The effect of intravenous and oral disopyramide on the mechanisms of the arrhythmia were studied in 11 patients with the common type of atrioventricular (AV) nodal paroxysmal reentrant tachycardia. Programmed electric stimulation of the heart was used to initiate and terminate tachycardia and to evaluate the effect of disopyramide on mode of initiation and termination of tachycardia. Disopyramide was given intravenously to all patients during tachycardia. This resulted in termination of tachycardia, by block in the anterograde slow pathway in 1 and in the retrograde fast pathway in 3 patients. In all 4 patients, reinitiation of tachycardia was no longer possible. In these 4 patients, oral disopyramide prevented spontaneous and pacing-induced AV nodal tachycardia. In 4 of the remaining 7 patients in whom tachycardia was not terminated by intravenous disopyramide, reinitiation of the arrhythmia during programmed stimulation was prevented by the drug. In these 4 patients, oral disopyramide was also effective in preventing spontaneous occurrence of tachycardia. In 3 patients, tachycardia was not terminated and its reinitiation was not prevented by intravenous disopyramide. Only 1 of these 3 patients received disopyramide by mouth, and it failed to prevent reinitiation and spontaneous tachycardia. In conclusion, disopyramide is an effective drug in patients with AV nodal paroxysmal reentrant tachycardia. A good correlation was found between intravenous and oral effect of disopyramide on the mechanisms of the arrhythmia. The study of the effect of intravenous disopyramide predicted the outcome of oral disopyramide therapy.