title: GP IIb/IIIa inhibition with eptifibatide lowers levels of soluble CD40L and RANTES after percutaneous coronary intervention.
abstract: Platelets are the most abundant blood source of CD40L, a proinflammatory and prothrombotic costimulatory molecule implicated in atherosclerosis. Agonist stimulation results in the secretion of a soluble form of CD40L (sCD40L) and GP IIb/IIIa receptor inhibition blocks secretion of sCD40L in vitro. However, the effect of GP IIb/IIIa inhibition on sCD40L levels in humans is unknown. Plasma sCD40L and inflammatory markers were measured (t = 0, 0.5, 2, and 24 hr post-PCI) in a cohort of patients receiving abciximab (n = 15), eptifibatide (n = 15), or no GP IIb/IIIa inhibitor (n = 15). PCI in the absence of GP IIb/IIIa inhibitor was associated with a small but measurable rise in sCD40L and the platelet-derived chemokine RANTES. In contrast, eptifibatide significantly lowered baseline sCD40L (P = 0.018) and RANTES (P = 0.006) levels. This effect was not observed with abciximab. GP IIb/IIIa inhibition with eptifibatide lowers levels of sCD40L and RANTES post-stenting, possibly conferring anti-inflammatory as well as antithrombotic effects.
authors.affiliation: West Roxbury VA Medical Center, West Roxbury, Massachusetts, USA. welt@mit.edu
authors.forename: Frederick G P
authors.initials: FG
authors.lastname: Welt
authors.forename: Sarah D
authors.initials: SD
authors.lastname: Rogers
authors.forename: Xiaobin
authors.initials: X
authors.lastname: Zhang
authors.forename: Raila
authors.initials: R
authors.lastname: Ehlers
authors.forename: Zhiping
authors.initials: Z
authors.lastname: Chen
authors.forename: Lisa
authors.initials: L
authors.lastname: Nannizzi-Alaimo
authors.forename: David R
authors.initials: DR
authors.lastname: Phillips
authors.forename: Daniel I
authors.initials: DI
authors.lastname: Simon
mesh_terms: D000077284:Abciximab; D000368:Aged; D000704:Analysis of Variance; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D023201:CD40 Ligand / Q000097:blood*; D018946:Chemokine CCL5 / Q000097:blood*; D003327:Coronary Disease / Q000097:blood* / Q000601:surgery*; D004797:Enzyme-Linked Immunosorbent Assay; D000077542:Eptifibatide; D005260:Female; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000494:pharmacology*; D010865:Pilot Projects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D018709:Statistics, Nonparametric; D015607:Stents; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D018946:Chemokine CCL5; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D023201:CD40 Ligand; D006493:Heparin; D000077542:Eptifibatide; D001241:Aspirin; D000077284:Abciximab