The effects of intravenous verapamil on the electrophysiologic properties of the accessory pathway in 12 patients with symptomatic Wolff-Parkinson-White syndrome were studied using intracardiac electrical recordings. In 11 of the 12 patients it was possible to induce a reentrant supraventricular tachycardia with programmed atrial or ventricular pacing. After verapamil it was still possible to induce supraventricular tachycardia in 6 of the 11 patients; however, the mean cycle of length of the tachycardia increased from a control value of 330 +/- 20 ms (mean +/- standard error of mean) to 369 +/- 21 ms (p less than 0.05). Although verapamil had no significant effect on the anterograde refractory period of the accessory pathway as measured by the extrastimulus technique, it significantly increased maximal 1:1 atrioventricular (AV) conduction through the accessory pathway to incremental high rate atrial pacing in 10 of the 12 patients (control value 227 +/- 10 beats/min, value after verapamil 258 +/- 14 beats/min, p less than 0.001). In 4 patients in whom episodes of atrial fibrillation could be compared before and after verapamil, the drug decreased the average R-R interval from a control value of 327 +/- 27 ms to 282 +/- 28 ms (p less than 0.05) and decreased the shortest R-R interval between preexcited beats from a control value of 237 +/- 21 ms to 209 +/- 18 ms (p less than 0.05). It is concluded that in patients with symptomatic Wolff-Parkinson-White syndrome, verapamil may increase the ventricular response through the accessory pathway if atrial fibrillation occurs. This finding, which is of potential clinical significance, could not have been predicted from conventional anterograde refractory period estimations.