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GP IIb/IIIa inhibition with eptifibatide lowers levels of soluble CD40L and RANTES after percutaneous coronary intervention

Authors

  • Frederick G.P. Welt MD,

    Corresponding author
    1. West Roxbury VA Medical Center, West Roxbury, Massachusetts
    2. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
    3. Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, Massachusetts
    • Cardiac Catheterization Laboratory, West Roxbury VA Medical Center, 1400 VFW Parkway, Boston, MA 02132
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  • Sarah D. Rogers PA-C,

    1. West Roxbury VA Medical Center, West Roxbury, Massachusetts
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  • Xiaobin Zhang MD,

    1. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
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  • Raila Ehlers MD,

    1. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
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  • Zhiping Chen,

    1. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
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  • Lisa Nannizzi-Alaimo,

    1. Millennium Pharmaceuticals, Inc., South San Francisco, California
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  • David R. Phillips PhD,

    1. Millennium Pharmaceuticals, Inc., South San Francisco, California
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  • Daniel I. Simon MD

    1. West Roxbury VA Medical Center, West Roxbury, Massachusetts
    2. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
    3. Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, Massachusetts
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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. Catheter Cardiovasc Interv 2004;61:185–189. © 2004 Wiley-Liss, Inc.

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