Copyright © 1992 by the European Society of Cardiology.
© 1992 The European Society of Cardiology
Electrophysiological and electropharmacological studies in pre-excitation syndromes: results with propafenone therapy and isoproterenol infusion testing
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Electrophysiology Laboratories, Tzaneio State Hospital Athens, Greece
*Department of Cardiology, Tzaneio State Hospital Athens, Greece
Division of Cardiology, Tufts/New England Medical Center, Tufts University School of Medicine Boston, MA, U.S.A.
Received 29 October 1991; revised 20 May 1992; .
Correspondence A. S. Manolis, MD, Associate Director, Electrophysiology and Pacemaker Laboratory, Assistant Professor of Medicine, Box 868, Tufts/New England Medical Center, 750 Washington Street, Boston, MA 02111, U.S.A.
Abstract
To study the electrophysiological effects of oral propafenone on accessory pathways and determine the potential for catecholamine-mediated reversal of these effects, comprehensive electrophysiology studies (EPS) were conducted in 11 patients with manifest (n = 9) or concealed (n = 2) pre-excitation syndrome. EPS were performed at baseline (in the drug-free state), after oral propafenone loading, and with isoproterenol infusion during propafenone therapy. The study group included 10 men and 1 woman with a mean age of 39±13 years, who presented with symptoms of palpitations (n = 6), presyncope (n = 3) and syncope (n = 2). The clinical arrhythmia was atrioventricular reciprocating tachycardia (n = 6), atrial flutter/fibrillation (n = 3), or both (n = 2). During the baseline EPS the accessory pathway location was identified as left (n = 6) or septa (n = 5). The mean anterograde effective refractory period was 265±42 ms, the shortest pre-excited RR interval 259 ± 20 ms and the retrograde refractory period 258 ± 39 ms. Orthodromic atrioventricular reciprocating tachycardia was induced in 10 patients (mean cycle length = 324±31 ms). Antidromic reciprocating tachycardia was induced in one patient (cycle length = 340 ms).
In all the 11 patients EPS were repeated after 4 days of oral propafenone loading (668 ± 226 mg daily) when drug steady state was expected to have been achieved. One additional patient had baseline EPS but developed clinical arrhythmia recurrences after propafenone loading and thus he was excluded from the study; follow-up EPS were conducted on procainamide. Propafenone caused complete anterograde block in the accessory pathway in four patients and increased the anterograde refractory period from 270 ±24 ms to 393 ± 124 ms in the other patients, with resultant anterograde conduction occurring exclusively via the atrioventricular node during atrial fibrillation in another three patients. The drug caused retrograde block in three patients, and significantly increased the retrograde refractory period in the other patients (from 248±33 ms to 353±96ms) (P = 0·015). Orthodromic reciprocating tachycardia was rendered non-inducible in six patients or slower and/or non-sustained in the other five patients (cycle length = 400±19 ms, P = 0·012).
Isoproterenol infusion testing (3·6±1·6 µg . min–1) was performed in nine patients during the follow-up EPS. Among the four patients with anterograde block and one of two patients with retrograde block in the accessory pathway, isoproterenol did not restore conduction. However, the anterograde refractory period in three patients decreased from 430 ± 121 to 270±61 ms (P>0·05) and retrograde conduction that was blocked by propafenone was now restored in one patient, while the retrograde refractory period in six patients decreased from 358 ± 106 ms to 295 ±89 ms (P = 0·004). Furthermore, atrial fibrillation rendered non-inducible or non-sustained by propafenone was sustained during isoproterenol infusion, and in four patients in whom reciprocating tachycardia had been rendered slower (cycle length = 405±17 ms) or non-sustained by propafenone, a faster (cycle length = 338 ± 13 ms, P = 0·004) and sustained tachycardia was induced during isoproterenol testing.
At a mean long-term follow-up period of 9±6 months, among 10 patients discharged on a combined regimen of propafenone and ß-blocker, there have been no supraventricular arrhythmia recurrences and no major drug side-effects. The patient who had no follow-up EPS on propafenone due to clinical arrhythmia recurrences, underwent radiofrequency ablation of his left-sided bypass tract. In conclusion, propafenone constitutes effective drug therapy for patients with pre-excitation syndrome. Its electrophysiological effects on accessory pathways can be partially or completely reversed with acute isoproterenol infusion, suggesting an adjunctive role for beta-blocker therapy.
Key Words: Pre-excitation • electrophysiological studies • propafenone • isoproterenol • Wolff-Parkinson-White syndrome
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