Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.
BACKGROUND
Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification.


RESULTS
Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion.


CONCLUSIONS
Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.
Markowitz
S M
SM
Department of Medicine, New York Hospital-Cornell University Medical Center, New York 10021, USA.
Stein
K M
KM
Lerman
B B
BB
D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000209:etiology / Q000503:physiopathology; D001283:Atrioventricular Node / Q000187:drug effects / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D002316:Cardiotonic Agents / Q000627:therapeutic use; D017115:Catheter Ablation; D005260:Female; D006339:Heart Rate; D006801:Humans; D007545:Isoproterenol / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009431:Neural Conduction / Q000187:drug effects; D012032:Refractory Period, Electrophysiological; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000503:physiopathology* / Q000601:surgery*; D016276:Ventricular Function / Q000187:drug effects
D002316:Cardiotonic Agents; D007545:Isoproterenol