Effects of oral disopyramide phosphate on induction and sustenance of atrioventricular reentrant tachycardia incorporating retrograde accessory pathway conduction

H. C. Kou, J. S. Hung, Y. S. Lee, D. Wu

Research output: Contribution to journalJournal Article peer-review

7 Scopus citations

Abstract

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 (≤ 287 ± 4 to ≥ 392 ± 22 msec, p < 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 < 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 primarily by depression of the retrograde limb of the reentrant circuit.

Original languageEnglish
Pages (from-to)454-462
Number of pages9
JournalCirculation
Volume66
Issue number2 I
DOIs
StatePublished - 1982
Externally publishedYes

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