Endothelial function in obstructive sleep apnea.
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.
Atkeson
Amy
A
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Yeh
Susie Yim
SY
Malhotra
Atul
A
Jelic
Sanja
S
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D001777:Blood Coagulation; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D045422:Continuous Positive Airway Pressure; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D019186:Mandibular Advancement / Q000295:instrumentation; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D012038:Regeneration; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D012892:Sleep Deprivation / Q000503:physiopathology
D000975:Antioxidants; D018836:Inflammation Mediators; D009569:Nitric Oxide