Oxidative stress mediated arterial dysfunction in patients with obstructive sleep apnoea and the effect of continuous positive airway pressure treatment

Maria Del Ben,Teresa Augelletti,Francesco Angelico,Francesco Violi,Licia Polimeni,Lorenzo Loffredo,Marco Brunori,Mario Fabiani,Fabiana Albanese,Francesco Baratta,Roberto Carnevale

doi:10.1186/1471-2466-12-36

Abstract

BackgroundSeveral studies suggest an increase of oxidative stress and a reduction of endothelial function in obstructive sleep apnoea syndrome (OSAS). We assessed the association between OSAS, endothelial dysfunction and oxidative stress. Further aim was to evaluate the effect of nasal continuous positive airway pressure (nCPAP) on oxidative stress and arterial dysfunction.MethodsWe studied 138 consecutive patients with heavy snoring and possible OSAS. Patients underwent unattended overnight home polysomnography. Ten patients with severe OSAS were revaluated after 6 months of nCPAP therapy. To assess oxidative stress in vivo, we measured urinary 8-iso-PGF2α and serum levels of soluble NOX2-derived peptide (sNOX2-dp). Serum levels of nitrite/nitrate (NOx) were also determined. Flow-mediated brachial artery dilation (FMD) was measured to asses endothelial function.ResultsPatients with severe OSAS had higher urinary 8-iso-PGF2α (p<0.001) and serum NOX2 and lower NOx. A negative association was observed between FMD and OSA severity. Apnea/hypopnea index was significantly correlated with the indices of central obesity and with urinary 8-isoprostanes (r=0.298, p<0.001). The metabolic syndrome (t=-4.63, p<0.001) and urinary 8-isoprostanes (t=-2.02, p<0.05) were the only independent predictors of FMD. After 6-months nCPAP treatment, a significant decrease of serum NOX2, (p<0.005) and urinary 8-iso-PGF2α (p<0.01) was observed, while serum NOx showed only a minor increase. A statistically significant increase of FMD was observed (from 3.6% to 7.0%).ConclusionsThe results of our study indicate that patients with OSAS and cardiometabolic comorbidities have increased oxidative stress and arterial dysfunction that are partially reversed by nCPAP treatment.

Highlights

Several studies suggest an increase of oxidative stress and a reduction of endothelial function in obstructive sleep apnoea syndrome (OSAS)
The majority of OSAS patients show the cluster of metabolic and non-metabolic cardiovascular risk factors of the metabolic syndrome and it has suggested that OSA may be a manifestation of metabolic syndrome (MS) [2,3,4]
A strong positive association was observed between OSA severity and the indices of central obesity, i.e. body mass index (p=

Summary

Introduction

Several studies suggest an increase of oxidative stress and a reduction of endothelial function in obstructive sleep apnoea syndrome (OSAS). We assessed the association between OSAS, endothelial dysfunction and oxidative stress. Previous studies have demonstrated that total nitrate and nitrite (NOx) production is lower in OSAS patients than in controls [12,13]. Both oxidative stress and inflammation are major components in the initiation and development of endothelial dysfunction, which is widely accepted as an early marker of atherosclerosis. Endothelial function, which is the result of a reduction in NO bioavailability, is markedly reduced in patients with moderate/severe OSAS [17,18,19,20,21,22,23]. The biological mechanisms which may explain the association of OSA with endothelial dysfunction are still under debate

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