LOCAL CAPTURE BY ATRIAL-PACING IN SPONTANEOUS CHRONIC ATRIAL-FIBRILLATION

Citation
C. Pandozi et al., LOCAL CAPTURE BY ATRIAL-PACING IN SPONTANEOUS CHRONIC ATRIAL-FIBRILLATION, Circulation, 95(10), 1997, pp. 2416-2422
Citations number
20
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
95
Issue
10
Year of publication
1997
Pages
2416 - 2422
Database
ISI
SICI code
0009-7322(1997)95:10<2416:LCBAIS>2.0.ZU;2-R
Abstract
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 rece ntly in experimental AF or induced AF in humans. Methods and Results T his 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 chr onic AF, not taking antiarrhythmic drugs. A Franz catheter (for pacing and monophasic action potential recording) and a recording quadripola r catheter positioned about 10 mm apart were used. Local capture was a chieved in 41 (87.2%) sites for a total of 100 captures. In 71 episode s the capture was lost within 15 seconds, while in the remaining 29, p acing was stopped after 15 seconds of stable capture. The AF types imm ediately before capture were type 1 in 83 and type 2 in 17 episodes. T ype 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 duri ng type 1 and type 2 AF but not type 3 AF, and (3) pacing before captu re accelerates AF, probably by transient or local capture. These findi ngs suggest that an excitable gap is present in chronic AF, therefore supporting the hypothesis that leading circle reentry is not the uniqu e electrophysiological mechanism maintaining the arrhythmia.