Mechanisms and clinical significance of adenosine-induced dormant accessory pathway conduction after catheter ablation.
BACKGROUND
Adenosine can unmask dormant pulmonary vein conduction after isolation. The role of adenosine in uncovering dormant accessory pathway (AP) conduction after AP ablation is unknown.


RESULTS
We evaluated 109 consecutive patients (age, 41 ± 28 years; 62 [57%] men) who were administered adenosine after successful AP ablation. Dormant AP conduction was defined as adenosine-induced recurrent AP conduction, as demonstrated by recurrent preexcitation or change in retrograde ventriculoatrial activation patterns. Dormant AP conduction was identified in 13 (12%) patients. Adenosine led to transient retrograde AP conduction in 6 patients and transient anterograde AP conduction in 8 patients. In all these cases, adenosine-induced AP conduction occurred during the bradycardia phase of adenosine effect and resulted in dormant AP conduction times shorter than atrioventricular nodal conduction times before adenosine administration. On the basis of analysis of timing of occurrence of dormant AP conduction, the mechanism of adenosine-induced AP conduction was determined to be caused by AP excitability recovery in ≥ 12 (92%) cases. The presence of dormant AP conduction was a significant predictor of chronic recurrent AP conduction requiring repeat ablation (odds ratio, 8.54; 95% confidence interval, 1.09-66.9; P=0.041).


CONCLUSIONS
Adenosine can unmask dormant AP conduction after catheter ablation. Direct effects of adenosine on the AP, possibly via AP membrane potential hyperpolarization, are the dominant mechanism of adenosine-induced AP conduction after ablation. Dormant AP conduction is associated with higher rates of recurrent AP conduction requiring repeat ablation.
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
Michelle D
MD
Spotnitz
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
Steven M
SM
Markowitz
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
Christopher F
CF
Liu
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
George
G
Thomas
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
James E
JE
Ip
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
Joshua
J
Liez
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY.
Bruce B
BB
Lerman
From the Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, NY. jac9029@med.cornell.edu.
Jim W
JW
Cheung
D058606:Accessory Atrioventricular Bundle / Q000503:physiopathology / Q000601:surgery*; D000200:Action Potentials; D000241:Adenosine; D000293:Adolescent; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery*; D017115:Catheter Ablation; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011237:Predictive Value of Tests; D011667:Pulmonary Veins / Q000503:physiopathology / Q000601:surgery*; D012008:Recurrence; D012189:Retrospective Studies; D012307:Risk Factors; D016896:Treatment Outcome; D055815:Young Adult
D000241:Adenosine
Wolff–Parkinson–White syndrome; accessory conducting pathways; adenosine; catheter ablation