Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris

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dc.contributor.authorErcan E.
dc.contributor.authorBozdemir H.
dc.contributor.authorTengiz I.
dc.contributor.authorSekuri C.
dc.contributor.authorAliyev E.
dc.contributor.authorAkilli A.
dc.contributor.authorAkin M.
dc.date.accessioned2019-10-27T00:22:35Z
dc.date.available2019-10-27T00:22:35Z
dc.date.issued2004
dc.departmentEge Üniversitesien_US
dc.description.abstractAim: The inflammatory response, initiated by neutrophil and monocyte adhesion to endothelial cells, is important in the pathogenesis of acute coronary syndromes. Platelets play an important role in inflammatory process by interacting with monocytes and neutrophils. In this study, we investigated the effect of tirofiban on the levels of cell adhesion molecules (soluble intercellular adhesion molecule-1, sICAM-1, and vascular cell adhesion molecule-1, sVCAM-1) in patients with unstable angina pectoris (AP). Methods: Thirty-five patients with unstable AP (Group I), ten patients with stable AP (Group II) and ten subjects who had angiographycally normal coronary arteries (Group III) were included the study. Group I was divided into two subgroups for the specific treatment regimens: Group IA (n = 15) received tirofiban and Group IB (n = 20) did not. Blood samples for investigating the cell adhesion molecules were drawn at zero time (baseline; 0 h) in all patients and at 72 h in Group I. Results: The baseline levels of sICAM-1 and sVCAM-1 were higher in Group I than in Groups II and III. They were higher in Group IA than in Group IB. However, the sICAM-1 and sVCAM-1 levels decreased significantly in Group IA after tirofiban infusion. In contrast, these levels remained unchanged or were increased above the baseline value in Group IB at 72 h. Conclusion: The levels of cell adhesion molecules in patients with unstable AP decreased significantly after tirofiban infusion. Inhibition of platelet function by specific glycoprotein IIb/IIIa antagonists may decrease platelet-mediated inflammation and the ischemic end-point. © 2004 Ercan et al; licensee BioMed Central Ltd.en_US
dc.identifier.doi10.1186/1477-9560-2-4
dc.identifier.issn1477-9560
dc.identifier.issn1477-9560en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1186/1477-9560-2-4
dc.identifier.urihttps://hdl.handle.net/11454/22616
dc.identifier.volume2en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.relation.ispartofThrombosis Journalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGP IIb/IIIa antagonistsen_US
dc.subjectInflammationCell adhesion moleculesen_US
dc.subjectUnstable angina pectorisen_US
dc.titleDecreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectorisen_US
dc.typeArticleen_US

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