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Sleep Apnea and Atrial Fibrillation
Abstract & Commentary
By John P. DiMarco, MD, PhD, Professor of Medicine, Division of Cardiology, University of Virginia, Charlottesville. Dr. DiMarco is a consultant for Novartis, and does research for Medtronic and Guidant.
This article originally appeared in the April 2007 issue of Clinical Cardiology Alert. It was edited by Michael Crawford, MD, and peer reviewed by Rakesh Mishra, MD.
Synopsis: Obesity and the magnitude of nocturnal oxygen desaturation, which is an important pathophysiological consequence of OSA, are independent risk factors for incident AF in individuals <65 years of age.
Source: Gami AS, et al. Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. J Am Coll Cardiol. 2007;49:565-571.
Gami and colleagues from the Mayo Clinic describe in this paper relationships between obesity, obstructive sleep apnea, and atrial fibrillation (AF). Gami et al identified adult residents living in Olmsted County, Minnesota, who underwent diagnostic polysomnography between 1987 and 2003. Patients with a previous history of atrial fibrillation were excluded. Subjects were defined as having obstructive sleep apnea (OSA) if they had an apnea-hypopnea index during their sleep study ≥ 5. The occurrence of incident AF was timed from the date of the sleep study by querying the Mayo Clinic electronic medical index. Any diagnosis of AF or atrial flutter was made during any medical contact if the occurrence of AF was confirmed by an electrocardiogram was considered an event. Time-to-event analyses were performed using Kaplan-Meier methods to identify univariate predictors of incident AF. The parameters included subject, age, gender, body mass index, relevant comorbidities, OSA status and severity, and physiological sleep variables. Multivariate analyses were performed using Cox proportional hazards regressions methods. Furthermore, in an analysis that included only subjects with OSA, the effect of continuous positive airway pressure after the sleep study was introduced into the multivariate model.
During the period of the study, 3542 subjects underwent polysomnography, and OSA was present in 2626 (74%). After an average follow up of 4.7 years (up to 15 years), incident AF occurred in 133 subjects, for a cumulative frequency of 14%. By univariate analysis, age, male gender, hypertension, the presence of coronary disease, heart failure, a history of smoking, the presence of diabetes, body mass index, obstructive sleep apnea, and measures of the severity of sleep apnea, all were related to the risk of incident atrial fibrillation. There was a significant interaction between OSA and age.
Therefore, Gami et al performed a stratified analysis for subjects younger than 65 years, as well as 65 years or older. Among the subjects less than 65 years old, age, male gender, body mass index, and a history of coronary artery disease independently predicted incident AF. The decrease in nocturnal oxygen saturation was also an independent predictor of incident AF. In contrast, for subjects ≥ 65 years old, only heart failure independently predicted incident AF. In a multivariate regression model that included only subjects with OSA, the use of continuous positive airway pressure did not positively or negatively affect the incidence of AF. In the multivariate regression model, both OSA and obesity independently predicted incident AF.
Gami et al conclude that obesity and the magnitude of nocturnal oxygen desaturation are independent risk factors for incident AF in individuals less than 65 years of age.
A number of arrhythmias are commonly seen in patients with organic sleep apnea. This paper shows that atrial fibrillation is strongly related to the presence of OSA. A number of mechanisms may be responsible for this. OSA is associated with diastolic dysfunction, which can lead to increases in atrial size and atrial stretch. Rapid swings in intracardiac pressures can activate atrial ion channels that may contribute to AF initiation. Surges in autonomic nervous system activity may also occur. During OSA-associated bradycardia, atrial repolarization prolongs and, then with elevation of sympathetic activity during apnea catecholamine sensitive ion channels, may lead to increased automaticity. This combination should be a potent mechanism for AF initiation. Finally, OSA has been reported to be associated with systemic inflammation, another potential cause of atrial fibrillation.
It is disappointing that Gami et al cannot demonstrate that the use of continuous positive airway pressure (CPAP) favorably influenced the risk for atrial fibrillation. However, in this study, CPAP was used mostly in the patients with the most severe form of OSA, and a prospective study will likely be required to see if CPAP has a favorable influence on the incidence of AF.
In conclusion, physicians should consider sleep apnea as an important potential cause of atrial fibrillation. Weight reduction and treatment of OSA should be part of the management of AF in patients at risk.