Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome.

We evaluated the electrophysiologic effects of disopyramide phosphate in 12 patients with the Wolff-Parkinson-White syndrome

C R Kerr; E N Prystowsky; W M Smith; L Cook; J J Gallagher


Scholarcy highlights

  • Oral disopyramide in a mean dose of 279 ± 33 mg every 6 hours caused a significant prolongation of cycle length of reciprocating tachycardia, from 331 ± 53 to 370 ± 68 msec due to a prolongation of the minimum ventriculoatrial interval from 100 ± 27 to 133 + 42 msec
  • We examined the effects of disopyramide on the shortest and mean RR intervals during atrial flutter-fibrillation and the shortest atrial pacing cycle length at which 1:1 atrioventricular conduction occurred over the accessory pathway
  • The electrophysiologic effects of disopyramide phosphate have been studied in sinus node, atrioventricular node and atrial and ventricular muscle.6"18 The effects of the drug reflect a balance between the direct prolongation of refractoriness and the anticholinergic effect of the drug
  • Bennett"9 studied the effects of i.v. disopyramide in six patients with Wolff-Parkinson-White syndrome and showed a prolongation of the shortest and mean RR intervals during AF and a variable effect on reciprocating tachycardia
  • It slows conduction retrogradely through the pathway, as evidenced by prolongation of the ventriculoatrial intervals during reciprocating tachycardia. This resulted plexes can enter the circuit and initiate a tachycardia may be prolonged, resulting in easier induction of the reentrant tachycardia. This explains why reciprocating tachycardia was induced after disopyramide in patient 5, whereas it could not be induced in the control state
  • The primary importance of this drug is in the control of atrial flutter-fibrillation, where it prolongs refractoriness in the accessory pathway and slows the ventricular response

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