GPIIb-IIIa antagonists reduce thromboinflammatory processes in patients with acute coronary syndromes undergoing percutaneous coronary intervention
dc.contributor.author | Furman, Mark I. | |
dc.contributor.author | Krueger, Lori A. | |
dc.contributor.author | Linden, Matthew Dean | |
dc.contributor.author | Fox, Marsha L. | |
dc.contributor.author | Ball, Steven P. | |
dc.contributor.author | Barnard, Marc R. | |
dc.contributor.author | Frelinger, Andrew L. III | |
dc.contributor.author | Michelson, Alan D. | |
dc.date | 2022-08-11T08:10:10.000 | |
dc.date.accessioned | 2022-08-23T16:58:29Z | |
dc.date.available | 2022-08-23T16:58:29Z | |
dc.date.issued | 2005-02-01 | |
dc.date.submitted | 2012-04-25 | |
dc.identifier.citation | J Thromb Haemost. 2005 Feb;3(2):312-20. doi 10.1111/j.1538-7836.2005.01124.x | |
dc.identifier.issn | 1538-7836 (Linking) | |
dc.identifier.doi | 10.1111/j.1538-7836.2005.01124.x | |
dc.identifier.pmid | 15670038 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/43378 | |
dc.description.abstract | OBJECTIVE: To investigate the effects of abciximab, eptifibatide and no GPIIb-IIIa antagonist (control) on soluble CD40 ligand (sCD40L) and the formation of leukocyte-platelet aggregates (LPA) in 98 ACS patients undergoing percutaneus coronary intervention (PCI). BACKGROUND: sCD40L and LPA are increased in patients with ACS. METHODS: sCD40L was measured by enzyme-linked immunosorbent assay (ELISA) and LPA by whole blood flow cytometry. RESULTS: There were no baseline differences between the three groups in sCD40L and LPA. At the end of PCI, sCD40L was unchanged in the controls, decreased by 30% (P andlt; 0.001) in the abciximab group and by 11% (P andlt; 0.02) in the eptifibatide group. Eighteen to 24 h after PCI, sCD40L was unchanged in the controls, reduced 30% (P andlt; 0.001) in the abciximab-treated group and 9% (P andlt; 0.01) in the eptifibatide-treated group. At the end of PCI, circulating monocyte-platelet aggregates (MPA) were reduced by 12% (P = NS) in the abciximab-treated group, 13% in the eptifibatide-treated group (P = NS), but slightly increased in the controls (P = NS). Eighteen to 24 h after PCI, MPA were reduced by 41% (P andlt; 0.001) compared to baseline in the abciximab-treated group, by 23% (P = NS) in the eptifibatide-treated group, and 15% (P = NS) in the controls. In contrast to control patients presenting while on clopidogrel, control patients presenting not on clopidogrel demonstrated a reduction in sCD40L and LPA 18-24 h post-PCI (P = NS). At low receptor occupancy, GPIIb-IIIa antagonists did not augment the release of sCD40L or the number of circulating LPA. CONCLUSIONS: GPIIb-IIIa antagonists reduce circulating sCD40L and LPA formation in patients with ACS undergoing PCI. At low receptor occupancy, GPIIb-IIIa antagonists do not activate platelets. | |
dc.language.iso | en_US | |
dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15670038&dopt=Abstract">Link to article in PubMed</a> | |
dc.relation.url | http://dx.doi.org/10.1111/j.1538-7836.2005.01124.x | |
dc.subject | Acute Disease | |
dc.subject | Aged | |
dc.subject | Angioplasty, Balloon, Coronary | |
dc.subject | Antibodies, Monoclonal | |
dc.subject | Blood Platelets | |
dc.subject | CD40 Ligand | |
dc.subject | Coronary Disease | |
dc.subject | Female | |
dc.subject | Humans | |
dc.subject | Immunoglobulin Fab Fragments | |
dc.subject | Inflammation | |
dc.subject | Leukocytes | |
dc.subject | Male | |
dc.subject | Middle Aged | |
dc.subject | Platelet Adhesiveness | |
dc.subject | Platelet Aggregation Inhibitors | |
dc.subject | Platelet Glycoprotein GPIIb-IIIa Complex | |
dc.subject | Ticlopidine | |
dc.subject | Hematology | |
dc.subject | Oncology | |
dc.subject | Pediatrics | |
dc.title | GPIIb-IIIa antagonists reduce thromboinflammatory processes in patients with acute coronary syndromes undergoing percutaneous coronary intervention | |
dc.type | Journal Article | |
dc.source.journaltitle | Journal of thrombosis and haemostasis : JTH | |
dc.source.volume | 3 | |
dc.source.issue | 2 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/peds_hematology/55 | |
dc.identifier.contextkey | 2796543 | |
html.description.abstract | <p>OBJECTIVE: To investigate the effects of abciximab, eptifibatide and no GPIIb-IIIa antagonist (control) on soluble CD40 ligand (sCD40L) and the formation of leukocyte-platelet aggregates (LPA) in 98 ACS patients undergoing percutaneus coronary intervention (PCI).</p> <p>BACKGROUND: sCD40L and LPA are increased in patients with ACS.</p> <p>METHODS: sCD40L was measured by enzyme-linked immunosorbent assay (ELISA) and LPA by whole blood flow cytometry.</p> <p>RESULTS: There were no baseline differences between the three groups in sCD40L and LPA. At the end of PCI, sCD40L was unchanged in the controls, decreased by 30% (P andlt; 0.001) in the abciximab group and by 11% (P andlt; 0.02) in the eptifibatide group. Eighteen to 24 h after PCI, sCD40L was unchanged in the controls, reduced 30% (P andlt; 0.001) in the abciximab-treated group and 9% (P andlt; 0.01) in the eptifibatide-treated group. At the end of PCI, circulating monocyte-platelet aggregates (MPA) were reduced by 12% (P = NS) in the abciximab-treated group, 13% in the eptifibatide-treated group (P = NS), but slightly increased in the controls (P = NS). Eighteen to 24 h after PCI, MPA were reduced by 41% (P andlt; 0.001) compared to baseline in the abciximab-treated group, by 23% (P = NS) in the eptifibatide-treated group, and 15% (P = NS) in the controls. In contrast to control patients presenting while on clopidogrel, control patients presenting not on clopidogrel demonstrated a reduction in sCD40L and LPA 18-24 h post-PCI (P = NS). At low receptor occupancy, GPIIb-IIIa antagonists did not augment the release of sCD40L or the number of circulating LPA.</p> <p>CONCLUSIONS: GPIIb-IIIa antagonists reduce circulating sCD40L and LPA formation in patients with ACS undergoing PCI. At low receptor occupancy, GPIIb-IIIa antagonists do not activate platelets.</p> | |
dc.identifier.submissionpath | peds_hematology/55 | |
dc.contributor.department | Department of Pediatrics | |
dc.source.pages | 312-20 |