RELATIONSHIP BETWEEN ATRIAL-FIBRILLATION AND TYPICAL ATRIAL-FLUTTER IN HUMANS - ACTIVATION SEQUENCE CHANGES DURING SPONTANEOUS CONVERSION

Citation
Fx. Roithinger et al., RELATIONSHIP BETWEEN ATRIAL-FIBRILLATION AND TYPICAL ATRIAL-FLUTTER IN HUMANS - ACTIVATION SEQUENCE CHANGES DURING SPONTANEOUS CONVERSION, Circulation, 96(10), 1997, pp. 3484-3491
Citations number
18
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
96
Issue
10
Year of publication
1997
Pages
3484 - 3491
Database
ISI
SICI code
0009-7322(1997)96:10<3484:RBAATA>2.0.ZU;2-8
Abstract
Background A transitional rhythm precedes the spontaneous onset of atr ial flutter in an animal model, but few data are available in man. Met hods and Results In 10 patients, 16 episodes of atrial fibrillation (1 66 +/- 236 seconds) converting into atrial flutter during electrophysi ological evaluation were analyzed. A 20-pole catheter was used for map ping the right atrial free wall. Preceding the conversion was a charac teristic sequence of events: (1) a gradual increase in atrial fibrilla tion cycle length (150 +/- 25 ms after onset, 166 +/- 25 ms before con version, P < .01); (2) an electrically silent period (267 +/- 45 ms) ( 3) ''organized atrial fibrillation'' (cycle length, 184 +/- 24 ms) wit h the same right atrial free wall activation direction as during atria l flutter; (4) another delay on the lateral right atrium (283 +/- 52 m s); and (5) typical atrial flutter (cycle length, 245 +/- 38 ms). The coronary sinus generally had a different rate than the right atrial fr ee wall until the beat that initiated flutter, when right atrium and c oronary sinus were activated in sequence. During 1313 seconds of fibri llation, there were 171 episodes of ''organized atrial fibrillation.'' An additional activation delay at least 30 ms longer than the mean or ganized atrial fibrillation cycle length was sensitive (100%) and spec ific (99%) for impending organization into atrial flutter. During orga nized atrial fibrillation: right atrial free wall activation was crani ocaudal in 70% and caudocranial in 30%, which may explain why counterc lockwise flutter is a more common clinical rhythm than clockwise flutt er, Atrial flutter never degenerated into fibrillation. even after ade nosine infusion. Conclusions Anatomic barriers, along with statistical properties of conduction and refractoriness during atrial fibrillatio n, may explain the remarkably stereotypical pattern of endocardial act ivation during the initiation of atrial flutter via fibrillation and t he rarity of degeneration of flutter to fibrillation once it stabilize s.