Published ahead of print on November 1, 2007, doi:10.1164/rccm.200608-1190PP
© 2008 American Thoracic Society doi: 10.1164/rccm.200608-1190PP
Cardiovascular Morbidity in Obstructive Sleep ApneaOxidative Stress, Inflammation, and Much More1 Kosair Children's Hospital Research Institute, and Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Louisville, Kentucky Correspondence and requests for reprints should be addressed to David Gozal, M.D., Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, 570 South Preston Street, Suite 204, Louisville, KY 40202. E-mail: david.gozal{at}louisville.edu ABSTRACT Sleep-disordered breathing and obstructive sleep apnea (OSA) are highly prevalent disorders throughout the lifespan, which may affect up to 2–10% of the population, and have now been firmly associated with an increased risk for cardiovascular and neurobehavioral complications. Nevertheless, the overall pathophysiologic mechanisms mediating end-organ injury in OSA remain undefined, particularly due to the very frequent coexistence of other disease states, such as obesity, that clearly complicate the potential cause–effect relationships. Two major, and to some extent overlapping, mechanisms have been proposed to explain the morbid consequences of OSA, namely increased generation and propagation of reactive oxygen species and initiation and amplification of inflammatory processes. The evidence supporting the validity of these concepts as well as that detracting from such mechanisms will be critically reviewed in the context of clinical and laboratory-based approaches. In addition, some of the contradictory issues raised by such evaluation of the literature will be interpreted in the context of putative modifications of the individual responses to OSA, as determined by genetic variants among susceptibility-related genes, and also by potential environmental modulators of the phenotypic expression of any particular end-organ morbidity associated with OSA.
Key Words: inflammation • oxidative stress • reactive oxygen species • intermittent hypoxia • sleep fragmentation Related articles in AJRCCM:
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