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Obstructive Sleep Apnea and Vascular Diseases

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ABSTRACT

Obstructive sleep apnea (OSA) affects a large proportion of adults, and is as an independent risk factor for cerebrovascular and cardiovascular disease. The repetitive airway obstruction that characterizes OSA results in intermittent hypoxia, intrathoracic pressure swings, and sleep fragmentation, which in turn lead to sympathetic activation, oxidative stress, inflammation, and endothelial dysfunction. This review outlines the associations between OSA and vascular diseases and describes basic mechanisms that may be responsible for this association, in both the micro‐ and macrocirculation. It also reports on interventional studies that aim to ameliorate OSA and thereby reduce vascular disease burden. © 2016 American Physiological Society. Compr Physiol 6:1519‐1528, 2016.

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Figure 1. Figure 1. Possible mechanisms linking OSA with vascular disease.
Figure 2. Figure 2. Pathways linking OSA to endothelial dysfunction. ↑, upregulation; ↓, downregulation; Angio II, angiotensin II receptor; CRP, C‐reactive protein; eNOS, endothelial nitric oxide synthetase; EPCs, endothelial progenitor cells; HIF, hypoxia‐inducible facto; ICAM, intercellular adhesion molecule; IL 6, interleukin 6; IL 8, interleukin 8; NADPH, nicotinamide adenine dinucleotide phosphate; NF‐KB, nuclear factor‐ kB; RNS, reactive nitrogen species; ROS, reactive oxygen species; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor.
Figure 3. Figure 3. Endothelial function, as measured by flow‐mediated dilation of the brachial artery, is impaired in subjects with OSA, as compared with control subjects, in a subgroup of subjects younger than 50 years of age. The box encompasses the 25% to 75% quartiles, and the median is represented by the horizontal line within the box. The whiskers extend to the highest and lowest values within the higher and lower limits, respectively (129).
Figure 4. Figure 4. Intervention of CPAP on OSA pathway. ↑, increase; OSA: obstructive sleep apnea; CPAP, continuous positive airway pressure; CVD, cardiovascular disease.


Figure 1. Possible mechanisms linking OSA with vascular disease.


Figure 2. Pathways linking OSA to endothelial dysfunction. ↑, upregulation; ↓, downregulation; Angio II, angiotensin II receptor; CRP, C‐reactive protein; eNOS, endothelial nitric oxide synthetase; EPCs, endothelial progenitor cells; HIF, hypoxia‐inducible facto; ICAM, intercellular adhesion molecule; IL 6, interleukin 6; IL 8, interleukin 8; NADPH, nicotinamide adenine dinucleotide phosphate; NF‐KB, nuclear factor‐ kB; RNS, reactive nitrogen species; ROS, reactive oxygen species; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor.


Figure 3. Endothelial function, as measured by flow‐mediated dilation of the brachial artery, is impaired in subjects with OSA, as compared with control subjects, in a subgroup of subjects younger than 50 years of age. The box encompasses the 25% to 75% quartiles, and the median is represented by the horizontal line within the box. The whiskers extend to the highest and lowest values within the higher and lower limits, respectively (129).


Figure 4. Intervention of CPAP on OSA pathway. ↑, increase; OSA: obstructive sleep apnea; CPAP, continuous positive airway pressure; CVD, cardiovascular disease.
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Dimitrios Baltzis, Jessie P. Bakker, Sanjay R. Patel, Aristidis Veves. Obstructive Sleep Apnea and Vascular Diseases. Compr Physiol 2016, 6: 1519-1528. doi: 10.1002/cphy.c150029