Mechanisms of endothelial dysfunction in obstructive sleep apnea

Abstract

Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic susceptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA.

Keywords: dysfunction; endothelial; inflammation; obstructive sleep apnea.

Figure 1

Intermediary mechanisms that mediate increased cardiovascular risk in obstructive sleep apnea (OSA). Repetitive hypoxia/reoxygenation associated with transient cessation of breathing while asleep promotes endothelial dysfunction in patients with OSA by increasing vascular inflammation, oxidative stress and apoptosis while reducing nitric oxide availability. Sleep fragmentation and deprivation resulting from repetitive arousals during sleep compound the effects of hypoxia/reoxygenation injury by independently promoting vascular inflammation. Genetic susceptibility may contribute to cardiovascular risk associated with OSA.