Author + information
- Received June 20, 1983
- Revision received September 26, 1983
- Accepted September 30, 1983
- Published online March 1, 1984.
- Kevin F. Browne, MD,
- Eric N. Prystowsky, MD, FACC,
- Douglas P. Zipes, MD, FACC,
- Donald A. Chilson, MD and
- James J. Heger, MD, FACCa
- ↵aAddress for reprints: James J. Hegel MD, Associate Professor of Medicine, Indiana University School of Medicine, 1100 West Michigan Street, Indianapolis, Indiana 46223.
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 < 0.001), QRS duration increased 17% (p < 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 < 0.02) and functional (247 ± 18 to 264 ± 25 ms, p < 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. Among six patients receiving cibenzoline during follow-up, one patient died of recurrent myocardial infarction, two patients stopped taking cibenzoline because of recurrent veutricular tachycardia and three patients have continued taking cibenzoline for 10 ± 4 months with control of symptomatic arrhythmias.
Thus, cibenzoliue suppressed ventricular tachycardia and premature veutricular complexes in some patients unresponsive to conventional drugs and was well tolerated. Cibenzoline significantly prolonged ventricular effective and functional refractory periods and had minimal negative hemodynamic effects.
This study was supported in part by the Herman C. Krannert Fund, Indianapolis, Indiana; Grants HL-06308 and HL-07182 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; Public Health Service Grant RR00750, General Clinical Research Center; The American Heart Association, Indiana Affiliate, Indiana; and by the Veterans Administration Medical Center, Indianapolis, Indiana.
- Received June 20, 1983.
- Revision received September 26, 1983.
- Accepted September 30, 1983.
- American College of Cardiology Foundation