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Titolo:
Platelet aggregation inhibition with glycoprotein IIb-IIIa inhibitors
Autore:
Proimos, G;
Indirizzi:
Epsworth Hosp, Victorian Heart Ctr, Richmond 3121, Australia Epsworth Hosp Richmond Australia 3121 eart Ctr, Richmond 3121, Australia
Titolo Testata:
JOURNAL OF THROMBOSIS AND THROMBOLYSIS
fascicolo: 2, volume: 11, anno: 2001,
pagine: 99 - 110
SICI:
0929-5305(200104)11:2<99:PAIWGI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERCUTANEOUS CORONARY INTERVENTION; MURINE MONOCLONAL-ANTIBODY; ISCHEMIC-HEART-DISEASE; CHIMERIC 7E3 FAB; ARG-GLY-ASP; GPIIB/IIIA INHIBITORS; PLASMA-MEMBRANES; CALCIUM-BINDING; UNSTABLE ANGINA; BLEEDING-TIME;
Keywords:
platelet aggregation; inhibition; GP IIb-IIIa inhibitors; pharmacology;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Proimos, G Epsworth Hosp, Victorian Heart Ctr, Consulting Rooms,Level 6,Suite 6-1,80 Bridge Rd, Richmond 3121, Australia Epsworth Hosp Consulting Rooms,Level 6,Suite 6-1,80 Bridge Rd Richmond Australia 3121
Citazione:
G. Proimos, "Platelet aggregation inhibition with glycoprotein IIb-IIIa inhibitors", J THROMB TH, 11(2), 2001, pp. 99-110

Abstract

Inhibitors of the platelet receptor glycoprotein (GP) IIb-IIIa are a noveland potent class of antithrombotic drugs for the management of patients with non-ST-segment elevation acute coronary syndromes (ACS) and those undergoing percutaneous coronary intervention (PCI). Pharmacodynamic studies withthree currently approved agents in this class (abciximab [ReoPro (R), Centocor, Inc., Malvern, Pennsylvania, and Eli Lilly & Company, Indianapolis, Indiana]; eptifibatide [INTEGRILIN (R), COR Therapeutics, Inc., South San Francisco, California, and Key Pharmaceuticals, Inc., Kenilworth, New Jersey]; and tirofiban HCI [Aggrastat (R), Merck & Co., Inc., Whitehouse Station, New Jersey]) all sought to identify dosing regimens that would establish and maintain > 80 % inhibition of ex vivo platelet aggregation throughout theduration of intravenous infusion. Direct comparison of these prior studiesis difficult, however, because the assays used different anticoagulants (sodium citrate [abciximab, tirofiban HCI] or D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone [PPACK] [eptifibatide]) and different concentrations of the platelet agonist adenosine diphosphate (ADP) (5 mu mol [tirofiban HCI] or 20 mu mol [abciximab, eptifibatide]). More recent work has attempted to overcome these limitations by using similar assay conditions for all GP IIb-IIIa inhibitors. These studies have indicated that the concentrationsof all three agents required to provide the targeted effect for platelet inhibition are considerably higher in the presence of an anticoagulant that does not chelate calcium ions (e.g., heparin or PPACK) than in the presenceof calcium-chelating anticoagulant (i.e., sodium citrate). Of the three currently approved GP IIb-IIIa inhibitors, eptifibatide is the only agent whose approved dosing is based on an ex vivo platelet aggregation assay that uses such an anticoagulant. Additionally, Kereiakes et al. have recently reported that the high levels of platelet inhibition (> 80 %), using PPACK as an anticoagulant and ADP (20 mu mol) as an agonist, are more consistently achieved with the approved dosing regimen of eptifibatide. The antiplatelet effect of abciximab showed more interpatient variability, whereas the median inhibition of ex vivo platelet aggregation with the approved dosing regimen for tirofiban HCl was < 80 % at almost all time points during drug infusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 01:12:42