The electrophysiologic effects of intravenous (i.v.) and oral
propafenone were evaluated in 14 patients with
Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (
AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with
Wolff-Parkinson-White syndrome, i.v.
propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral
therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the
supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral
propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral
therapy. There was no difference in the electrophysiologic effects between i.v. and oral
propafenone. The induction of SVT was prevented by i.v.
propafenone in 10 of 20 patients and in 4 additional patients with oral
propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic
drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible
tachycardia had recurrences of SVT. Thus, in patients with SVT,
propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement
tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)