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The electrophysiologic effects of encainide were studied in 10 patients with Wolff–Parkinson– White syndrome after intravenous (1 mg kg in 60 minutes) and oral administration of two dose regimens (75 and 150 mg daily). Under control conditions atrial fibrillation (AF) with a rapid ventricular response was induced in all patients andatrioventricular reciprocating tachycardia (A VRT) in 9 patients. After intravenous encainide AF was no longer induced in 3/9 patients; in 3 of the remaining the accessory pathway (AP) was totally blocked and in the others the shortest RR interval increased from 213 ±6 to 297 ±91 ms and the mean RR interval from 293 ± 39 to 362 ± 79 ms. The lower dose of oral encainide prolonged the shortest RR interval from 206 ± 24 to 273 ± 64 ms and the mean RR interval from 280 ± 48 to 368 ±52 ms in 6 patients; in 2 cases no preexcitedbeats were recorded and in 1 AF was not inducible. After the higher dose of oral encainide A F was still inducible in 7/8 cases; in 3 the A P was blocked and in the others the shortest and mean RR intervals increased from 202 ±30 to 280 ± 24 ms and from 276 ±59 to 436 ± 80 ms, respectively. After intravenous encainide antegrade conduction over the A P was blocked in 4/9 patients and the antegrade effective refractory period (ERP) was prolonged in another 4. Oral encainide blocked A P conduction in 4 cases and prolonged ERP considerably in the others. Induction of A V RT was prevented in 1/8 patients after intravenous and in 5/9 patients after oral encainide; in the 4 patients in whom AVRTremained inducible cycle length increasedfrom 306±31 to 3 54 ±49 ms after intravenous encainide and to 392 ±46 ms after oral administration. All patients were discharged on encainide (mean maintenance dose, 127 mg daily) and followed for 21 ±7 months; no recurrence of AF was observed; two patients complained of transient mild side effects. These data show that in patients with Wolff-Parkinson- White syndrome encainide prolongs refractoriness and slows conduction over the AP; it prevents induction of AVRT and markedly slows ventricular response during AF, thus protecting patients against life-threatening arrhythmias [ABSTRACT FROM PUBLISHER]