ELECTROPHYSIOLOGICAL MECHANISMS OF ACTION OF ETHMOZINE THAT EXPLAIN ITS ANTIARRHYTHMIC EFFICACY IN THE LATE-STAGE OF EXPERIMENTAL MYOCARDIAL-INFARCTION IN DOGS

The effects of intravenous ethmozine (3 mg.gk-1) on electrophysiologic al parameters of ischaemically damaged myocardium and induced ventricu lar tachyarrhythmias were studied by programmed stimulation in 17 cons cious dogs with 4 to 8 day-old ligation of the left anterior descendin g coronary artery. Ethmozine showed a beneficial effect on sustained v entricular tachycardia by suppressing its inducibility in five of 14 a nimals or by slowing its rate in six of 14 animals. Ethmozine prolonge d 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 p otentials recorded from the infarction zone. The QT interval was only slightly increased with ethmozine. Our findings indicate an antiarrhyt hmic action of ethmozine in the late stage of myocardial infarction. M ajor mechanisms accounting for its efficacy may predominantly be assoc iated with marked depression of slow conduction in the infarction zone , as well as with prolongation of ventricular refractoriness without s ignificant changes of ventricular repolarization.