Electrophysiologic effects of oral propafenone in Wolff-Parkinson-White syndrome studied by programmed electrical stimulation.

ABSTRACT

We studied the electrophysiologic effects of oral propafenone on induction of supraventricular tachycardia (SVT) in 10 patients with Wolff-Parkinson-White syndrome (5 manifest and 5 concealed accessory pathways). Nine patients had orthodromic SVT and one patient had atrial fibrillation with preexcited QRS (shortest RR 220 msec). Electrophysiologic studies were performed during control and 48 hours after oral propafenone administered in a dose of 300 mg every eight hours. Propafenone caused complete anterograde accessory pathway conduction block in 4 of 5 patients with manifest delta waves. Retrograde conduction through the accessory pathway was abolished in 6 of 9 patients in whom it was present during control. Sustained SVT was inducible in all 9 patients during control. Propafenone prevented induction of SVT in 8 of 9 patients (88.9%) and slowed the rate of induced SVT in one patient. In the patient with atrial fibrillation (AF) the accessory pathway was blocked and AF was not inducible. There was a significant increase in the effective refractory period (ERP) of the atrium (208 +/- 40 msec to 257 +/- 25 msec, p less than 0.01), atrioventricular (AV) node (less than or equal to 256 +/- 34 msec to greater than or equal to 324 +/- 35 msec, p less than 0.001) and ventricle (204 +/- 14 msec to 262 +/- 51 msec, p less than 0.01). The atrial paced cycle length at AV nodal block also increased from 288 +/- 51 msec to 389 +/- 51 msec (p less than 0.01) after the drug. Thus propafenone has potent inhibitory effects on accessory pathways and has additional significant effects on atrial, AV nodal and ventricular refractoriness.