Kunze K P, Kuck K H, Schlüter M, Kuch B, Bleifeld W
Am J Cardiol. 1984 Aug 1;54(3):323-9. doi: 10.1016/0002-9149(84)90191-7.
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)
