Electrophysiological effects of lorcainide in sinoatrial disease and in Wolff-Parkinson-White syndrome*

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Abstract
The influence of lorcainide on sinus node function and intracardiac conduction was studied in 34 patients, including seven patients with sinoatrial disease and 14 patients with Wolff-Parkinson-White syndrome. Programmed cardiac stimulation and His bundle electrography were undertaken. Lorcainide, 2 mg/kg body weight, was given intravenously over a period of 10 min. In normal subjects, a slight increase of sinus rate was observed; lorcainide did not change corrected sinus node recovery time (CSNRT) and sinoatrial conduction time (SACT), calculated by use of the premature stimulus technique. In sinoatrial disease, however, three out of seven patients demon-strated a decrease of heart rate due to sinus node exit block, and CSNRT was markedly prolonged under the influence of the drug. Sinus node entrance block to premature atrial beats was observed in two controls and two patients with sinoatrial disease. Spontaneous sinus node exit block developed in two patients with sinoatrial dysfunction after administration of lorcainide. Refractory periods of the right atrium, right ventricle and conduction through the A V node (AH intervals) were unaffected by lorcainide, while HQ, QRS and QT intervals were prolonged. In Wolff-Parkinson-White syndrome, antegrade conduction via the accessory pathway was blocked in six out of 12 patients. After lorcainide, refractory periods of the accessory pathway increased in both the antegrade and retrograde direction. The ventricular rate during reciprocating tachycardia and during atrial fibril-lation was decreased by lorcainide. The results identify slowing of intraventricular conduction as the main action oflorcainide. In sinoatrial disease, lorcainide may aggravate sinus node dysfunction.

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