At the inflammatory point of view, the levels of TNF-α, IL-6, hsCRP, adhesion molecules, and monocyte chemoattractant protein-1 were markedly and significantly elevated in patients with sleep apnea than those in normal control subjects.8–9 IL-6 and hsCRP levels were independently associated with OSAS severity as indicated by the AHI. In addition, hsCRP level is associated with visceral adipose tissue and is significantly associated with the components of insulin resistance syndrome.5 These data support the belief that inflammatory processes and metabolic syndrome are activated in atherosclerotic lesions in patients with OSAS. C-reactive protein and other inflammatory cytokines accelerate the progression of atherosclerosis in patients with OSAS. In addition, increase in circulating levels of adenosine and urinary uric acid in patients with obstructive sleep apnea are implicated with increased production of reactive oxygen species. Activation of redox-sensitive gene expression is suggested by the increase in some protein products of these genes, including vascular endothelial growth factor, erythropoietin, endothelin-1, inflammatory cytokines, and adhesion molecules.10–11 These results implicate the participation of redox-sensitive transcription factors as hypoxia-inducible factor-1, activator protein-1 and nuclear factor-κB.