Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?

Hdl Handle:
http://hdl.handle.net/10147/207616
Title:
Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?
Authors:
Ryan, S; Taylor, C T; McNicholas, W T
Affiliation:
Sleep Research Laboratory, St Vincent's University Hospital, Dublin, Ireland.
Citation:
Thorax. 2009 Jul;64(7):631-6.
Journal:
Thorax
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207616
DOI:
10.1136/thx.2008.105577
PubMed ID:
19561283
Abstract:
Obstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and is recognised as a major public health burden. Large-scale epidemiological studies have demonstrated an independent relationship between OSAS and various cardiovascular disorders. The pathogenesis of cardiovascular complications in OSAS is not completely understood but a multifactorial aetiology is likely. Inflammatory processes have emerged as critical in the pathogenesis of atherosclerosis at all stages of atheroma formation. Increased levels of various circulating markers of inflammation including tumour necrosis factor alpha (TNFalpha), interleukin 6 (IL6), IL-8 and C-reactive protein (CRP) have been reported as associated with future cardiovascular risk. There is increasing evidence of elevated inflammatory markers in OSAS with a significant fall after effective treatment with continuous positive airway pressure. This evidence is particularly strong for TNFalpha, whereas studies on IL6 and CRP have yielded conflicting results possibly due to the confounding effects of obesity. Cell culture and animal studies have significantly contributed to our understanding of the underlying mechanisms of the association between OSAS and inflammation. Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.
Language:
eng
MeSH:
Cardiovascular Diseases/*etiology; Humans; Inflammation/*complications; Inflammation Mediators/blood; Obesity/complications; Sleep Apnea, Obstructive/blood/*complications
ISSN:
1468-3296 (Electronic); 0040-6376 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorRyan, Sen_GB
dc.contributor.authorTaylor, C Ten_GB
dc.contributor.authorMcNicholas, W Ten_GB
dc.date.accessioned2012-02-01T10:32:58Z-
dc.date.available2012-02-01T10:32:58Z-
dc.date.issued2012-02-01T10:32:58Z-
dc.identifier.citationThorax. 2009 Jul;64(7):631-6.en_GB
dc.identifier.issn1468-3296 (Electronic)en_GB
dc.identifier.issn0040-6376 (Linking)en_GB
dc.identifier.pmid19561283en_GB
dc.identifier.doi10.1136/thx.2008.105577en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207616-
dc.description.abstractObstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and is recognised as a major public health burden. Large-scale epidemiological studies have demonstrated an independent relationship between OSAS and various cardiovascular disorders. The pathogenesis of cardiovascular complications in OSAS is not completely understood but a multifactorial aetiology is likely. Inflammatory processes have emerged as critical in the pathogenesis of atherosclerosis at all stages of atheroma formation. Increased levels of various circulating markers of inflammation including tumour necrosis factor alpha (TNFalpha), interleukin 6 (IL6), IL-8 and C-reactive protein (CRP) have been reported as associated with future cardiovascular risk. There is increasing evidence of elevated inflammatory markers in OSAS with a significant fall after effective treatment with continuous positive airway pressure. This evidence is particularly strong for TNFalpha, whereas studies on IL6 and CRP have yielded conflicting results possibly due to the confounding effects of obesity. Cell culture and animal studies have significantly contributed to our understanding of the underlying mechanisms of the association between OSAS and inflammation. Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.en_GB
dc.language.isoengen_GB
dc.subject.meshCardiovascular Diseases/*etiologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshInflammation/*complicationsen_GB
dc.subject.meshInflammation Mediators/blooden_GB
dc.subject.meshObesity/complicationsen_GB
dc.subject.meshSleep Apnea, Obstructive/blood/*complicationsen_GB
dc.titleSystemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?en_GB
dc.contributor.departmentSleep Research Laboratory, St Vincent's University Hospital, Dublin, Ireland.en_GB
dc.identifier.journalThoraxen_GB
dc.description.provinceLeinster-
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