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Obstructive sleep apnea (OSA) is currently considered to be an inflammatory disorder. Evidence suggests that the chronic intermittent hypoxia and, possibly, sleep loss and fragmentation associated with OSA increase the levels of various markers of inflammation, oxidative stress, and procoagulant and thrombotic activity. These alterations may contribute to the development of endothelial and metabolic dysfunction, atherosclerosis and cardiovascular disorders associated with OSA. However, these alterations are also associated with OSA comorbidities, making it difficult to discern which effects are attributable to OSA and/or these other conditions. Well-designed longitudinal and interventional studies that take confounding variables into account are needed to demonstrate a causal link between OSA and inflammation, to assess specific mechanisms that could explain these alterations and to address whether they may be improved by continuous positive airway pressure therapy.
A. Lurie (Sat,) studied this question.