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GP IIb/IIIa inhibition with eptifibatide lowers levels of soluble CD40L and RANTES after percutaneous coronary intervention
Author(s) -
Welt Frederick G.P.,
Rogers Sarah D.,
Zhang Xiaobin,
Ehlers Raila,
Chen Zhiping,
NannizziAlaimo Lisa,
Phillips David R.,
Simon Daniel I.
Publication year - 2004
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.10763
Subject(s) - eptifibatide , medicine , abciximab , platelet , pharmacology , percutaneous coronary intervention , conventional pci , proinflammatory cytokine , platelet activation , immunology , inflammation , myocardial infarction
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. Catheter Cardiovasc Interv 2004;61:185–189. © 2004 Wiley‐Liss, Inc.