Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil.
We examined the electrophysiologic effects of verapamil in eight patients with the Wolff-Parkinson-White syndrome. Verapamil shortened the antegrade effective refractory period of the accessory pathway in three patients and abbreviated the shortest cycle length with 1:1 conduction over the accessory pathway in two patients. More significantly, verapamil decreased the shortest RR interval between preexcited ventricular complexes during atrial fibrillation (279 +/- 20 msec vs 236 +/- 18 msec, mean +/- SEM; p less than 0.01). After verapamil, two patients required cardioversion for hemodynamic deterioration after acceleration of the ventricular response during atrial fibrillation. In the four patients with predominantly preexcited ventricular complexes during atrial fibrillation the ventricular rate accelerated after verapamil, whereas in patients with predominantly normal ventricular complexes, the average ventricular rate decreased or did not change after verapamil. Verapamil may result in significant acceleration of ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome. The safety of verapamil in individual patients with the Wolff-Parkinson-White syndrome should be established by electrophysiologic testing before its use.
D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000188:drug therapy*; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D013268:Stimulation, Chemical; D014700:Verapamil / Q000494:pharmacology / Q000627:therapeutic use*; D014927:Wolff-Parkinson-White Syndrome / Q000188:drug therapy*
D014700:Verapamil