SNOWMASS, COLO. – The association between obstructive sleep apnea and atrial fibrillation is now so firmly supported that prevention of recurrent atrial fibrillation can be added to the list of indications for treatment of the sleep disorder, Dr. Bernard J. Gersh said at a conference sponsored by the Society for Cardiovascular Angiography and Interventions.
“Before I consider patients for pulmonary vein isolation and ablation, I make sure that they don't have sleep apnea,” added Dr. Gersh, professor of medicine at the Mayo Clinic, Rochester, Minn.
He was a coinvestigator in a Mayo Clinic study that showed the risk of recurrence of atrial fibrillation in the year following direct current cardioversion of the arrhythmia in patients with obstructive sleep apnea (OSA) was halved by continuous positive airway pressure (CPAP) therapy (Circulation 2003;107:2589-94).
Until recently, it was unclear how much of the association between OSA and atrial fibrillation is caused by the OSA and how much is caused by obesity, hypertension, diabetes, and other comorbid conditions common in OSApatients.
An answer finally was provided by a recent retrospective cohort study of 3,542 Olmsted County, Minn., adults free of a history of atrial fibrillation when referred for diagnostic polysomnography. During a mean 4.7-year follow-up, the incidence of new-onset atrial fibrillation was 14%. Obesity and OSA proved to be independent risk factors for atrial fibrillation in persons aged 65 years or less. For each 0.5-U log decrease in nocturnal oxygen saturation at baseline–an important measure of OSA severity–the risk of developing atrial fibrillation climbed 3.3-fold. And for each 5-kg/m
Other independent predictors of new-onset atrial fibrillation in this study were male gender and the presence of coronary artery disease.
At least 25 million Americans have OSA; 60%−80% of whom are undiagnosed. Atrial fibrillation is the most common sustained cardiac arrhythmia, and the worsening obesity epidemic combined with the large number of individuals with undiagnosed and untreated OSA and an aging general population portends a dramatic increase in the atrial fibrillation problem, Dr. Gersh noted at the conference, cosponsored by the American College of Cardiology.
A few years ago when Dr. Gersh cochaired a National Heart, Lung, and Blood Institute workshop on the cardiovascular consequences of sleep-disordered breathing (Circulation 2004; 109:951-7), an unresolved issue was whether OSA is a cause of acute MI, stroke, and other cardiovascular events or a surrogate marker for traditional cardiovascular risk factors. He cited two studies that have provided evidence that OSA is an independent cardiovascular risk factor.
In one observational cohort study of 1,022 consecutive patients who underwent poly-somnography, researchers at Yale University, New Haven, showed that OSA at baseline was independently associated with a twofold increased risk of subsequent stroke or death from any cause after adjusting for numerous potential confounders, including hypertension, smoking and alcohol-consumption status, age, gender, atrial fibrillation, and diabetes. The more severe the OSA as reflected in the apnea-hypopnea index, the greater the risk of the composite end point (N. Engl. J. Med. 2005;353:2034-41).
In the other study, physicians at University Hospital, Zaragoza (Spain), followed more than 1,000 men with CPAP-treated or untreated OSA, 377 simple snorers, and 264 healthy men. During a mean 10.1-year follow-up, men with untreated severe OSA had about threefold greater risks of fatal and nonfatal cardiovascular events than did the healthy controls. The CPAP-treated patients had cardiovascular event rates similar to those of controls (Lancet 2005;365:1046-53).