Optimal Use of Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Patients Undergoing Percutaneous Coronary Interventions
- 1 October 2011
- journal article
- review article
- Published by Springer Science and Business Media LLC in Drugs
- Vol. 71 (15), 2009-2030
- https://doi.org/10.2165/11595010-000000000-00000
Abstract
Discovery of the central role of platelets in the pathogenesis of acute coronary syndromes (ACS) and ischaemic complications of percutaneous coronary interventions (PCI) has led to the widespread use of oral and parenteral platelet inhibitors to treat these conditions. Glycoprotein (GP) IIb/IIIa (also known as αIIbβ3) receptors on the surface of platelets play an essential role in platelet aggregation and serve as a key mediator in the formation of arterial thrombus. When activated, GP IIb/IIIa receptors bind to fibrinogen, which serves as the ‘final common pathway’ in platelet aggregation. Of the numerous agents developed for modulating platelet activity, intravenous platelet GP IIb/IIIa receptor antagonists are the most potent. There are four agents in clinical use, including abciximab, eptifibatide, tirofiban and lamifiban, although lamifiban is not approved for use in the US. While all agents block fibrinogen binding to GP IIb/IIIa, they do so by different mechanisms. Abciximab is a humanized form of a murine monoclonal antibody directed against GP IIb/IIIa, eptifibatide is a synthetic, cyclic heptapeptide that contains a lysine-glycine-aspartic acid (KGD) sequence that mimics the arginine-glycine-aspartic acid (RGD) sequence found on GP IIb/IIIa, tirofiban is a non-peptide antagonist derived by optimization of the tyrosine analogue that structurally mimicks the RGD-containing loop of the disintegrin echistatin, and lamifiban is a synthetic, non-cyclic, non-peptide, low-molecular-weight compound. In clinical trials, use of these agents reduces ischaemic adverse cardiovascular events in patients with ACS undergoing PCI, but at a cost of increased bleeding.Keywords
This publication has 121 references indexed in Scilit:
- Activation of Protease-Activated Receptors 3 and 4 Accelerates Tissue Factor–Induced Thrombin Generation on the Surface of Vascular Smooth Muscle CellsArteriosclerosis, Thrombosis, and Vascular Biology, 2010
- Megakaryocyte impairment by eptifibatide-induced antibodies causes prolonged thrombocytopeniaBlood, 2009
- P2Y12 inhibitors: differences in properties and mechanisms of action and potential consequences for clinical useEuropean Heart Journal, 2009
- ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction) Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency MedicineJournal of the American College of Cardiology, 2007
- Clinical Pharmacokinetics of Tirofiban, a Nonpeptide Glycoprotein IIb/IIIa Receptor AntagonistClinical Pharmacokinetics, 2002
- LamifibanDrugs, 1999
- Aspirin, Heparin, or Both to Treat Acute Unstable AnginaNew England Journal of Medicine, 1988
- Aspirin and Dipyridamole in the Prevention of Re-Stenosis after Percutaneous Transluminal Coronary AngioplastyNew England Journal of Medicine, 1988
- Aspirin, Sulfinpyrazone, or Both in Unstable AnginaNew England Journal of Medicine, 1985
- Protective Effects of Aspirin against Acute Myocardial Infarction and Death in Men with Unstable AnginaNew England Journal of Medicine, 1983