The electrophysiologic effects of nicardipine hydrochloride in man

Nicardipine hydrochloride is an investigational antianginal calcium channel blocking agent with potent vasodilating properties. To study its acute electrophysiological effects in man, 12 patients (mean age 66, range 58-84), 6 with normal conduction and 6 with bifascicular block were evaluated. Each subject underwent electrophysiologic studies before and after a bolus and an intravenous infusion of nicardipine titrated to lower the mean blood pressure by at least 10%. The actual drop in mean blood pressure was 17% (p less than .01). The mean bolus was 2.2 +/- 1.2 mg (mean +/- standard deviation). The infusion rate was .21 +/- .06 mg/min. The drop in mean blood pressure was associated with an increase in heart rate of 13% (p less than .01). Maximum sinus node recovery time and sinoatrial conduction time decreased (p less than .01). The QT interval decreased (p less than .01), although the corrected QT remained unchanged. There was a tendency for a decrease in the atrioventricular nodal effective refractory period, functional refractory period, paced atrioventricular and ventriculoatrial conduction times. Intra-atrial, intraventricular and infranodal conduction times did not change. The administration of intravenous nicardipine produces hemodynamic effects consistent with arteriolar vasodilatation and a reflex sympathetic increase in heart rate. Except for the changes in sinus node function, the lack of marked electrophysiologic effects with intravenous nicardipine suggests that reflex sympathetic activity masks its direct slow channel blocking electrophysiologic effects in man.