Atrial remodeling in obstructive sleep apnea: implications for atrial fibrillation.
BACKGROUND
There is a known association between obstructive sleep apnea (OSA) and atrial fibrillation (AF); however, how OSA affects the atrial myocardium is not well described.


OBJECTIVE
To determine whether patients with OSA have an abnormal atrial substrate.


METHODS
Forty patients undergoing ablation of paroxysmal AF and in sinus rhythm (20 with OSA [apnea-hypopnea index ≥ 15] and 20 reference patients with no OSA [apnea-hypopnea index < 15] by polysomnography) were studied. Multipolar catheters were positioned at the lateral right atrium (RA), coronary sinus, crista terminalis, and RA septum to determine the effective refractory period at 5 sites, conduction time along linear catheters at the RA and the coronary sinus, conduction at the crista terminalis, and sinus node function (corrected sinus node recovery time). Biatrial electroanatomic maps were created to determine the voltage, conduction, and distribution of complex electrograms (duration ≥ 50 ms).


RESULTS
The groups had no differences in the prevalence of established risk factors for AF. Patients with OSA had the following compared with those without OSA: no difference in effective refractory period (P = .9), prolonged conduction times along the coronary sinus and RA (P = .02), greater number (P = .003) and duration (P = .03) of complex electrograms along the crista terminalis, longer P-wave duration (P = .01), longer corrected sinus node recovery time (P = .02), lower atrial voltage (RA, P <.001; left atrium, P <.001), slower atrial conduction velocity (RA, P = .001; left atrium, P = .02), and more widespread complex electrograms in both atria (RA, P = .02; left atrium, P = .01).


CONCLUSIONS
OSA is associated with significant atrial remodeling characterized by atrial enlargement, reduction in voltage, site-specific and widespread conduction abnormalities, and longer sinus node recovery. These features may in part explain the association between OSA and AF.
Centre for Heart Rhythm Disorders (CHRD), Discipline of Medicine, University of Adelaide, Adelaide, Australia.
Hany
H
Dimitri
Michelle
M
Ng
Anthony G
AG
Brooks
Pawel
P
Kuklik
Martin K
MK
Stiles
Dennis H
DH
Lau
Nicholas
N
Antic
Andrew
A
Thornton
David A
DA
Saint
Doug
D
McEvoy
Ral
R
Antic
Jonathan M
JM
Kalman
Prashanthan
P
Sanders
D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D006328:Cardiac Catheterization / Q000379:methods; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods; D005260:Female; D006325:Heart Atria / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D017286:Polysomnography; D015985:Precipitating Factors; D012849:Sinoatrial Node / Q000503:physiopathology*; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology