Author + information
- Received July 29, 1992
- Revision received February 18, 1993
- Accepted February 24, 1993
- Published online September 1, 1993.
- Bruce D. Lindsay, MD, FACC∗,
- Mina K. Chung, MD,
- M. Carolyn Gamache, MD,
- Robert A. Luke, MD,
- Kenneth B. Schechtman, PhD,
- Judy L. Osborn, RN and
- Michael E. Cain, MD, FACC
- ↵∗Address for correspondence: Bruce D. Lindsay, MD, Washington University School of Medicine, Cardiology, Box 8086, 660 South Euclid Avenue, Saint Louis, Missouri 63110.
Objectives. The purpose off this prospective study was to test the hypothesis that the elimination of inducible repetitive atrioventricular (AV) node reentry the persistence of slow AV pathway conduction is a valid end point for radiofrequency catheter ablation procedures in patients with supraventricular tachycardia due to AV node reentry.
Background. Although modification of AV node physiology by radiofrequency current can eliminate AV node reentrant tachycardia, therapeutic end points that are definitive of a satisfactory result in patients undergoing modification of the slow AV pathway have not been established. Applications of radiofrequency current at selected sites may eliminate all evidence of slow pathway conduction or sufficiently modify the refractory properties of the slow pathway to preclude sustained arrhythmias. Accordingly, total abolition of dual AV node physiology may not be necessary to prevent arrhythmia recurrence.
Methods. Radiofrequency catheter ablation of the slow AV pathway was attempted in 59 patients with typical AV node reentry. Tissue ablation was performed with a continuous wave of 500-kHz radiofrequency current. Twenty-five to 35 W was applied for 60 s at the site selected for destruction.
Results. Dual AV node physiology was eliminated completely in 35 patients (59%), persisted without inducible AV node reentry in 13 patients (22%) and persisted with inducible single AV reentrant beats in 11 patients (19%). In patients with persistent dual AV node physiology, the maximal difference between the effective refractory period of the fast and slow pathways was reduced from 104 ± 62 ms before the procedure to 37 ± 37 ms after AV conduction had been modified (p < 0.001). During a mean follow-up interval of 15 months (range 4 to 28), only one patient (2%) had a recurrence of the tachycardia.
Conclusions. Resulte demonstrate that when complete elimination of dial AV node physiology is difficult, modification of slow pathway conduction to the extent that repetitive AV node reentry cannot be induced is a definitive end point that portends a good prognosis.
- Received July 29, 1992.
- Revision received February 18, 1993.
- Accepted February 24, 1993.