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Gene expression profiling in chronic obstructive pulmonary disease.

Gozal (4) argue that recurrent hypoxia–reoxygenation arising from OSA can unleash a cascade of oxygen free radicals and inflammatory mediators that contribute to vascular endothelial dysfunction through nitric oxide–mediated pathways. In concert with dysregulation of lipid metabolism, these factors may promote atherosclerosis. Such a pathophysiologic scheme could help to explain epidemiologic associations between OSA and a variety of cardiovascular diseases. Indeed, recent articles have demonstrated that, compared with subjects without OSA, those with OSA have greater evidence of subclinical atherosclerosis that is partially reversible by treatment with CPAP (15–17). The authors of these articles have done an admirable job in providing readers with fresh insights into pathophysiologic, clinical, and therapeutic implications of sleep-related breathing disorders. They have also raised awareness of deficiencies in our knowledge and of controversies in need of resolution. As the broad scope and high quality of these articles make abundantly clear, respiratory sleep medicine has truly come of age: nevertheless, exciting challenges remain.