Sleep Strategies

What are we missing when it comes to obstructive sleep apnea and atrial fibrillation?


 

Is the lack of efficacy due to starting CPAP too late in the course of OSA?

It has been proposed that there may be a critical early period after the onset of OSA when intervention with CPAP (or alternative therapies) will be most effective in preventing adverse cardiovascular outcomes. An answer will almost certainly necessitate a long-term prospective study enrolling people before they develop OSA. Additionally, the AHI is used in most trials to determine the presence and severity of OSA. However, the AHI has been shown to have a poor correlation with sleep-related symptoms, and it may fail to capture key OSA pathophysiologic stressors (e.g., hyperadrenergic drive, cyclical hypoxemia, etc), which may increase the risk of AF. Other disease characteristics and polysomnographic features may better capture disease severity and the cardiovascular risk factors associated with it. The respiratory arousal threshold, arousal index, degree of loop gain, hypoxic burden, heart rate variability, and cardiopulmonary coupling are some examples of such features.

Another possible explanation is that AF is not causally related, and the demonstrated association between the two is because both conditions share risk factors such as age and BMI, among others. Or, if they are causally linked, OSA may be a minor contributor, and the magnitude of that contribution is insufficient to reduce the risk of AF significantly by treating OSA. More research is needed to define the salient intervenable aspects of OSA better and design the optimal timing and duration of intervention.

Dr. Mudrakola is with the Department of Pulmonary & Critical Care Medicine, Summa Health, Akron, Ohio. Dr. Selim is with the Department of Pulmonary & Critical Care Medicine, Mayo Clinic, Rochester, Minnesota.

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