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Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?
  1. S Ryan1,2,
  2. C T Taylor2,
  3. W T McNicholas1,2
  1. 1
    Sleep Research Laboratory, St Vincent’s University Hospital, Dublin, Ireland
  2. 2
    School of Medicine and Medical Science, The Conway Institute, University College Dublin, Ireland
  1. Correspondence to Professor W T McNicholas, Department of Respiratory Medicine, St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland; walter.mcnicholas{at}


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 α (TNFα), 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 TNFα, 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-κB) 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.

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  • This is a reprint of a paper that first appeared in Thorax, July 2009, volume 64, pages 631–6

  • Funding Health Research Board (Ireland), Science Foundation of Ireland, Wellcome Trust

  • Competing interests None.