title: [GPIIb-IIIa inhibitors].
abstract: Therapy involving the use of anti-GPIIb-IIIa inhibitors has progressively evolved in recent years for patients undergoing percutaneous coronary intervention or with acute coronary syndromes. Patients receiving anti-GP IIb-IIIa therapy have a lower risk of death or myocardial infarction than those receiving the classic anti-agregant, aspirin, alone. Two classes of products have been used in clinic, the chimeric monoclonal antibody Fab fragment, c7E3 or abciximab (ReoPro), which has been the pioneer, and synthetic peptides or peptidomimetics such as eptifibatide (Integrilin) or tirofiban (Agrastat). Abciximab is a long-acting, high-affinity receptor blocker, whereas eptifibatide and tirofiban have much shorter biological half-lives. Another property that differentiates these compounds is that the peptides bind exclusively to GP IIb-IIIa whereas c7E3 also binds to alpha v beta 3, the vitronectin receptor. The potent inhibitory effect of these compounds increases the risk of bleeding. By carefully controlling the levels of heparin and by removing the sheath as early as possible, the hemorrhagic problems may be limited. Another potential complication is the rapid development of thrombocytopenia. The cause has yet to be found and for c7E3 no correlation with the development of HACA (human anti-chimeric antibodies) has been observed. Because of the chronic nature of coronary artery disease, evaluation of the readministration of c7E3 to the same patient two or even more times is under investigation. The first results do not show major problems. The best biological way to investigate the efficiency of anti-GPIIb-IIIa has to be determined. Interestingly, a new point-of-care test has been proposed, while monoclonal antibodies are available that differentiate between nonoccupied and occupied GPIIb-IIIa complexes.
authors.affiliation: Laboratoire d'hémobiologie-UMR 5533 CNRS, hôpital cardiologique, 33604 Pessac, France. Paquita.Nurden@cnrshl.u-bordeaux2.fr
authors.forename: P
authors.initials: P
authors.lastname: Nurden
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D003327:Coronary Disease / Q000188:drug therapy*; D000077542:Eptifibatide; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000517:prevention & control; D010455:Peptides / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban; D000077542:Eptifibatide; D001241:Aspirin; D000077284:Abciximab