Electrophysiologic effects and clinical efficacy of oral propafenone therapy in patients with ventricular tachycardia

Donald A. Chilson, James J. Heger, Douglas P. Zipes, Kevin F. Browne, Eric N. Prystowsky

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37 Scopus citations

Abstract

The effects of the antiarrhythmic agent propafenone were evaluated in 25 patients with recurrent symptomatic ventricular tachycardia. Oral propafenone was given to a maximal dose of 300 mg every 8 hours. Ten of the 25 patients developed side effects or had inadequate suppression of spontaneous ventricular arrhythmias during propafenone therapy. Electrophysiologic studies were performed before and during drug therapy on the 15 patients who had a satisfactory clinical response. Propafenone increased the PR interval from 168 ± 46 to 188 ± 25 ms (p < 0.007), the HV interval from 47 ± 10 to 65 ± 13 ms (p < 0.005), the shortest atrial pacing cycle length to maintain 1:1 atrioventricular (AV) nodal conduction from 385 ± 44 to 436 ± 42 ms (p < 0.005), the ventricular effective refractory period from 231 ± 17 to 255 ± 19 ms (p < 0.001) and the ventricular functional refractory period from 260 ± 15 to 278 ± 17 ms (p < 0.002). Before propafenone therapy, all 15 patients had ventricular tachycardia induced by programmed ventricular stimulation. During propafenone treatment, 12 patients still had ventricular tachycardia induced, and the tachycardia cycle length significantly increased fom 236 ± 44 to 374 ± 103 ms (p < 0.001). Ten patients were considered to have satisfactory electrophysiologic response to propafenone on the basis of either the inability to initiate ventricular tachycardia or a marked increase in ventricular tachycardia cycle length associated with lack of symptoms during the induced tachycardia. These patients were discharged receiving propafenone. During a mean follow-up period of 11 months, 8 of the 10 patients have remained free of ventricular tachycardia, while 2 have had a recurrence. Propafenone significantly depresses AV nodal and His-Purkinje conduction, lengthens ventricular refractoriness and markedly increases ventricular tachycardia cycle length. Furthermore, preliminary data suggest that induction of ventricular tachycardia at electrophysiologic study does not always augur recurrence of spontaneous tachycardia.

Original languageEnglish (US)
Pages (from-to)1407-1413
Number of pages7
JournalJournal of the American College of Cardiology
Volume5
Issue number6
DOIs
StatePublished - Jan 1 1985

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ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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