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dc.contributor.authorMcNicholas, Walter T
dc.date.accessioned2012-02-01T10:28:26Z
dc.date.available2012-02-01T10:28:26Z
dc.date.issued2012-02-01T10:28:26Z
dc.identifier.citationProg Cardiovasc Dis. 2009 Mar-Apr;51(5):392-9.en_GB
dc.identifier.issn1532-8643 (Electronic)en_GB
dc.identifier.issn0033-0620 (Linking)en_GB
dc.identifier.pmid19249445en_GB
dc.identifier.doi10.1016/j.pcad.2008.10.005en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207021
dc.description.abstractThe pathogenesis of cardiovascular complications in obstructive sleep apnea syndrome (OSAS) is not fully understood but is likely multifactorial in origin. Inflammatory processes play an important role in the pathogenesis of atherosclerosis, and circulating levels of several markers of inflammation have been associated with future cardiovascular risk. These include cell adhesion molecules such as intercellular adhesion molecule-1 and selectins, cytokines such as tumour necrosis factor alpha and interleukin 6, chemokines such as interleukin 8, and C-reactive protein. There is also increasing evidence that inflammatory processes play an important role in the cardiovascular pathophysiology of OSAS and many of the inflammatory markers associated with cardiovascular risk have been reported as elevated in patients with OSAS. Furthermore, animal and cell culture studies have demonstrated preferential activation of inflammatory pathways by intermittent hypoxia, which is an integral feature of OSAS. The precise role of inflammation in the development of cardiovascular disease in OSAS requires further study, particularly the relationship with oxidative stress, metabolic dysfunction, and obesity.
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshAnoxia/immunologyen_GB
dc.subject.meshBiological Markers/metabolismen_GB
dc.subject.meshC-Reactive Protein/metabolismen_GB
dc.subject.meshCardiovascular Diseases/*immunologyen_GB
dc.subject.meshCell Adhesion Molecules/metabolismen_GB
dc.subject.meshHumansen_GB
dc.subject.meshInflammation/*immunologyen_GB
dc.subject.meshInflammation Mediators/*metabolismen_GB
dc.subject.meshInterleukins/metabolismen_GB
dc.subject.meshObesity/immunologyen_GB
dc.subject.meshOxidative Stressen_GB
dc.subject.meshRisk Factorsen_GB
dc.subject.meshSleep Apnea, Obstructive/complications/*immunologyen_GB
dc.subject.meshTumor Necrosis Factor-alpha/metabolismen_GB
dc.titleObstructive sleep apnea and inflammation.en_GB
dc.contributor.departmentSleep Research Laboratory, St. Vincent's University Hospital, Dublin, Ireland., walter.mcnicholas@ucd.ieen_GB
dc.identifier.journalProgress in cardiovascular diseasesen_GB
dc.description.provinceLeinster
html.description.abstractThe pathogenesis of cardiovascular complications in obstructive sleep apnea syndrome (OSAS) is not fully understood but is likely multifactorial in origin. Inflammatory processes play an important role in the pathogenesis of atherosclerosis, and circulating levels of several markers of inflammation have been associated with future cardiovascular risk. These include cell adhesion molecules such as intercellular adhesion molecule-1 and selectins, cytokines such as tumour necrosis factor alpha and interleukin 6, chemokines such as interleukin 8, and C-reactive protein. There is also increasing evidence that inflammatory processes play an important role in the cardiovascular pathophysiology of OSAS and many of the inflammatory markers associated with cardiovascular risk have been reported as elevated in patients with OSAS. Furthermore, animal and cell culture studies have demonstrated preferential activation of inflammatory pathways by intermittent hypoxia, which is an integral feature of OSAS. The precise role of inflammation in the development of cardiovascular disease in OSAS requires further study, particularly the relationship with oxidative stress, metabolic dysfunction, and obesity.


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