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Authors
McNicholas, Walter TAffiliation
Sleep Research Laboratory, St. Vincent's University Hospital, Dublin, Ireland., walter.mcnicholas@ucd.ieIssue Date
2012-02-01T10:28:26ZMeSH
AnimalsAnoxia/immunology
Biological Markers/metabolism
C-Reactive Protein/metabolism
Cardiovascular Diseases/*immunology
Cell Adhesion Molecules/metabolism
Humans
Inflammation/*immunology
Inflammation Mediators/*metabolism
Interleukins/metabolism
Obesity/immunology
Oxidative Stress
Risk Factors
Sleep Apnea, Obstructive/complications/*immunology
Tumor Necrosis Factor-alpha/metabolism
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Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):392-9.Journal
Progress in cardiovascular diseasesDOI
10.1016/j.pcad.2008.10.005PubMed ID
19249445Abstract
The 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.Language
engISSN
1532-8643 (Electronic)0033-0620 (Linking)
ae974a485f413a2113503eed53cd6c53
10.1016/j.pcad.2008.10.005
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