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Relationship between atrial fibrillation and typical atrial flutter in humans: activation sequence changes during
F X Roithinger1, M R Karch, P R Steiner
1Department of Medicine and Cardiovascular Research Institute, University of California San Francisco, 94143-1354, USA.
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.