Oxidative stress and cardiovascular complications in sleep apnea.

A recent letter in CHEST (May 2004) by Teramoto and colleagues1 on the role of interleukin (IL)-6 in the pathogenesis of obesity and obstructive sleep apnea (OSA) supported our findings suggesting this measurement for screening and monitoring OSA.2 More importantly, their data show a good correlation between plasma concentrations of proinflammatory cytokines (IL-6 and tumor necrosis factor) and C-reactive protein (CRP) as markers of cardiovascular complications. This supports the idea that inflammatory processes are activated in atherosclerotic lesions in patients with OSA. We demonstrated that in these subjects, 8-isoprostane levels were elevated either in plasma or in exhaled breath condensate, indicating increased oxidative stress in OSA.2 Several mechanisms may be responsible for the oxidativeantioxidative imbalance in OSA patients, including recurrent hypoxia and reoxygenation during sleep, the increase in adrenergic activity, the marked reduction in rapid eye movement, and the continuous damage of upper airway mucosa as a result of recurred mechanical obstruction during the sleep.3 In addition, we showed a good correlation between IL-6 and 8-isoprostane. Proinflammatory cytokines, CRP, and oxidative stress could act in synergy to explain the acceleration in atherosclerosis progression, and the high frequency of cardiovascular consequence in OSA patients. Because continuous positive airway pressure treatment reduces the levels of IL-6, CRP, and, as we showed, 8-isoprostane, this therapy may suppress the systemic and local inflammation and oxidative-antioxidative imbalance in OSA, and thus reduce the progression of atherosclerotic lesions and reduce cardiovascular complications in OSA patients.