 22 patients and 97.5 mg in 2 patients. Cibenzoline abolished spontaneous episodes of ventricular tachycardia in 8 of 16 patients with ventricular tachycardia during a 72 hour control electrocardiographic recording, and 7 of 22 patients had greater than 83% decrease in premature ventricular complexes compared with control. The PR interval increased 14% (p less than 0.001), QRS duration increased 17% (p less than 0.001), QT interval did not change and mean ejection fraction in 10 patients did not change. Electrophysiologic studies were performed on 10 patients in the control period and during maximal cibenzoline dosage. Cibenzoline did not affect electrophysiologic properties of the atrium or atrioventricular (AV) node. It prolonged the ventricular effective (223 +/- 16 to 241 +/- 22 ms, p less than 0.02) and functional (247 +/- 18 to 264 +/- 25 ms, p less than 0.02) refractory periods. At control electrophysiologic studies, ventricular tachycardia was induced in 9 of 10 patients (mean cycle length 210 +/- 31 ms). Cibenzoline therapy prevented ventricular tachycardia induction in two patients, and in the other seven patients the mean ventricular tachycardia cycle length increased from 210 to 260 ms. The one patient with no ventricular arrhythmia induced during the control study still had no arrhythmia induced while receiving cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)