Elsevier

Heart Rhythm

Volume 9, Issue 3, March 2012, Pages 321-327
Heart Rhythm

Clinical
Atrial fibrillation
Atrial remodeling in obstructive sleep apnea: Implications for atrial fibrillation

This article was presented in part at the Annual Scientific Sessions of the Heart Rhythm Society, May 2011, San Francisco, USA, and published in abstract form in Heart Rhythm 2011;8:S244.
https://doi.org/10.1016/j.hrthm.2011.10.017Get rights and content

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).

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.

Introduction

Obstructive sleep apnea (OSA) is increasingly recognized as a potential risk factor for the development of atrial fibrillation (AF).1, 2, 3 In addition, OSA has been associated with a greater risk of recurrence of AF after cardioversion4 and catheter ablation.5 Despite the enormity of the problems associated with the epidemic of AF, the mechanisms by which OSA predisposes to the development or recurrence of AF remains unknown. Recent evidence has highlighted the importance of atrial structural and electrical remodeling in the substrate predisposing to AF.6, 7, 8, 9, 10, 11, 12, 13 We postulated that patients with OSA have evidence of atrial structural and electrical remodeling to account for their predisposition to AF.

Section snippets

Study population

The study comprised 40 patients undergoing first-time ablation of paroxysmal AF. These patients were dichotomized by polysomnography into OSA (moderate to severe OSA: apnea–hypopnea index ≥ 15; n = 20) and a reference group (none to mild OSA: apnea–hypopnea index < 15; n = 20). Patients with significant central sleep apnea were excluded from the study. A total of 96 consecutive patients were screened to obtain 40 patients fulfilling the study criteria. To avoid the remodeling due to arrhythmia

Baseline characteristics

Baseline characteristics are summarized in Table 1. There were no significant differences in the use of β-blockers (P = .3), calcium-channel blockers (P = .5), or angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers (P = .7) between the groups. Patients with OSA demonstrated significantly larger atria indexed to body surface area (P = .009). Left ventricular function was normal for all patients. University of Toronto AFSS duration and frequency scores were similar between the

Major findings

This study utilized detailed electrophysiologic and electroanatomic mapping to characterize electrophysiologic and electroanatomic atrial abnormalities in patients with OSA. Those with OSA demonstrated the following compared with reference patients:

  • 1

    Structural change with increased atrial size and extensive areas of low voltage and regions of electrical silence, perhaps suggesting loss of atrial myocardium, fibrosis, or underlying conduction dissociation.

  • 2

    Conduction abnormalities characterized

Conclusion

Patients with OSA demonstrate significant atrial remodeling characterized by structural abnormalities with a reduction in atrial myocardial voltage regions of electrical silence, conduction slowing, and sinus node dysfunction. These factors may account for the development and maintenance of AF in patients with OSA.

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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.

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