Cardiac Effects of the Class III Antiarrhythmic Drugs Amiodarone and Nibentan

Abstract

The effects of Amiodarone and Nibentan on the postextrasystolic and postrest reactions were stud- ied with normal rat myocardium and (for Amiodarone only) with myocardial strips isolated from patients with coronary heart disease (CHD). One-third of the patient samples displayed spontaneous activity that could be effectively suppressed by Amiodarone. All other samples displayed postrest inotropic effects of two types, with 30 or 70% decreases in the parameters of the contraction-relaxation cycle. Amiodarone did not influence the reaction of the first type but increased the postrest inotropic response of the second type. Both Amiodarone and Nibentan decreased the postextrasystolic inotropic response of the normal rat myocardium and simultaneously increased the postextrasystolic contraction. In addition, these drugs nearly doubled postrest potentiation. In the patient myocardium samples, however, Amiodarone did not decrease the amplitude of the extrasystolic contrac- tion but increased postextrasystolic potentiation. It was supposed that, in the myocardium of some CHD patients (as well as in the rat myocardium), Amiodarone increases the ability of the sarcoplasmic reticulum to accumulate calcium ions. The same was supposed for the effects observed for Nibentan in tests with the rat myocardium. This phenomenon may contribute to the suppression of abnormal activity of the myocardium and strengthen the direct antiarrhythmic effect of Amiodarone.