Sleep Apnea Severity as Atrial Fibrillation Risk
Obstructive sleep apnea (OSA) is the most common clinically significant respiratory abnormality during sleep. It is very common in patients with atrial fibrillation (AF) and promotes arrhythmogenesis and impairs the effectiveness of treatment.
Breathing disorders during sleep cause recurrent episodes of nocturnal hypoxemia, sympathetic nerve activation, and cortical excitation, often associated with excessive daytime sleepiness. Disordered breathing during sleep is common in people with or at risk of cardiovascular disease, including those who are obese or have high blood pressure, coronary artery disease, heart failure, or atrial fibrillation. Current therapy for obstructive sleep apnea includes weight loss (for obesity), exercise, and positive airway pressure (PAP) therapy.
Obstructive sleep apnea is associated with increased cardiovascular risk, but PAP treatment has not been shown to improve cardiovascular outcomes in randomized trials. Central sleep apnea (CSA) is not generally associated with daytime sleepiness in heart failure or atrial fibrillation and is a marker of increased cardiovascular risk, but PAP is harmful in a randomized trial. The benefits of better phenotyping, targeting higher-risk patients, and a more personalized therapeutic approach are being explored in ongoing studies.
The prevalence of OSA ranges from 3% to 49% in population studies and from 21% to 74% in patients with atrial fibrillation. The diagnosis and treatment of OSA in patients with atrial fibrillation requires close interdisciplinary collaboration between electrophysiologists, cardiologists, and sleep specialists. Because OSA prevalence is high in patients with atrial fibrillation and most do not report daytime sleepiness, a sleep study assessment may be useful for patients being considered for the rhythm control strategy.
Atrial electrophysiological changes associated with acute transient apnea and increased occurrences of AF triggers associated with brief episodes of intermittent deoxygenation and re-oxygenation, changes in intrathoracic pressure during obstructed respiratory effort, and vagal sympathetic activation together constitute a stimulus to AF triggers and a complex and dynamic substrate for AF during sleep.
Long-term recurrent episodes of OSA are ultimately associated with structural remodeling and changes in electrical conduction in the atrium. Observational data suggest that OSA reduces the effectiveness of pharmacological and catheter-based antiarrhythmic therapy. Non-randomized studies have shown that treatment of OSA with continuous positive airway pressure can help maintain sinus rhythm after electrical cardioversion and catheter ablation in patients with atrial fibrillation. However, it remains unclear which sleep apnea metric should be used to determine the severity and guide such treatment in patients with atrial fibrillation.
Sleep breathing disorders (SDB) are common in patients with atrial fibrillation, heart failure, and hypertension and are associated with an increased risk of mortality, cardiovascular (CV) events, and arrhythmias. The current assessment of the severity of SDB is mainly based on the apnea-hypopnea index (AHI), which represents the number of hypopneas and apneas per hour of sleep. However, this event-based parameter alone may not adequately reflect the complex pathophysiological mechanisms underlying RRT that may contribute to the risk of cardiovascular outcomes.
Conclusions and Relevance
Data from non-randomized trials in patients with atrial fibrillation suggest that treatment of OSA with continuous positive airway pressure may help maintain sinus rhythm after electrical cardioversion and improve survival rates. Randomized clinical trials are needed to confirm the association between OSA and atrial fibrillation, the benefits of OSA treatment, and the necessity and cost-effectiveness of routine OSA screening and treatment.
OSA is associated with significant atrial remodeling characterized by atrial enlargement, voltage reduction, generalized and site-specific conduction abnormalities, and prolonged sinus node recovery. These features may partially explain the association between OSA and AF.