The antiarrhythmic efficacy and proarrhythmic potential of the class IC antiarrhythmic agent
encainide were assessed in subacute and chronic postinfarction canine models, respectively. In conscious dogs with spontaneous premature ventricular complexes (PVCs) at 48 h after anterior
myocardial infarction (MI), cumulative intravenous (i.v.) administration of 1.0 and 3 mg/kg
encainide significantly reduced
PVC frequency. However, in anesthetized dogs studied more chronically after anterior MI (range 8-44 days), i.v. administration of 0.3-3 mg/kg
encainide resulted in induction of new
ventricular tachyarrhythmias by programmed ventricular stimulation in 6 of 10 dogs with no inducible arrhythmias prior to
encainide. Newly induced arrhythmias after
encainide administration included unimorphic and polymorphic
ventricular tachycardia (VT) as well as VT degenerating rapidly into
ventricular fibrillation (VF). The incidences of new
arrhythmia induction after cumulative i.v. administration of
encainide were 3 of 9 after 0.3 mg/kg i.v.
encainide, 4 of 9 after 1.0 mg/kg i.v.
encainide, and 5 of 10 after 3.0 mg/kg i.v.
encainide. Time elapsed between MI and electrophysiologic testing tended to predict proarrhythmic response to
encainide, with the six preparations with newly induced arrhythmias tested earlier than the four preparations that remained nonresponsive to postencainide programmed stimulation (13.2 +/- 3.1 vs. 26.5 +/- 6.5 days postinfarction, respectively, p = 0.07). There was also a trend toward larger underlying anterior MIs in the six preparations with newly induced arrhythmias as compared with the four preparations that remained nonresponsive to postencainide programmed stimulation (13.2 +/- 2.9 vs. 7.5 +/- 2.1% of left ventricle, respectively, p = 0.19).(ABSTRACT TRUNCATED AT 250 WORDS)