(Circulation. 1997;96:3484-3491.)
© 1997 American Heart Association, Inc.
Articles |
Relationship Between Atrial Fibrillation and Typical Atrial Flutter in Humans
Activation Sequence Changes During Spontaneous Conversion
From the Section of Cardiac Electrophysiology, Department of Medicine and Cardiovascular Research Institute, University of California San Francisco.
Correspondence to Michael D. Lesh, MD, Section of Cardiac Electrophysiology, Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco, 500 Parnassus Ave, Room MU 428, Box 1354, San Francisco, CA 94143-1354. E-mail lesh{at}ep4.ucsf.edu
Background A transitional rhythm precedes the spontaneous onset of atrial flutter in an animal model, but few data are available in man.
Methods and Results In 10 patients, 16 episodes of atrial fibrillation (166±236 seconds) converting into atrial flutter during electrophysiological evaluation were analyzed. A 20-pole catheter was used for mapping the right atrial free wall. Preceding the conversion was a characteristic sequence of events: (1) a gradual increase in atrial fibrillation cycle length (150±25 ms after onset, 166±28 ms before conversion, P<.01); (2) an electrically silent period (267±45 ms); (3) "organized atrial fibrillation" (cycle length, 184±24 ms) with the same right atrial free wall activation direction as during atrial flutter; (4) another delay on the lateral right atrium (283±52 ms); and (5) typical atrial flutter (cycle length, 245±38 ms). The coronary sinus generally had a different rate than the right atrial free wall until the beat that initiated flutter, when right atrium and coronary sinus were activated in sequence.
During 1313 seconds of fibrillation, there were 171 episodes of "organized atrial fibrillation." An additional activation delay at least 30 ms longer than the mean organized atrial fibrillation cycle length was sensitive (100%) and specific (99%) for impending organization into atrial flutter. During organized atrial fibrillation, right atrial free wall activation was craniocaudal in 70% and caudocranial in 30%, which may explain why counterclockwise flutter is a more common clinical rhythm than clockwise flutter. Atrial flutter never degenerated into fibrillation, even after adenosine infusion.
Conclusions Anatomic barriers, along with statistical properties of conduction and refractoriness during atrial fibrillation, may explain the remarkably stereotypical pattern of endocardial activation during the initiation of atrial flutter via fibrillation and the rarity of degeneration of flutter to fibrillation once it stabilizes.
Key Words: fibrillation • atrial flutter • mapping
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