THERAPEUTIC END-POINTS FOR THE TREATMENT OF ATRIOVENTRICULAR NODE REENTRANT TACHYCARDIA BY CATHETER-GUIDED RADIOFREQUENCY CURRENT

Citation
Bd. Lindsay et al., THERAPEUTIC END-POINTS FOR THE TREATMENT OF ATRIOVENTRICULAR NODE REENTRANT TACHYCARDIA BY CATHETER-GUIDED RADIOFREQUENCY CURRENT, Journal of the American College of Cardiology, 22(3), 1993, pp. 733-740
Citations number
20
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
22
Issue
3
Year of publication
1993
Pages
733 - 740
Database
ISI
SICI code
0735-1097(1993)22:3<733:TEFTTO>2.0.ZU;2-9
Abstract
Objectives. The purpose of this prospective study was to test the hypo thesis that the elimination of inducible repetitive atrioventricular ( AV) node reentry despite 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 radiofreque ncy current can eliminate AV node reentrant tachycardia, therapeutic e nd points that are definitive of a satisfactory result in patients und ergoing modification of the slow AV pathway have not been established. Applications of radiofrequency current at selected sites may eliminat e all evidence of slow pathway conduction or sufficiently modify the r efractory properties of the slow pathway to preclude sustained arrhyth mias. 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 co ntinuous wave of 500-kHz radiofrequency current. Twenty-five to 35 W w as applied for 60 s at the site selected for tissue destruction. Resul ts. 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 maxim al difference between the effective refractory period of the fast and slow pathways was reduced from 104 +/- 62 ms before the procedure to 3 7 +/- 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 patie nt (2%) had a recurrence of the tachycardia. Conclusions. Results demo nstrate that when complete elimination of dual AV node physiology is d ifficult, modification of slow pathway conduction to the extent that r epetitive AV node reentry cannot be induced is a definitive end point that portends a good prognosis.