Electrophysiologic and clinical effects of intravenous and oral encainide in accessory atrioventricular pathway

Abstract

The effect of intravenous and oral encainide was studied in 12 patients with an accessory atrioventricular pathway (AP). Eight patients had Wolff-Parkinson-White syndrome and 4 had a concealed AP. Electrophysiologic studies were performed before and after intravenous encainide, 1.0 to 1.5 mg/kg, and 4 weeks after oral encainide, 75 to 200 mg/day. Mean follow-up was 19 ± 6 months. During sinus rhythm, intravenous and oral encainide significantly prolonged the AH and HV intervals. In patients with Wolff-Parkinson-White syndrome, after intravenous encainide, anterograde conduction over the AP was blocked in 3 patients, and the anterograde effective refractory period (ERP) of the AP was markedly increased in 3. Five of these 6 patients had a control value of the anterograde AP ERP of less than 270 ms. Anterograde AP block was maintained in 2 patients after oral encainide therapy. Retrograde AP block or marked increase of retrograde AP ERP was seen in 4 of 9 patients after intravenous encainide and in 2 of 7 after oral therapy. Encainide either prevented induction of circus movement tachycardia (intravenous, 4 of 11 patients; oral, 2 of 7 patients) or significantly prolonged tachycardia cycle length (intravenous, 7 of 11 patients; oral, 5 of 7 patients). During long-term follow-up of 9 patients, 6 patients had no recurrences of tachyarrhythmia after individual adjustment of encainide dosage. One patient had worsening of supraventricular tachycardia after intravenous encainide therapy and 4 patients complained of visual blurring; in 1 patient it was so severe that it required withdrawal of the drug. No correlation was found between plasma concentration of encainide or its metabolites and changes of electrophysiologic or clinical variables. Thus, in most patients with an AP, encainide blocks or prolongs anterograde conduction over the AP and has a beneficial effect on circus movement tachycardia, either by preventing induction of tachycardia or by prolonging tachycardia cycle length.