Platelet Glycoprotein IIb/IIIa Inhibitors and an Invasive Strategy

Abstract

With the importance of plaque rupture and thrombosis in acute coronary syndromes (ACS) and the problem of distal embolization during percutaneous coronary intervention (PCI) (1), inhibition of platelet aggregation by platelet glycoprotein (GP) IIB/IIIA receptor antagonists has taken on a central role. By preventing the final common pathway of platelet aggregation, i.e., fibrinogen-mediated crosslinkage of platelets via the GPIIB/IIIA receptor, these agents can potently inhibit platelet aggregation caused by all types of stimuli (e.g., thrombin, ADP, collagen, and others). Three agents, abciximab, tirofiban, and eptifibatide, are now approved for use in coronary angioplasty, and the latter two are also approved for treatment of unstable angina/non-ST elevation myocardial infarction (UA/ NSTEMI) in patients not necessarily undergoing angioplasty. Abciximab is a monoclonal antibody Fab fragment directed at the GPIIB/IIIA receptor. Eptifibatide, a synthetic heptapeptide, and tirofiban, a nonpeptide molecule, are antagonists of the GPIIB/IIIA receptor whose structure mimics the arginine-glycine-aspartic acid (abbreviated RGD) amino acid sequence by which fibrinogen binds to the GPIIB/IIIA receptor.