Clinical electrophysiologic effects of lorcainide in patients and its effect on the conduction of accessory pathway in Wolff-Parkinson-White syndrome

The electrophysiologic effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 20 patients with and without Wolff-Parkinson-White (WPW) syndromes. Lorcainide shortened the sinus cycle length from 721.0 +/- 125.9 to 649.5 +/- 100.1 ms (P less than 0.001), but did not influence sinus node function and AV node conduction and refractoriness, slightly increased atrial effective period (ERP) (P less than 0.02) and did not change ventricular ERP (P less than 0.2), obviously lengthened atrial conduction time, H, H-V interval and the width of V wave. Lorcainide caused complete antegrade block of the accessory pathway (AP) in six of 9 WPW patients and resulted in exclusive conduction over the AV nodal. His conduction in two patients with atrial flutter. It also prolonged the retrograde conduction time and refractoriness of AP, and prevented initiation of orthodromic atrioventricular tachycardia (O-AVRT) in six of 12 patients by blocking of the retrograde conduction of the AP, increased the cycle length of tachycardia from 321.7 +/- 43.6 to 361.7 +/- 54.9 ms (P less than 0.005) by marked prolongation of retrograde AP conduction time in 6 patients in whom O-AVRT could still be induced. It is concluded that intravenous lorcainide does not affect sinus node and AV node function, slightly influences atrial and ventricular refractoriness, obviously suppresses atrial, His bundle and intraventricular conduction, and is an effective antiarrhythmic drug for patients with WPW by blocking both the antegrade and retrograde conduction of the AP.