Successful surgical ablation of atrioventricular (AV) accessory connections may be confirmed during postoperative electrophysiologic testing by the absence of accessory connection conduction in both the anterograde and retrograde directions. Whereas the former may be readily apparent by examination of the surface electrocardiogram during sinus rhythm or atrial pacing, assessment of the latter may be complicated by the frequent presence of enhanced retrograde AV nodal conduction in the postoperative period. Consequently, availability of interventions that selectively affect AV nodal conduction and refractoriness without concomitant effects on accessory connections may be helpful for assessing the success of the surgical procedure. In this study the effects of combined propranolol and verapamil administration on electrophysiologic properties of the AV node and the accessory AV connection were assessed both pre- and postoperatively in 17 patients (12 men and 5 women, mean age 33 years) undergoing surgical ablation of accessory connections. Preoperatively, electrophysiologic characteristics of all but 1 of the accessory AV connections were unaffected by propranolol and verapamil administration. Postoperatively, on the other hand, propranolol and verapamil significantly prolonged both the retrograde AV node effective refractory period (baseline: 272 ± 34 ms vs after drugs: 384 ± 70 ms [p < 0.0001]) and the shortest cycle length maintaining 1:1 ventriculoatrial conduction (baseline: 357 ± 99 ms vs after drugs: 485 ± 64 ms [p < 0.0001]). Late postoperative electrophysiologic evaluation (7 ± 3 weeks) revealed no evidence of residual accessory AV connection conduction, and all patients remain asymptomatic at 21 ± 10 months follow-up. Thus, thecombined administration of propranolol and verapamil may prove helpful for differentiating between retrograde AV nodal and residual accessory connection conduction during early postoperative assessment of patients undergoing surgery for accessory AV connection ablation.
Bibliographical noteFunding Information:
From the Departments of Medicine (Cardiovascular Division), Pediatrics and Surgery, University of Minnesota Medical School, Minneapolis, Minnesota. Dr. Milstein was supported in part by a grant from the American Heart Association-Minnesota Affiliate, Minneapolis, Minnesota.D r. Buetikofer was supported in part by a fellowship grant from the North American Society of Pacing and Electrophysiology. This study was completed in part during Dr. Benditt’s tenure as an Established Investigator of the American Heart Association, Dallas, Texas. Manuscript received May 3, 1990; revised manuscript received July 2, 1990, and accepted July 3.
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