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Should I evaluate my patient with atrial fibrillation for sleep apnea?

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Yes. The prevalence of sleep apnea is exceedingly high in patients with atrial fibrillation—50% to 80% compared with 30% to 60% in respective control groups.1–3 Conversely, atrial fibrillation is more prevalent in those with sleep-disordered breathing than in those without (4.8% vs 0.9%).4

Sleep-disordered breathing comprises obstructive sleep apnea and central sleep apnea. Obstructive sleep apnea, characterized by repetitive upper-airway obstruction during sleep, is accompanied by intermittent hypoxia, rises in carbon dioxide, autonomic nervous system fluctuations, and intrathoracic pressure alterations.5 Central sleep apnea may be neurally mediated and, in the setting of cardiac disease, is characterized by alterations in chemosensitivity and chemoresponsiveness, leading to a state of high loop gain—ie, a hypersensitive ventilatory control system leading to ventilatory drive oscillations.6

Both obstructive and central sleep apnea have been associated with atrial fibrillation. Experimental data implicate obstructive sleep apnea as a trigger of atrial arrhythmogenesis,7,8 and epidemiologic studies support an association between central sleep apnea, Cheyne-Stokes respiration, and incident atrial fibrillation.9

HOW SLEEP APNEA COULD LEAD TO ATRIAL FIBRILLATION

In experiments in animals, intermittent upper-airway obstruction led to forced inspiration, substantial negative intrathoracic pressure, subsequent left atrial distention, and increased susceptibility to atrial fibrillation.10 The autonomic nervous system may be a mediator of apnea-induced atrial fibrillation, as apnea-induced atrial fibrillation is suppressed with autonomic blockade.10

Emerging data also support the hypothesis that intermittent hypoxia7 and resolution of hypercapnia,8 as observed in obstructive sleep apnea, exert atrial electrophysiologic changes that increase vulnerability to atrial arrhythmogenesis.

In a case-crossover study,11 the odds of paroxysmal atrial fibrillation occurring after a respiratory disturbance were 17.9 times higher than after normal breathing (95% confidence interval [CI] 2.2–144.2), though the absolute rate of overall arrhythmia events (including both atrial fibrillation and nonsustained ventricular tachycardia) associated with respiratory disturbances was low (1 excess arrhythmia event per 40,000 respiratory disturbances).

EFFECT OF SLEEP APNEA ON ATRIAL FIBRILLATION MANAGEMENT

Sleep apnea also seems to affect the efficacy of a rhythm-control strategy for atrial fibrillation. For example, patients with obstructive sleep apnea have a higher risk of recurrent atrial fibrillation after cardioversion (82% vs 42% in controls)12 and up to a 25% greater risk of recurrence after catheter ablation compared with those without obstructive sleep apnea (risk ratio 1.25, 95% CI 1.08–1.45).13

Several observational studies showed a higher rate of atrial fibrillation after pulmonary vein isolation in obstructive sleep apnea patients who do not use continuous positive airway pressure (CPAP) than in those who do.14–17 CPAP therapy appears to exert beneficial effects on cardiac structural remodeling; cardiac magnetic resonance imaging shows that patients with sleep apnea who received less than 4 hours of CPAP per night had larger left atrial dimensions and increased left ventricular mass compared with those who received more than 4 hours of CPAP at night.17 However, a need remains for high-quality, large randomized controlled trials to eliminate potential unmeasured biases due to differences that may exist between CPAP users and non-users, such as general adherence to medical therapy and healthcare interventions.

An additional consideration is that the overall utility and value of obtaining a diagnosis of obstructive sleep apnea strictly as it pertains to atrial fibrillation management is affected by whether a rhythm- or rate-control strategy is pursued. In other words, if a patient is deemed to be in permanent atrial fibrillation and a rhythm-control strategy is therefore not pursued, the potential effect of untreated obstructive sleep apnea on atrial fibrillation recurrence could be less important. In this case, however, the other beneficial cardiovascular and systemic effects of diagnosing and treating underlying obstructive sleep apnea would remain.

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