Obstructive sleep apnea, Oxidative stress and Endotelial Dysfunction
F. Angelico, M. Del Ben, M. Fabiani,
Department of Internal Medicine and Medical Specialities, Sapienza University, Rome, Italy
Several studies have provided evidence supporting an increase of oxidative stress in OSAS. Oxidative stress is a major component in the initiation and development of endothelial dysfunction, which is widely accepted as an early marker of atherosclerosis. Endothelial dysfunction is markedly reduced in patients with moderate/severe OSAS.
Aim of our study was to assess the association between OSAS, endothelial dysfunction and oxidative stress. Further aim was to evaluate the effect of nasal continuous positive airway pressure (CPAP) on oxidative stress and arterial dysfunction.
We studied 138 consecutive patients who were referred because of suspected metabolic disorders with heavy snoring. Patients underwent unattended overnight home polysomnography. Furthermore, 10 patients with severe OSAS were revaluated after 6 months of nCPAP therapy. To assess oxidative stress in vivo, we measured urinary 8-iso-PGF2α, which is a reliable marker of lipoperoxidation. Flow-mediated brachial artery dilation (FMD) was measured to assess endothelial function.
As compared to non-OSAS, patients with severe OSAS had statistically significant higher urinary 8-iso-PGF2α (p Our results suggest that OSAS may cause oxidative stress, thus promoting arterial dysfunction. An open question is whether OSA itself results in oxidative stress and arterial dysfunction or it is simply a consequence of metabolic comorbidities frequently associated to OSAS. In fact, in a previous paper, we provided evidence that patients with metabolic syndrome have lower FMD and increased urinary 8-iso-PGF2α, as compared to controls.
After 6 months on nCPAP treatment, a decrease of urinary 8-iso-PGF2α (p suggesting a reduction of oxidative stress and an improvement of endothelial dysfunction. This is the first study to demonstrate the efficacy of nCPAP therapy on oxidative stress and arterial dysfunction independent from weight loss and risk factor management.
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