Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction. Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal. Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes. In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.