Coronary Artery Disease
GP IIb/IIIa inhibition with eptifibatide lowers levels of soluble CD40L and RANTES after percutaneous coronary intervention
Article first published online: 23 JAN 2004
Copyright © 2004 Wiley-Liss, Inc.
Catheterization and Cardiovascular Interventions
Volume 61, Issue 2, pages 185–189, February 2004
How to Cite
Welt, F. G.P., Rogers, S. D., Zhang, X., Ehlers, R., Chen, Z., Nannizzi-Alaimo, L., Phillips, D. R. and Simon, D. I. (2004), GP IIb/IIIa inhibition with eptifibatide lowers levels of soluble CD40L and RANTES after percutaneous coronary intervention. Cathet. Cardiovasc. Intervent., 61: 185–189. doi: 10.1002/ccd.10763
- Issue published online: 23 JAN 2004
- Article first published online: 23 JAN 2004
- Manuscript Accepted: 14 OCT 2003
- Manuscript Received: 3 JUL 2003
- National Institutes of Health. Grant Numbers: R01 HL57506, R01 DK55656, AG00294-17
- Millennium Pharmaceuticals, Inc.
- GPIIb/IIIa inhibitors
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.