The effects of tiapamil were studied in 10 patients with antegrade preexcitation using programmed stimulation of the heart. Before administration of the drug, it was possible to initiate sustained orthodromic tachycardia in 7 patients, antidromic tachycardia in 2 and atrial echoes in 1 case by premature atrial and/or ventricular stimulation. An intravenous bolus of 2 mg/kg tiapamil terminated the tachycardia in 7 out of 8 cases by blocking the A-V node. The tachycardia continued at a reduced heart rate in 1 case with a nodoventricular bypass. Tiapamil lengthened the effective A-V nodal refractory period in 1 patient in whom it could be measured and the atrial effective refractory period in 1 case but did not prolong the antegrade or retrograde refractory periods of the accessory pathway. Only in 1 case was the antegrade effective refractory period of the accessory pathway shortened by tiapamil. The A-V nodal conduction time (A-H interval) was prolonged. Following tiapamil it was not possible to initiate the tachycardia in 4 cases and atrial echoes in 1 case; in 2 patients the tachycardia zone widened and in 3 it was not altered. In the latter, the cycle length of the tachycardia increased. Tiapamil appears to be of therapeutic value for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the initiation of tachycardia. The delayed A-V nodal conduction during sinus rhythm augments the area of ventricular preexcitation which may facilitate the electrocardiographic localization of the accessory pathway.