Electrophysiological properties in chronic lone atrial fibrillation.
BACKGROUND
Although the electrophysiological mechanisms underlying self-sustaining atrial fibrillation (AF) are unclear, recent studies suggest that one requirement for reentry, slow conduction, is frequently present in patients with AF. However, these observations limited to paroxysmal AF may not necessarily apply to chronic AF. Therefore, electrophysiological properties of the atrium and sinus nodal function in chronic lone AF were evaluated.


RESULTS
Electrophysiological studies were performed after electrocardioversion in 12 patients with chronic lone AF. Atrial enlargement was absent in the patients with AF. Twelve patients without atrial arrhythmias served as the control group. The patients with AF had a higher incidence of sinus nodal dysfunction, a shorter atrial effective refractory period (215 +/- 19 msec versus 238 +/- 23 msec, p less than 0.02), and a longer P wave duration than control patients (115 +/- 16 msec versus 86 +/- 16 msec, p less than 0.01). The conduction delay zone was significantly greater in patients with AF (60 +/- 12 msec) than that in the control patients (8 +/- 13 msec, p less than 0.01), and the maximal conduction delay was also greater in the study patients than those in the control group, both to the His bundle region (31 +/- 12 msec versus 10 +/- 15 msec, p less than 0.01) and to the coronary sinus (41 +/- 15 msec versus 15 +/- 11 msec, p less than 0.01). The fragmented atrial activity zone was wider in the study group (23 +/- 25 msec) than in control subjects (1.7 +/- 4 msec, p less than 0.02). Repetitive atrial firing was observed in four patients with AF but it was not seen in the control group.


CONCLUSIONS
These electrophysiological features, which are manifestations of the abnormal atrial electrophysiology, would favor production of atrial reentry in chronic lone AF.
Cardiovascular Center, Kawanami Hospital, Fukuoka, Japan.
K
K
Kumagai
S
S
Akimitsu
K
K
Kawahira
F
F
Kawanami
Y
Y
Yamanouchi
T
T
Hiroki
K
K
Arakawa
D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy; D016275:Atrial Function / Q000502:physiology*; D002304:Cardiac Pacing, Artificial; D002908:Chronic Disease; D004554:Electric Countershock; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012849:Sinoatrial Node / Q000503:physiopathology*