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European Heart Journal 1994 15(12):1698-1704;
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Electrophysiological mechanisms of action of ethmozine that explain its antiarrhythmic efficacy in the late stage of experimental myocardial infarction in dogs

I. AIDONIDIS, E. EGEL, T. HILBEL, I. RIZOS, W. KUEBLER and J. BRACHMANN

Department of Cardiology, University of Heidelberg Heidelberg, Germany

Received 20 October 1993; accepted 9 June 1994.

Correspondence. PD Dr J Brachmann, Abt. Innere Median III (Kardiolo-gie), Med. Universitaetsldinik Heidelberg, Bergheimer Str. 58, D-69115 Heidelberg, Germany.

Abstract

The effects of intravenous ethmozine (3 mg. kg–1) on electrophysiological parameters of ischaemically damaged myocardium and induced ventricular tachyarrhythmias were studied by programmed stimulation in 17 conscious dogs with 4 to 8 day-old ligation of the left anterior descending coronary artery. Ethmozine showed a beneficial effect on sustained ventricular tachycardia by suppressing its inducibility in five of 14 animals or by slowing its rate in six of 14 animals. Ethmozine prolonged the ventricular effective refractory period in normal and infarcted myocardium, and impaired depressed conduction in ischaemically damaged tissue. The latter was indicated by significant lengthening of late potentials recorded from the infarction zone. The QT interval was only slightly increased with ethmozine. Our findings indicate an antiarrhythmic action of ethmozine in the late stage of myocardial infarction. Major mechanisms accounting for its efficacy may predominantly be associated with marked depression of slow conduction in the infarction zone, as well as with prolongation of ventricular refractoriness without significant changes of verticular repolarization.

Key Words: Late myocardial infarction • conscious dog • programmed stimulation • ventricular arrhythmia • ethmozine


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