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.