Obstructive Sleep Apnea: An Emerging Risk Factor for Atherosclerosis
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 betw...
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Veröffentlicht in: | Chest 2011-08, Vol.140 (2), p.534-542 |
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description | 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. |
doi_str_mv | 10.1378/chest.10-2223 |
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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.</description><identifier>ISSN: 0012-3692</identifier><identifier>EISSN: 1931-3543</identifier><identifier>DOI: 10.1378/chest.10-2223</identifier><identifier>PMID: 21813534</identifier><identifier>CODEN: CHETBF</identifier><language>eng</language><publisher>Northbrook, IL: American College of Chest Physicians</publisher><subject>Animals ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - diagnosis ; Atherosclerosis - etiology ; Atherosclerosis - physiopathology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. 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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.</description><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - diagnosis</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Pneumology</subject><subject>Postgraduate Education Corner</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>Risk Factors</subject><subject>Sleep Apnea, Obstructive - complications</subject><subject>Sleep Apnea, Obstructive - physiopathology</subject><issn>0012-3692</issn><issn>1931-3543</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUE1Lw0AUXESxtXr0KrmIp9T9SrLrQQi1VaFQ8OMcXjebdjVf7iYF_70rxq_De4_HDDPDIHRK8JSwRFyqrXbdlOCQUsr20JhIRkIWcbaPxhgTGrJY0hE6cu4F-5_I-BCNKBGERYyP0c1q7Trbq87sdPBYat0GaVtruArSOphX2m5MvQkejHsNFqC6xgaFn7Tbats4VX5u447RQQGl0yfDnaDnxfxpdhcuV7f3s3QZtlRGXVgUkeYCKPFJIWYMEilVhHGOIRFUJh6PocgVVyr3-TTGqpCYK5wLLQXkbIKuv3Tbfl3pXOm6s1BmrTUV2PesAZP9R2qzzTbNLmNECi6pF7gYBGzz1vvisso4pcsSat30LhOCYCGxb2-Czv5a_Xh8N-cJ5wMBnIKysFAr4355nFMexwn7APu1fjQ</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>DRAGER, Luciano F</creator><creator>POLOTSKY, Vsevolod Y</creator><creator>LORENZI-FILHO, Geraldo</creator><general>American College of Chest Physicians</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110801</creationdate><title>Obstructive Sleep Apnea: An Emerging Risk Factor for Atherosclerosis</title><author>DRAGER, Luciano F ; POLOTSKY, Vsevolod Y ; LORENZI-FILHO, Geraldo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p295t-ff5e48a21223a633a799c500d0a78297ff56afdc4ccd813e00cf904c0d8e98ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - diagnosis</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Pneumology</topic><topic>Postgraduate Education Corner</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>Risk Factors</topic><topic>Sleep Apnea, Obstructive - complications</topic><topic>Sleep Apnea, Obstructive - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DRAGER, Luciano F</creatorcontrib><creatorcontrib>POLOTSKY, Vsevolod Y</creatorcontrib><creatorcontrib>LORENZI-FILHO, Geraldo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Chest</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DRAGER, Luciano F</au><au>POLOTSKY, Vsevolod Y</au><au>LORENZI-FILHO, Geraldo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Obstructive Sleep Apnea: An Emerging Risk Factor for Atherosclerosis</atitle><jtitle>Chest</jtitle><addtitle>Chest</addtitle><date>2011-08-01</date><risdate>2011</risdate><volume>140</volume><issue>2</issue><spage>534</spage><epage>542</epage><pages>534-542</pages><issn>0012-3692</issn><eissn>1931-3543</eissn><coden>CHETBF</coden><abstract>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.</abstract><cop>Northbrook, IL</cop><pub>American College of Chest Physicians</pub><pmid>21813534</pmid><doi>10.1378/chest.10-2223</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Atherosclerosis (general aspects, experimental research) Atherosclerosis - diagnosis Atherosclerosis - etiology Atherosclerosis - physiopathology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Humans Medical sciences Pneumology Postgraduate Education Corner Respiratory system : syndromes and miscellaneous diseases Risk Factors Sleep Apnea, Obstructive - complications Sleep Apnea, Obstructive - physiopathology |
title | Obstructive Sleep Apnea: An Emerging Risk Factor for Atherosclerosis |
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