Cardiovascular Disease

Recent studies provide strong evidence that OSA is associated with several physiologic processes that could increase risk for cardiovascular disease. First, it has been well established that OSA is associated with sympathetic activation (65). This is most pronounced in association with obstructive apneas and hypopneas during

FIGURE 4 (See color Insert.) Potential interactions between OSA, systemic inflammation, and their possible link to cardiovascular disease. Abbreviations: ROS, reactive oxygen species; ICAM-1, intercellular adhesion molecule-1; IL-8, interleukin-8; MCP-1, monocyte chemoattractant protein-1; NO, nitric oxide; OSA, obstructive sleep apnea.

FIGURE 4 (See color Insert.) Potential interactions between OSA, systemic inflammation, and their possible link to cardiovascular disease. Abbreviations: ROS, reactive oxygen species; ICAM-1, intercellular adhesion molecule-1; IL-8, interleukin-8; MCP-1, monocyte chemoattractant protein-1; NO, nitric oxide; OSA, obstructive sleep apnea.

sleep, but OSA patients also have evidence of increased sympathetic activity that persists during wakefulness (66). There is also evidence that therapy for OSA can reduce sympathetic activation, during both sleep and wakefulness (67). Obstructive apneas and hypopneas can thereby trigger significant surges in systemic blood pressure, and there is compelling evidence that OSA also increases risk for diurnal hypertension (68-70). An association between OSA and hypertension may at least partly explain the increased risk for heart disease reported in patients with OSA (71-73).

Evidence has also accumulated that OSA represents a state of oxidative stress, with increased levels of reactive oxygen species that could trigger a proinflamma-tory cytokine cascade (74). Proinflammatory cytokines, such as TNF-alpha, IL-6, and IL-8, as well as the adhesion molecules ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1), are all increased in the presence of OSA (Fig. 4). It has been demonstrated that C-reactive protein, a strong marker of cardiovascular risk, is also elevated in patients with OSA (75). There is evidence that effective therapy for OSA can reduce these proinflammatory cytokines. Since cardiovascular disease is now widely thought to involve inflammatory processes, at least at the site of localized vascular lesions, the potential role of OSA as a promoter of inflammation also warrants consideration when assessing risk for cardiovascular disease.

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