Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris
<p>Abstract</p> <p>Aim</p> <p>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 monocy...
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Language: | English |
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BMC
2004-04-01
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Series: | Thrombosis Journal |
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Online Access: | http://www.thrombosisjournal.com/content/2/1/4 |
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author | Aliyev Emil Sekuri Cevad Tengiz Istemihan Bozdemir Huseyin Ercan Ertugrul Akilli Azem Akin Mustafa |
author_facet | Aliyev Emil Sekuri Cevad Tengiz Istemihan Bozdemir Huseyin Ercan Ertugrul Akilli Azem Akin Mustafa |
author_sort | Aliyev Emil |
collection | DOAJ |
description | <p>Abstract</p> <p>Aim</p> <p>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).</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p> |
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id | doaj.art-73cb7999240e453dadca368570ead4df |
institution | Directory Open Access Journal |
issn | 1477-9560 |
language | English |
last_indexed | 2024-12-22T08:45:23Z |
publishDate | 2004-04-01 |
publisher | BMC |
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series | Thrombosis Journal |
spelling | doaj.art-73cb7999240e453dadca368570ead4df2022-12-21T18:32:07ZengBMCThrombosis Journal1477-95602004-04-0121410.1186/1477-9560-2-4Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectorisAliyev EmilSekuri CevadTengiz IstemihanBozdemir HuseyinErcan ErtugrulAkilli AzemAkin Mustafa<p>Abstract</p> <p>Aim</p> <p>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).</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p>http://www.thrombosisjournal.com/content/2/1/4Unstable angina pectorisGP IIb/IIIa antagonistsInflammationCell adhesion molecules |
spellingShingle | Aliyev Emil Sekuri Cevad Tengiz Istemihan Bozdemir Huseyin Ercan Ertugrul Akilli Azem Akin Mustafa Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris Thrombosis Journal Unstable angina pectoris GP IIb/IIIa antagonists Inflammation Cell adhesion molecules |
title | Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
title_full | Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
title_fullStr | Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
title_full_unstemmed | Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
title_short | Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
title_sort | decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris |
topic | Unstable angina pectoris GP IIb/IIIa antagonists Inflammation Cell adhesion molecules |
url | http://www.thrombosisjournal.com/content/2/1/4 |
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