Atrioventricular nodal reentrant tachycardia in patients referred for atrial fibrillation ablation: response to ablation that incorporates slow-pathway modification.
BACKGROUND
Although the most common sites of atrial ectopy that trigger atrial fibrillation (AF) are in or around the pulmonary veins (PVs), atrioventricular nodal reentrant tachycardia (AVNRT) can also cause or coexist with AF. We sought to characterize patients with AF and AVNRT and assess clinical outcomes after ablation.


RESULTS
To determine the prevalence of concomitant AVNRT and AF, 629 consecutive patients referred for catheter ablation between November 1998 and March 2005 were studied. Electrophysiological studies with programmed stimulation during isoproterenol infusion identified atrial ectopy that initiated AF and the presence of inducible AVNRT. AF ablation consisted of proximal isolation of PVs and elimination of any non-PV trigger of AF, including AVNRT. There were 27 patients (4.3%) who had inducible AVNRT at the time of AF ablation. Of these, 13 underwent AVNRT ablation without PV isolation. Compared with the rest of the cohort, patients with AVNRT and AF were younger at the time of symptom onset (age 36.8+/-13.8 versus 48.2+/-11.7 years; P<0.01). Freedom from AF with or without previously ineffective antiarrhythmic medication was similar in both groups (96.3% versus 90.7%; mean follow-up 21.4+/-9.4 months); however, patients with AVNRT targeted for ablation were more likely to be AF free while not taking any antiarrhythmic medication after a single procedure during the follow-up period (87.5% versus 54.7%; P<0.01) and had fewer complications (0% versus 2.5%; P=0.30). Twelve of the 13 patients who underwent slow-pathway ablation without left atrial ablation remained AF free without the need for antiarrhythmic medication after a single procedure.


CONCLUSIONS
AVNRT is an uncommon AF trigger seen more frequently in younger patients. Ablation of AVNRT in patients with AF was associated with improved outcomes compared with those with other triggers of AF.
Sauer
William H
WH
Electrophysiology Section, Cardiovascular Division, Department of Medicine, University of Pennsylvania Health System, Philadelphia, PA, USA.
Alonso
Concepcion
C
Zado
Erica
E
Cooper
Joshua M
JM
Lin
David
D
Dixit
Sanjay
S
Russo
Andrea
A
Verdino
Ralph
R
Ji
Sen
S
Gerstenfeld
Edward P
EP
Callans
David J
DJ
Marchlinski
Francis E
FE
D000328:Adult; D001281:Atrial Fibrillation / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000503:physiopathology* / Q000601:surgery; D017115:Catheter Ablation; D015331:Cohort Studies; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D015995:Prevalence; D011667:Pulmonary Veins / Q000503:physiopathology; D012044:Regression Analysis; D013610:Tachycardia / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery; D013997:Time Factors