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
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.