title: Oxidative stress mediated arterial dysfunction in patients with obstructive sleep apnoea and the effect of continuous positive airway pressure treatment.
abstract: BACKGROUND
  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. Further aim was to evaluate the effect of nasal continuous positive airway pressure (nCPAP) on oxidative stress and arterial dysfunction.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Patients 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%).
  
  
  CONCLUSIONS
  The 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.
authors: Department of Internal Medicine and Medical Specialities, Sapienza University, Rome, Italy. francesco.angelico@uniroma1.it.
authors: Maria
authors: M
authors: Del Ben
authors: Mario
authors: M
authors: Fabiani
authors: Lorenzo
authors: L
authors: Loffredo
authors: Licia
authors: L
authors: Polimeni
authors: Roberto
authors: R
authors: Carnevale
authors: Francesco
authors: F
authors: Baratta
authors: Marco
authors: M
authors: Brunori
authors: Fabiana
authors: F
authors: Albanese
authors: Teresa
authors: T
authors: Augelletti
authors: Francesco
authors: F
authors: Violi
authors: Francesco
authors: F
authors: Angelico
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D045422:Continuous Positive Airway Pressure; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000097:blood; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D018384:Oxidative Stress; D017286:Polysomnography; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000097:blood / Q000503:physiopathology* / Q000628:therapy / Q000652:urine; D016896:Treatment Outcome; D014463:Ultrasonography; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D008562:Membrane Glycoproteins; D009566:Nitrates; D009573:Nitrites; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; C056558:CYBB protein, human; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases