Abstract

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 < 0.05) after i.v. application, and from 336 ± 65 ms to 367 ± 65 ms (p < 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 < 0.05) after i.v. infusion, and from 333 ± 57 ms to 369 ± 75 ms (p < 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. Electrophysiologic drug testing with propafenone predicts its efficacy during chronic therapy in most patients.

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