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Official Journal of the Italian Society of Thoracic Endoscopy
Indexed/Abstracted in: EMBASE, Scopus
Online ISSN 1827-1723
Carpagnano G. E., Lacedonia D., Bergantino L., Sabato R., Forte L., Foschino-Barbaro M. P.
Department of Medical and Occupational Sciences, Institute of Respiratory Disease, University of Foggia, Foggia, Italy
Obstructive sleep apnea syndrome (OSAS) is gaining recognition as a cardiovascular and cerebrovascular risk factor. The putative mechanisms involved in the pathogenesis of cardiovascular disease in OSA, among others, include oxidative stress, systemic inflammation and endothelial dysfunction. Various mechanisms such as intermittent hypoxia, mechanical trauma of the airway, or obesity could cause systemic and local inflammation and excessive formation of reactive oxygen species. Further studies are required to pin-point the relationship with these processes and the development of cardiovascular disease in OSAS. Several markers of inflammation have been associated with future cardiovascular risk. These include cell adhesion molecules such ICAM-1, cytokines such as tumor necrosis factor alpha and interleukin 6, chemokines such as interleukin 8, C-reactive protein, and many others. However, despite increasing evidence that inflammatory processes play an important role in the pathogenesis of cardiovascular complications in OSAS and even though many of the markers of inflammation and oxidative stress associated with cardiovascular risk have been reported as being elevated in patients with OSAS, their monitoring is not included in the current management of this disease. The aim of this review is to spread current knowledge on biomarkers of oxidative stress, inflammation and cardiovascular function in sleep apnea, focusing on the possibility to explore them using non-invasive methods.