Acute electrophysiologic effects of pirmenol in normal subjects and in patients with Wolff-Parkinson-White syndrome

Abstract

The acute electrophysiologic effects of pirmenol are reported in 8 normal subjects and in 8 patients with Wolff-Parkinson-White (WPW) syndrome. Standard electrophysiologic testing was performed before and after a 50-mg intravenous bolus and a 60-minute infusion of 150 mg of pirmenol. After pirmenol administration, AH interval, atrial refractory period, atrioventricular (AV) nodal functional refractory period and Wenckebach cycle length did not change; however, sinus cycle length decreased from 743 ±169 to 650 ± 133 ms (p < 0.001), sinoatrial conduction time from 103 ± 35 to 78 ± 37 ms (p < 0.05) and AV nodal effective refractory period from 308 ± 51 to 272 ± 23 ms (p < 0.01). Pirmenol increased the HV interval from 43 ± 5 to 48 ± 6 ms (p < 0.05) and ventricular functional refractory period from 247 ± 21 to 260 ± 21 ms (p < 0.005). Anterograde effective refractory period of the accessory AV pathway increased in 4 of 6 patients with ventricular preexcitation and retrograde effective refractory period increased in all patients. Pirmenol treatment prolonged the shortest preexcited RR interval from 253 ± 38 to 459 ± 19 ms (p < 0.05) and the average RR interval from 354 ± 26 to 421 ± 60 ms (p < 0.01) during atrial fibrillation in all 6 patients with preexcitation. Pirmenol did not influence the inducibility or cycle length of AV reciprocating tachycardia in the patients with WPW syndrome. The pirmenol infusions were well tolerated. Thus, pirmenol therapy has a direct depressant effect and an indirect vagolytic action on electrophysiologic measurements, a clinically beneficial effect in slowing the ventricular response to atrial fibrillation in WPW syndrome and little effect on reciprocating AV tachycardia.