The electrophysiologic effects and clinical efficacy of intravenous (i.v.) and oral
encainide were studied in 13 patients with accessory atrioventricular (AV) pathways (7 overt, 1 intermittent and 5 concealed) and
drug-resistant supraventricular arrhythmias (5
paroxysmal atrial fibrillation, 1 atrial
tachycardia and 7 with orthodromic circus movement
tachycardia). Previously,
therapy had failed with a mean of 3 conventional antiarrhythmic agents. In 5 patients,
amiodarone administration had also been unsuccessful. All patients underwent programmed electrical stimulation of the heart before and after 1.5 mg/kg of i.v.
encainide. Seven patients were restudied during oral
encainide therapy (mean 155.8 +/- 54.2 mg/day) 3 days to 6 weeks (average 21 days) later. Anterograde conduction over the accessory AV pathway blocked in 4 of 7 patients after i.v.
encainide. Oral
encainide blocked anterograde conduction over the accessory pathway or prolonged the refractory period of the accessory pathway in 3 of 4 patients. This change in anterograde conduction was independent of the predrug value for the anterograde refractory period of the accessory AV pathway. Intravenous and oral
encainide had minimal effects on retrograde conduction over the accessory AV pathway. The clinical effect of oral
encainide was studied in 12 patients. Four patients responded to oral
encainide and have been free of
arrhythmia or side effects for 2 to 20 months (average 10.5).
Encainide failed to prevent the clinical
arrhythmia in 2 patients. In 4 patients with atrial arrhythmias, circus movement
tachycardia developed during oral
encainide therapy. In 1 patient the frequency of circus movement
tachycardia increased with oral
encainide treatment.(ABSTRACT TRUNCATED AT 250 WORDS)