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Postgraduate Education Corner: CONTEMPORARY REVIEWS IN SLEEP MEDICINE |

Obstructive Sleep ApneaObstructive Sleep Apnea and Atherosclerosis: An Emerging Risk Factor for Atherosclerosis

Luciano F. Drager, MD, PhD; Vsevolod Y. Polotsky, MD, PhD; Geraldo Lorenzi-Filho, MD, PhD
Author and Funding Information

From the Hypertension Unit (Dr Drager), and the Sleep Laboratory, Pulmonary Division (Dr Lorenzi-Filho), Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil; and the Division of Pulmonary and Critical Care Medicine (Dr Polotsky), Johns Hopkins University School of Medicine, Baltimore, MD.

Correspondence to: Geraldo Lorenzi-Filho, MD, PhD, Sleep Laboratory, Pulmonary Division, Heart Institute (InCor), University of São Paulo Medical School, Av Dr Eneas Carvalho de Aguiar, 44, 05403-904, São Paulo, Brazil; e-mail: geraldo.lorenzi@incor.usp.br


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].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(2):534-542. doi:10.1378/chest.10-2223
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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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