TY - JOUR
T1 - Atrial remodeling in obstructive sleep apnea
T2 - Implications for atrial fibrillation
AU - Dimitri, Hany
AU - Ng, Michelle
AU - Brooks, Anthony G.
AU - Kuklik, Pawel
AU - Stiles, Martin K.
AU - Lau, Dennis H.
AU - Antic, Nicholas
AU - Thornton, Andrew
AU - Saint, David A.
AU - McEvoy, Doug
AU - Antic, Ral
AU - Kalman, Jonathan M.
AU - Sanders, Prashanthan
N1 - Funding Information:
Dr Dimitri is supported by Postgraduate Medical Scholarships from the Cardiac Society of Australia and New Zealand and jointly by the National Heart Foundation of Australia and the National Health and Medical Research Council of Australia. Dr Brooks, Dr Kuklik, and Dr Sanders are funded by the National Heart Foundation of Australia. Dr Stiles is supported by the National Heart Foundation of New Zealand and the Dawes Scholarship from the Royal Adelaide Hospital. Dr Lau is supported by a Postdoctoral Fellowship from the National Health and Medical Research Council of Australia. Dr Sanders reports having served on the advisory board of Bard Electrophysiology, Biosense-Webster, Medtronic, St Jude Medical, Sanofi-Aventis, and Merck, Sharpe and Dohme. Dr Sanders reports having received lecture fees and research funding from Bard Electrophysiology, Biosense-Webster, Medtronic, and St Jude Medical.
PY - 2012/3
Y1 - 2012/3
N2 - 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 [apneahypopnea index < 15] and 20 reference patients with no OSA [apneahypopnea 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). Conclusion: 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.
AB - 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 [apneahypopnea index < 15] and 20 reference patients with no OSA [apneahypopnea 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). Conclusion: 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.
KW - Arrhythmia
KW - Atrial fibrillation
KW - Hypoxia
KW - Remodeling
KW - Sleep apnea
UR - http://www.scopus.com/inward/record.url?scp=84857619245&partnerID=8YFLogxK
U2 - 10.1016/j.hrthm.2011.10.017
DO - 10.1016/j.hrthm.2011.10.017
M3 - Article
C2 - 22016075
AN - SCOPUS:84857619245
SN - 1547-5271
VL - 9
SP - 321
EP - 327
JO - Heart Rhythm
JF - Heart Rhythm
IS - 3
ER -