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8-isoprostanes and resistin as markers of vascular damage in non-hypersomnolent obstructive sleep apnoea patients

期刊

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING
卷 37, 期 6, 页码 695-702

出版社

WILEY
DOI: 10.1111/cpf.12361

关键词

isoprostanes; non-hypersomnolent; resistin; vascular damageOSA

资金

  1. Medical University, Sofia [42/2013]

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Background: Oxidative stress and inflammation are assumed as the main pathological triggers for vascular damage in hypersomnolent obstructive sleep apnoea (OSA) patients, whereas their exact role in less symptomatic population is currently unknown. Aim: To determine whether oxidative stress (urinary 8-isoprostane concentration) and inflammation (plasma resistin levels) are associated with vascular damage in non-hypersomnolent (Epworth Sleep Score <11) OSA patients. Methods: A total of 325 consecutive patients have undergone standard polysomnography, and 256 of them were diagnosed with OSA. Excessive daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). Only 86 patients with ESS <11 participated in the study. The control group was presented by 45 subjects without OSA. Endothelial function was assessed by ultrasonographic measurement of flow-mediated dilatation (FMD). Intima-media thickness (IMT) and ankle-brachial index (ABI) were determined by ultrasonography. Urinary 8-isoprostanes (Cayman Chemical, USA) were measured, applying mass spectrometry. Resistin (RayBio_ Human ResistinCat#:ELH-Resistin-001) plasma levels were detected by ELISA. Results: In patients with OSA, flow-mediated dilatation was significantly lower than in control subjects (4.62% 1.9) and (7.1% +/- 2.8), respectively (P: 0.013). The prevalence of plaques in a.carotis communis was higher in OSA (16% versus 4%). The same is observed regarding a.tibialis posterior (81% vs. 29%). The average IMT and ABI in OSA and in the control group were, respectively, (IMT - 800 mu m versus. 66 6 mu m); (ABI -1.06 versus 1.20). Urinary isoprostanes were higher in OSA patients (0.091 versus 0.078) and correlated negatively to FMD (r: -0.825, P: 0.00), IMT (r: -0.324, P: 0.003) and ABI (r: -0.226, P: 0.043). No association between resistin and the degree of vascular injury was found. Conclusions: In comparison with the control group, increased prevalence of endothelial dysfunction and vascular damage was established in OSA patients without excessive daytime sleepiness. Urinary 8-isoprostanes (oxidative stress markers) are closely associated with FMD (endothelial dysfunction), IMT and ABI (vascular damage). Resistin plasma levels correlated neither to FMD, nor to IMT or ABI.

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