Obstructive sleep apnea and inflammation

Prog Cardiovasc Dis. Mar-Apr 2009;51(5):392-9. doi: 10.1016/j.pcad.2008.10.005.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Biomarkers / metabolism
  • C-Reactive Protein / metabolism
  • Cardiovascular Diseases / immunology*
  • Cell Adhesion Molecules / metabolism
  • Humans
  • Hypoxia / immunology
  • Inflammation / immunology*
  • Inflammation Mediators / metabolism*
  • Interleukins / metabolism
  • Obesity / immunology
  • Oxidative Stress
  • Risk Factors
  • Sleep Apnea, Obstructive / complications
  • Sleep Apnea, Obstructive / immunology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Biomarkers
  • Cell Adhesion Molecules
  • Inflammation Mediators
  • Interleukins
  • Tumor Necrosis Factor-alpha
  • C-Reactive Protein