Published 2005
by Canadian Coordinating Office for Health Technology Assessment in Ottawa .
Written in English
Edition Notes
| Statement | Chuong Ho ... [et al.]. |
| Series | Technology report -- issue 49, Technology report (Canadian Coordinating Office for Health Technology Assessment) -- issue 49. |
| Contributions | Ho, Chuong., Canadian Coordinating Office for Health Technology Assessment. |
| The Physical Object | |
|---|---|
| Pagination | vi, 72 p. : |
| Number of Pages | 72 |
| ID Numbers | |
| Open Library | OL21393049M |
| ISBN 10 | 1894978544, 1894978552 |
Title: Intravenous Glycoprotein IIb / IIIa Antagonists: Their Benefits, Problems and Future Developments VOLUME: 10 ISSUE: 14 Author(s):Ronan Curtin Affiliation:Dept. of Clinical Pharmacology, Royal College of Surgeons in Ireland, Dublin, Ireland. Keywords:glycoprotein, abciximab, tirofiban, eptifibatide, lamifiban, partial-agonism, pia Abstract: The intravenous Glycoprotein (GP) IIb / IIIa. Abstract The rationale for developing platelet glycoprotein (GP) IIb/IIIa antagonists as antithrombotic agents for use in ischemic cardiovascular disease emerged from integrating data obtained in the early s by many different investigators working in diverse : Barry S. Coller. Peerlinck K, De Lepeleire I, Goldberg M, Farrell D, Barrett J, Hand E, Panebianco D, Deckmyn H, Vermylen J, Arnout J. MK (L,), a selective nonpeptide platelet glycoprotein IIb/IIIa antagonist, is active in man. Circulation ; – PubMed CrossRef Google ScholarCited by: 3. Glycoprotein IIb/IIIa (GPIIb/IIIa) antagonists, including abciximab and tirofiban, are administered concurrently with clopidogrel, a P2Y12antagonist, and aspirin in some patients undergoing percutaneous coronary intervention.
Glycoprotein IIb/IIIa inhibitors (GPIIb/IIIa) (e.g., tirofiban, eptifibatide and abciximab) block the contact between fibrinogen and the glycoprotein IIb/IIIa receptor on the surface of platelets (Patrono et al., ). Table 1. Guideline recommendations for available glycoprotein IIb/IIIa antagonists in the setting of PCI. Abciximab Tirofiban Eptifibatide Dosing for a minimum of 12 hours and up to 18 IV bolus of mg/kg, followed by µg/kg/min (max Glycoprotein IIb/IIIa inhibitors are frequently used during percutaneous coronary intervention (angioplasty with or without intracoronary stent placement). They work by preventing platelet aggregation and thrombus formation. They do so by inhibition of the GpIIb/IIIa receptor on the surface of the platelets. Although thrombolytic therapy is approved in several countries for treatment of ischemic stroke, only a small number of patients are eligible for treatment. Additional agents that could restore or improve cerebral flow are needed. Reperfusion agents such as platelet glycoprotein (GP) IIb/IIIa antagonists, alone or in combination with reduced doses of thrombolytic agents, have the potential for.
The glycoprotein IIb/IIIa receptor antagonists are a class of drugs used in the setting of acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). There are currently three glycoprotein receptor inhibitors (GPIs) in widespread use, abciximab, eptifibatide, and tirofiban, which have each been shown individually. Glycoprotein IIb/IIIa receptor antagonists. Routinely used in the absence of EPD (but not recommended if EPDs are used), GPIIb/IIIa receptor antagonists appear to reduce the risk of periprocedural stroke [].Careful heparin dosage (50 U/kg and ACT ~ seconds) is important to minimize the bleeding risk. Get this from a library! Glycoprotein IIb/IIIa antagonists: a systematic review of randomized clinical trials in patients undergoing percutaneous coronary intervention. [Chuong Ho; Canadian Coordinating Office for Health Technology Assessment.;]. Intravenous Antagonists The first glycoprotein IIb/IIIa antagonists developed were murine monoclonal antibodies to the glycoprotein IIb/IIIa complex. 18 The structure of the antibody was modified by replacing the constant domain of the murine antibody with the corresponding human sequence, producing a chimeric compound that was less immunogenic.
