We performed electrophysiologic studies before and after
oral administration of
disopyramide phosphate, 200 mg every 6 hours, in 20 patients with atrioventricular (AV) reentrant
tachycardia using a retrogradely conducting accessory pathway.
Disopyramide markedly depressed retrograde accessory pathway conduction by increasing the mean ventricular paced cycle length that produced ventriculoatrial block (less than or equal to 287 +/- 4 to greater than or equal to 392 +/- 22 msec, p less than 0.01); it also depressed antegrade normal pathway AV conduction by increasing the atrial paced cycle length that produced
AV block (287 +/- 9 to 328 +/- 7 msec, p less than 0.01). In 14 patients,
tachycardia could not be induced or sustained after
disopyramide phosphate. In 13 patients, this reflected depression of the retrograde limb with either absence of atrial echoes (nine patients) or induction of nonsustained
tachycardia that terminated after the QRS complex (four patients), and in one, it reflected depression of the antegrade limb with induction of a single atrial echo not followed by a QRS response. In six patients, sustained
tachycardia could still be induced after
disopyramide. Oral
disopyramide phosphate is effective in preventing induction of sustained AV reentrant
tachycardia in most patients. This effect is achieved by depression of the retrograde limb of the reentrant circuit.