The role of inflammation markers in triggering acute coronary events

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dc.contributor.authorTokaç, Mehmet
dc.contributor.authorÖzeren, Ali
dc.contributor.authorAktan, Murad
dc.contributor.authorAltunkeser, Bülent Behlül
dc.contributor.authorÖzdemir, Kurtuluş
dc.contributor.authorDüzenli, Akif
dc.contributor.authorGök, Hasan
dc.date.accessioned2020-03-26T16:46:15Z
dc.date.available2020-03-26T16:46:15Z
dc.date.issued2003
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractStudies have shown disparate results in relation to the role of plasma concentrations of inflammation markers such as fibrinogen, cytokines, and cell adhesion molecules in acute coronary syndromes. The differentiation of primary versus secondary alterations of these markers in response to acute coronary syndromes is not clear. The aim of this study was to investigate the effect of soluble cell adhesion molecules and some inflammatory markers on coronary plaque instability. The prospective study consisted of 15 patients with stable angina pectoris (SAP), 16 with unstable angina pectoris (UAP), and 16 who had undergone percutaneous transluminal coronary angioplasty (PTCA). Blood samples were obtained from the SAP group on admission, from the UAP group at the early stage of pain onset within 6h of pain, and again after 12h of pain. Samples from the PTCA group were collected before, 2, 14h after the procedure. Soluble vascular cell adhesion molecule-1 (VCAM-1), endothelial selectin, interleukin-1beta (IL-1beta) and interleukin-2 (IL-2), and C-reactive protein (CRP) were analyzed by enzyme-linked immunosorbent assay. CRP serum levels gradually increased although IL-2 gradually decreased in patients with UAP and PTCA. In addition, VCAM-1 levels were sharply decreased after the PTCA procedure. However, this value returned back to the preprocedure levels 14h after PTCA. Both CRP and IL-2 are directly involved in the triggering mechanisms of acute coronary events.en_US
dc.identifier.doi10.1007/s00380-003-0708-xen_US
dc.identifier.endpage176en_US
dc.identifier.issn0910-8327en_US
dc.identifier.issn1615-2573en_US
dc.identifier.issue4en_US
dc.identifier.pmid14520483en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage171en_US
dc.identifier.urihttps://dx.doi.org/10.1007/s00380-003-0708-x
dc.identifier.urihttps://hdl.handle.net/20.500.12395/18607
dc.identifier.volume18en_US
dc.identifier.wosWOS:000185649600002en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSPRINGERen_US
dc.relation.ispartofHEART AND VESSELSen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectadhesion moleculeen_US
dc.subjectcytokineen_US
dc.subjectfibrinogenen_US
dc.subjectC-reactive proteinen_US
dc.subjectacute coronary syndromeen_US
dc.titleThe role of inflammation markers in triggering acute coronary eventsen_US
dc.typeArticleen_US

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