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Current Vascular Pharmacology

Editor-in-Chief

ISSN (Print): 1570-1611
ISSN (Online): 1875-6212

Intracoronary Use of GP IIb/IIIa Inhibitors in Percutaneous Coronary Interventions

Author(s): Maria De Vita, Valentina Coluccia, Francesco Burzotta, Enrico Romagnoli and Carlo Trani

Volume 10, Issue 4, 2012

Page: [448 - 453] Pages: 6

DOI: 10.2174/157016112800812764

Price: $65

Abstract

The glycoprotein (GP) IIb/IIIa receptor is critical to the process of platelet aggregation and thrombus formation as it serves as the final common pathway for platelet aggregation. For this reason, the development of GP IIb/IIIa inhibitors that block fibrinogen binding to the receptor has become an attractive strategy for antiplatelet therapy with an expected strong and specific effect. Presently, there are three commercially available GP IIb/IIIa inhibitors: abciximab, eptifibatide and tirofiban. All three drugs are commonly administered intravenously, and large-scale clinical trials have demonstrated a clear clinical benefit and good safety profile in patients at high risk, especially those undergoing percutaneous coronary interventions (PCI). Recently, several studies tested the intracoronary (IC) route for GP IIb/IIIa inhibitors in order to verify its safety and its possible superiority as compared to the intravenous (IV) route. The majority of the studies testing the IC route were conducted using abciximab and in patients with STEMI with better results in terms of myocardial reperfusion and infarct size and also promising results in terms of clinical outcome. On the IC administration of eptifibatide and tirofiban only some, even if promising, data are available. Larger and randomized studies are warranted to confirm the superiority of the IC route of administration of the GP IIb/IIIa inhibitors to the IV one in patients with coronary artery disease undergoing PCI.

Keywords: Intracoronary GP IIb/IIIa inhibitors, abciximab, tirofiban, eptifibatide, platelet aggregation, fibrinogen, percutaneous coronary interventions, myocardial reperfusion, coronary artery disease, thromboxane A2


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