{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T03:56:15Z","timestamp":1771041375233,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T00:00:00Z","timestamp":1464912000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100009086","name":"Medical University Sofia","doi-asserted-by":"publisher","award":["42\/2013"],"award-info":[{"award-number":["42\/2013"]}],"id":[{"id":"10.13039\/100009086","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Physio Funct Imaging"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Oxidative stress and inflammation are assumed as the main pathological triggers for vascular damage in hypersomnolent obstructive sleep apnoea (<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>) patients, whereas their exact role in less symptomatic population is currently unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aim<\/jats:title><jats:p>To determine whether oxidative stress (urinary 8\u2010isoprostane concentration) and inflammation (plasma resistin levels) are associated with vascular damage in non\u2010hypersomnolent (Epworth Sleep Score &lt;11)<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A total of 325 consecutive patients have undergone standard polysomnography, and 256 of them were diagnosed with<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>. Excessive daytime sleepiness was assessed by the Epworth Sleepiness Scale (<jats:styled-content style=\"fixed-case\">ESS<\/jats:styled-content>). Only 86 patients with<jats:styled-content style=\"fixed-case\">ESS<\/jats:styled-content>&lt;11 participated in the study. The control group was presented by 45 subjects without<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>. Endothelial function was assessed by ultrasonographic measurement of flow\u2010mediated dilatation (<jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content>). Intima\u2010media thickness (<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>) and ankle\u2010brachial index (<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>) were determined by ultrasonography. Urinary 8\u2010isoprostanes (Cayman Chemical,<jats:styled-content style=\"fixed-case\">USA<\/jats:styled-content>) were measured, applying mass spectrometry. Resistin (RayBio_ Human ResistinCat#:<jats:styled-content style=\"fixed-case\">ELH<\/jats:styled-content>\u2010Resistin\u2010001) plasma levels were detected by<jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In patients with<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>, flow\u2010mediated dilatation was significantly lower than in control subjects (4\u00b762% \u00b11\u00b79) and (7\u00b71% \u00b12\u00b78), respectively (<jats:italic>P<\/jats:italic>: 0\u00b7013). The prevalence of plaques in a.carotis communis was higher in<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>(16% versus 4%). The same is observed regarding a.tibialis posterior (81% vs. 29%). The average<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>in<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>and in the control group were, respectively, (<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>\u2212 800\u00a0\u00b5m versus. 666\u00a0\u00b5m); (<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>\u22121\u00b706 versus 1\u00b720). Urinary isoprostanes were higher in<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>patients (0\u00b7091 versus 0\u00b7078) and correlated negatively to<jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content>(<jats:italic>r<\/jats:italic>: \u22120\u00b7825,<jats:italic>P<\/jats:italic>: 0\u00b700),<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>(<jats:italic>r<\/jats:italic>: \u22120\u00b7324,<jats:italic>P<\/jats:italic>: 0\u00b7003) and<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>(<jats:italic>r<\/jats:italic>: \u22120\u00b7226,<jats:italic>P<\/jats:italic>: 0\u00b7043). No association between resistin and the degree of vascular injury was found.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In comparison with the control group, increased prevalence of endothelial dysfunction and vascular damage was established in<jats:styled-content style=\"fixed-case\">OSA<\/jats:styled-content>patients without excessive daytime sleepiness. Urinary 8\u2010isoprostanes (oxidative stress markers) are closely associated with<jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content>(endothelial dysfunction),<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>(vascular damage). Resistin plasma levels correlated neither to<jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content>, nor to<jats:styled-content style=\"fixed-case\">IMT<\/jats:styled-content>or<jats:styled-content style=\"fixed-case\">ABI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cpf.12361","type":"journal-article","created":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T05:06:51Z","timestamp":1464930411000},"page":"695-702","source":"Crossref","is-referenced-by-count":15,"title":["8\u2010isoprostanes and resistin as markers of vascular damage in non\u2010hypersomnolent obstructive sleep apnoea patients"],"prefix":"10.1111","volume":"37","author":[{"given":"Radostina Vlaeva","family":"Cherneva","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Division of Pulmonary Medicine Medical University Sofia Georgi Sofiiski 1str Sofia Bulgaria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zheina 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