Electrophysiologic and clinical effects of oral encainide in paroxysmal atrioventricular node reentrant tachycardia

Abstract

The electrophysiologic effects of oral encainide (75 to 150 mg daily) were evaluated in 14 patients (6 male and 8 female, aged 49 ± 9 years) with atrioventricular (AV) node reentrant tachycardia of the slow-fast type. The patients were studied in control conditions and after 2 to 12 days of treatment.Encainide increased the AH interval from 67 ± 10 to 82 ± 23 ms (p < 0.02). Anterograde Wenckebach cycle length was increased in three patients, reduced in four, unchanged in one; it was not measurable in the remaining patients because tachycardia was induced. Retrograde Wenckebach periodicity increased from 307 ± 71 to 401 ± 92 ms (p < 0.005) in all nine patients in whom it was measurable; complete retrograde block was observed in one patient. At the control study, tachycardia was induced in all patients, with a mean cycle length of 341 ± 50 ms; after encainide, tachycardia was inducible in only 1 patient, with an increase in cycle length from 270 to 320 ms; in the other patients, tachycardia was not inducible because of a lack of retrograde (11 patients) or anterograde (2 patients) conduction. The mean plasma concentrations of encainide and its metabolites O-demethyl-encainide and 3-methoxy-O-demethyl-encainide measured in 13 patients during the repeat study were 161 ± 304, 128 ± 100 and 95 ± 85 ng/ml, respectively; three poor metabolizers who presented a high concentration of the parent compound were observed in this series.All patients were discharged on encainide at a mean daily dose of 112 ± 39 mg. One patient dropped out of the study 1 month later because of neurologic side effects (blurred vision and vertigo). During a mean follow-up period of 24 ± 11 months, nine patients are completely free of attacks, three patients had only one recurrence and one patient had a marked reduction of attacks; no one complained of side effects.Encainide appears to be highly effective in preventing AV node reentrant tachycardia, mainly by depressing conduction in the retrograde limb of the reentrant circuit. The drug demonstrates long-term clinical efficacy and does not induce any significant side effect at the doses used in this trial.