Oral disopyramide phosphate increased the mean ventricular paced cycle length producing ventriculoatrial block from ≤287 to ≥392 msec (P<0.01) and prevented tachycardia induction in 14 of 20 patients.
Does oral disopyramide phosphate prevent the induction of sustained AV reentrant tachycardia in patients with a retrogradely conducting accessory pathway?
Oral disopyramide phosphate effectively prevents the induction of sustained AV reentrant tachycardia by depressing the retrograde limb of the reentrant circuit.
Absolute Event Rate: 392% vs 287%
p-value: p=<0.01
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.
Kou et al. (Sun,) conducted a other in Atrioventricular (AV) reentrant tachycardia using a retrogradely conducting accessory pathway (n=20). Oral disopyramide phosphate vs. Baseline (before administration) was evaluated on Mean ventricular paced cycle length producing ventriculoatrial block (msec) (p=<0.01). Oral disopyramide phosphate increased the mean ventricular paced cycle length producing ventriculoatrial block from ≤287 to ≥392 msec (P<0.01) and prevented tachycardia induction in 14 of 20 patients.