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Circulation. 1997;95:2416-2422

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(Circulation. 1997;95:2416-2422.)
© 1997 American Heart Association, Inc.


Articles

Local Capture by Atrial Pacing in Spontaneous Chronic Atrial Fibrillation

Claudio Pandozi, MD; Leopoldo Bianconi, MD; Mauro Villani, MD; Antonio Castro, MD; Giuliano Altamura, MD; Salvatore Toscano, MD; Anna P. Jesi, MD; Giuseppe Gentilucci, MD; Fabrizio Ammirati, MD; Francesco Lo Bianco, MD; Massimo Santini, MD

the Department of Cardiac Diseases, San Filippo Neri Hospital, and Arrhythmia Control Unit (M.V.), I Clinica Medica La Sapienza Univerisity, Rome, Italy.

Correspondence to Dr Claudio Pandozi, Via Madonna Di Fatima, 22, 00147 Roma, Italy.

Background Atrial fibrillation (AF) is considered to be maintained by multiple reentrant circuits without or with a very short excitable gap. However, the possibility of local atrial capture has been shown recently in experimental AF or induced AF in humans.

Methods and Results This study was undertaken to evaluate the feasibility of atrial capture—suggestive of an excitable gap—in spontaneous chronic AF. Decremental pacing was performed in 47 right atrial sites in 14 patients with chronic AF, not taking antiarrhythmic drugs. A Franz catheter (for pacing and monophasic action potential recording) and a recording quadripolar catheter positioned about 10 mm apart were used. Local capture was achieved in 41 (87.2%) sites for a total of 100 captures. In 71 episodes the capture was lost within 15 seconds, while in the remaining 29, pacing was stopped after 15 seconds of stable capture. The AF types immediately before capture were type 1 in 83 and type 2 in 17 episodes. Type 3 AF was never captured. Pacing cycle at capture was 175.7±20.9 ms. The baseline atrial interval (FF) was 185.4±24.5, significantly longer than the FF recorded during pacing immediately before capture (176.0±19.8 ms) (P<.02).

Conclusions During spontaneous chronic AF in humans, (1) local capture by atrial pacing is possible up to at least 15 mm from the pacing site, (2) regional entrainment is possible during type 1 and type 2 AF but not type 3 AF, and (3) pacing before capture accelerates AF, probably by transient or local capture. These findings suggest that an excitable gap is present in chronic AF, therefore supporting the hypothesis that leading circle reentry is not the unique electrophysiological mechanism maintaining the arrhythmia.


Key Words: fibrillation • atrium • arrhythmia • reentry




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