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.(ABSTRACT TRUNCATED AT 250 WORDS)