Endothelial function in obstructive sleep apnea

Abstract

Untreated obstructive sleep apnea (OSA) is an independent risk factor for hypertension, myocardial infarction, and stroke. The repetitive hypoxia/reoxygenation and sleep fragmentation associated with OSA impair endothelial function. Endothelial dysfunction, in turn, may mediate increased risk for cardiovascular diseases. Specifically, in OSA, endothelial nitric oxide availability and repair capacity are reduced, whereas oxidative stress and inflammation are enhanced. Treatment of OSA improves endothelial vasomotor tone and reduces inflammation. We review the evidence and possible mechanisms of endothelial dysfunction as well as the effect of treatment on endothelial function in OSA.

Figures

Fig 1

Intermediary mechanisms associated with endothelial dysfunction in patients with OSA that potentially contribute to increased cardiovascular risks. Repetitive hypoxia/reoxygenation and sleep fragmentation associated with transient cessation of breathing in OSA adversely impact endothelial function by promoting oxidative stress, inflammation, and apoptosis, and reducing NO availability and repair capacity. Continuous positive airway pressure therapy ameliorates these alterations. Continuous positive airway pressure–induced reversal of vascular endothelial dysfunction may reduce and/or reverse increased cardiovascular risk in OSA.