Obstructive sleep apnea and inflammation: relationship to cardiovascular co-morbidity

Obstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and associated with cardiovascular morbidity and mortality. The pathogenesis of cardiovascular complications in OSAS is incompletely understood but a multifactorial etiology is likely. There is emerging evidence that inflammatory processes leading to endothelial dysfunction play a pivotal role. Various studies have demonstrated elevated inflammatory markers in OSAS patients in comparison to matched control subjects with a significant fall after effective treatment with continuous positive airway pressure. Cell culture and animal studies have significantly enhanced our understanding of the mechanisms of inflammation in OSAS. Intermittent hypoxia, the hallmark feature of OSAS, leads to a preferential activation of inflammatory pathways with the downstream consequence of expression of pro-inflammatory cytokines, chemokines and adhesion molecules that may contribute to endothelial dysfunction. Further studies are required to determine the precise role of inflammation in the cardiovascular pathogenesis of OSAS, particularly its interaction with oxidative stress, obesity and metabolic dysfunction.