The association of obstructive sleep apnea (OSA) with vascular disease and mortality was reported in clinical case series almost 3 decades ago and has since been confirmed in numerous prospective observational studies involving both sleep clinic patients and community-based cohorts. Physiological studies in animals and humans have suggested likely mechanisms whereby the intermittent hypercapnic hypoxemia and recurrent arousal from sleep that characterize OSA might cause vascular disease. The most strongly implicated mechanism is increased sympathetic nervous system activity, with considerable evidence as well for impaired glucose homeostasis, vascular inflammation, and oxidative stress.1 Numerous single-site and multicenter studies have demonstrated modest but clinically significant reductions in blood pressure with OSA treatment, an effect that is substantial during sleep.2-4 This effect alone would be expected to result in a reduction in risk of myocardial infarction and stroke. Clinical cohort studies comparing patients with OSA treated with positive airway pressure (PAP) with untreated patients with OSA have consistently demonstrated lower rates of death, myocardial infarction, and stroke among the treated patients.5 However, such observational studies carry a substantial risk of bias due to a “healthy adherer” effect, and randomized clinical trials (RCTs) are therefore necessary to demonstrate whether treatment of OSA does reduce cardiovascular risk.
Gottlieb DJ. Does Obstructive Sleep Apnea Treatment Reduce Cardiovascular Risk? It Is Far Too Soon to Say. JAMA. 2017;318(2):128–130. doi:10.1001/jama.2017.7966
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