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.
MeSH terms
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Animals
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Antioxidants / therapeutic use
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Blood Coagulation
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Cardiovascular Diseases / etiology*
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Cardiovascular Diseases / physiopathology
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Cardiovascular Diseases / prevention & control
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Continuous Positive Airway Pressure
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Endothelium, Vascular / metabolism
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Endothelium, Vascular / physiopathology*
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Hemodynamics
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Humans
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Hypoxia / physiopathology
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Inflammation / physiopathology
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Inflammation Mediators / metabolism
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Mandibular Advancement / instrumentation
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Nitric Oxide / metabolism
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Oxidative Stress
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Regeneration
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Sleep Apnea, Obstructive / complications
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Sleep Apnea, Obstructive / physiopathology*
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Sleep Apnea, Obstructive / therapy
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Sleep Deprivation / physiopathology
Substances
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Antioxidants
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Inflammation Mediators
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Nitric Oxide