TY - JOUR
T1 - Obstructive sleep apnea
T2 - An emerging risk factor for atherosclerosis
AU - Drager, Luciano F.
AU - Polotsky, Vsevolod Y.
AU - Lorenzi-Filho, Geraldo
N1 - Funding Information:
Funding/Support: This study was funded by the National Institutes of Health [Grants R01 HL80105, 5P50HL084945] ; Fundação Zerbini; Fundação de Amparo à Pesquisa do Estado de São Paulo [Research Fellowship Grant 2010/11681-0] ; and the American Heart Association [Grant-in-Aid 10GRNT3360001] .
PY - 2011/8/1
Y1 - 2011/8/1
N2 - Obstructive sleep apnea (OSA) is independently associated with death from cardiovascular diseases, including myocardial infarction and stroke. Myocardial infarction and stroke are complications of atherosclerosis; therefore, over the last decade investigators have tried to unravel relationships between OSA and atherosclerosis. OSA may accelerate atherosclerosis by exacerbating key atherogenic risk factors. For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. In addition, clinical data and experimental evidence in animal models suggest that OSA can have direct proatherogenic effects inducing systemic inflammation, oxidative stress, vascular smooth cell activation, increased adhesion molecule expression, monocyte/lymphocyte activation, increased lipid loading in macrophages, lipid peroxidation, and endothelial dysfunction. Several cross-sectional studies have shown consistently that OSA is independently associated with surrogate markers of premature atherosclerosis, most of them in the carotid bed. Moreover, OSA treatment with continuous positive airway pressure may attenuate carotid atherosclerosis, as has been shown in a randomized clinical trial. This review provides an update on the role of OSA in atherogenesis and highlights future perspectives in this important research area.
AB - Obstructive sleep apnea (OSA) is independently associated with death from cardiovascular diseases, including myocardial infarction and stroke. Myocardial infarction and stroke are complications of atherosclerosis; therefore, over the last decade investigators have tried to unravel relationships between OSA and atherosclerosis. OSA may accelerate atherosclerosis by exacerbating key atherogenic risk factors. For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. In addition, clinical data and experimental evidence in animal models suggest that OSA can have direct proatherogenic effects inducing systemic inflammation, oxidative stress, vascular smooth cell activation, increased adhesion molecule expression, monocyte/lymphocyte activation, increased lipid loading in macrophages, lipid peroxidation, and endothelial dysfunction. Several cross-sectional studies have shown consistently that OSA is independently associated with surrogate markers of premature atherosclerosis, most of them in the carotid bed. Moreover, OSA treatment with continuous positive airway pressure may attenuate carotid atherosclerosis, as has been shown in a randomized clinical trial. This review provides an update on the role of OSA in atherogenesis and highlights future perspectives in this important research area.
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U2 - 10.1378/chest.10-2223
DO - 10.1378/chest.10-2223
M3 - Review article
C2 - 21813534
AN - SCOPUS:80051479908
SN - 0012-3692
VL - 140
SP - 534
EP - 542
JO - CHEST
JF - CHEST
IS - 2
ER -