[Antiarrhythmic therapy with flecainide in acute experimental myocardial infarction (author's transl)]

Clinical and experimental studies indicate that ventricular arrhythmias, especially ventricular fibrillation, are in almost all cases the mechanism for sudden death occurring during the first 24 hours after the onset of an ischaemic myocardial event. Therefore a higher survival rate seems to depend on advances in antiarrhythmic therapy. The present study investigates the efficacy of the new local anaesthetic compound Flecainide in reducing or preventing ventricular arrhythmias and primary ventricular fibrillation, using a standardized experimental canine preparation. Our findings demonstrate that ventricular arrhythmias due to severe transmural myocardial infarction are reduced by 80-90% following the application of Flecainide. In some cases a complete abolition of the arrhythmias can be observed. The striking reduction in ventricular ectopics includes decreases in ventricular salves and R-on-T phenomena, which may lead to sudden death by precipitating ventricular fibrillation. The beneficial antiarrhythmic and antifibrillatory actions of Flecainide affect only the arrhythmias resulting from transmural necrosis of the myocardium ("in-hospital arrhythmias", 2nd-phase arrhythmias"), whereas the incidence of early ventricular arrhythmias, especially ventricular fibrillation occurring in the very inception of myocardial ischaemia ("pre-hospital arrhythmias", "1st-phase arrhythmias") is not prevented. Changes in hemodynamics and contractility due to Flecainide are not severe, even in myocardial infarction. Thus, our results indicate that the application of Flecainide in acute myocardial infarction in man may be successful in reducing therapy-resistant ventricular dysrhythmias.