Author + information
- Received July 29, 1985
- Revision received December 2, 1985
- Accepted December 11, 1985
- Published online May 1, 1986.
- Alejandro H. Haedo, MD1,
- Pablo A. Chiale, MD,
- Jorge D. Bandieri, MD,
- Julio O. Lázzari, MD,
- Marcelo V. Elizari, MD, FACC and
- Mauricio B. Rosenbaum, MD, FACCa
- ↵aAddress for reprints: Mauricio B. Rosenbaum, MD, Service of Cardiology, Ramos Mejía Hospital, Urquiza 609, Buenos Aires, 1221, Argentina.
The antiarrhythmic effects of verapamil, 17-monochloracetylajmaline, mexiletine and amiodarone were compared in 14 patients with chagasic myocarditis. Drugs and placebo were administered orally in the following order: placebo and verapamil, placebo and 17-monochloracetylajmaline, placebo and mexiletine (1 week each) and placebo and amiodarone (4 weeks each). A 24 hour ambulatory electrocardiographic recording was obtained after administration of each placebo and drug. Verapamil had no effect on the number of ventricular premature complexes, ventricular couplets and runs of ventricular tachycardia. 17-Monochloracetylajmaline did not reduce the number of ventricular premature complexes and ventricular couplets but caused a moderate reduction in runs of ventricular tachycardia. Mexiletine failed to significantly reduce ventricular premature complexes but caused a moderate decrease in both ventricular couplets and runs of ventricular tachycardia.
Amiodarone was the only one of the four drugs that caused a substantial reduction of ventricular premature complexes (logarithmic mean 97.8%; p < 0.001), total suppression of runs of ventricular tachycardia in 11 of 11 patients and suppression of ventricular couplets in 8 of 14 patients and a significant reduction in the remaining 6 patients. The much greater efficacy of amiodarone as compared with the two sodium channel modifiers (17-monochloracetylajmaline and mexiletine) and one calcium channel blocker (verapamil) suggests that its potent antiarrhythmic activity is probably related to other peculiar and still undefined electrophysiologic and pharmacologic properties.
↵1 Dr. Haedo was supported by a scholarship from the Concejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires.
This work was supported in part by the Fundación de Investigaciones Cardiológicas Einthoven, Buenos Aires.
- Received July 29, 1985.
- Revision received December 2, 1985.
- Accepted December 11, 1985.
- American College of Cardiology Foundation