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Glycoprotein Ilb/IIIa

Deshmukh VR, Fiorella DJ, Albuquerque FC, Frey J, Flaster M, Wallace RC, Spetzler RF, McDougall CG. Intra-arterial thrombolysis for acute ischemic stroke preliminary experience with platelet glycoprotein Ilb/IIIa inhibitors as adjunctive therapy. Neurosurgery 2005 56 46-54 [discussion 54 5]. [Pg.95]

Shuaib A, Yang Y, Nakada MT, Li Q, Yang T. Glycoprotein Ilb/IIIa antagonist, murine 7e3 f(ab ) 2, and tissue plasminogen activator in focal ischemia evaluation of efficacy and risk of hemorrhage with combination therapy. J Cereb Blood Flow Metab 2002 22 215-222. [Pg.119]

Administration of clopidogrel is recommended for all patients with STE ACS (Table 5—2).3 Clopidogrel blocks adenosine diphosphate receptors on platelets, preventing the expression of glycoprotein Ilb/IIIa receptors and thus platelet activation and aggregation. [Pg.97]

Abciximab is a first-line glycoprotein Ilb/IIIa receptor inhibitor for patients undergoing primary PCI3,15,18 who have not received fibrinolytics. It should not be administered for... [Pg.97]

In general, early pharmacotherapy of NSTE ACS (Fig. 5-3) is similar to that of STE ACS with three exceptions (1) fibrinolytic therapy is not administered (2) glycoprotein Ilb/IIIa receptor blockers are administered to high-risk patients for medical therapy as well as to PCI patients and (3) at this time, there are no standard quality indicators for patients with NSTE ACS who are not diagnosed with MI. [Pg.99]

In patients with NSTE ACS scheduled for early PCI, administration of either abciximab or eptifibatide (double bolus) is recommended. The use of tirofiban in these patients is not recommended, because it has been shown to be inferior to abciximab.2 Medical therapy with glycoprotein Ilb/IIIa receptor inhibitors in patients not undergoing PCI is reserved for higher-risk patients, such as those with positive troponin or ST-segment depression, and patients who have continued or recurrent ischemia despite other antithrombotic therapy.2... [Pg.100]

Doses and contraindications to glycoprotein Ilb/IIIa receptor blockers are described in Table 5-2. Major bleeding and rates of transfusion are increased with administration of a glycoprotein Ilb/IIIa receptor inhibitor in combination with aspirin and an anticoagulant,30 but there is no increased risk of intracranial hemorrhage in the absence of concomitant fibrinolytic treatment. The risk of thrombocytopenia with tirofiban and eptifibatide appears lower than that with abciximab. Bleeding risks appear similar between agents. [Pg.100]

Because the costs for chronic preventative pharmacotherapy are the same for primary and secondary prevention, while the risk of events is higher with secondary prevention, secondary prevention is more cost effective than primary prevention of CHD. Pharmacotherapy demonstrating cost effectiveness to prevent death in the ACS and post-MI patient includes fibrinolytics ( 2,000 to 33,000 cost per year of life saved), aspirin, glycoprotein Ilb/IIIa receptor blockers ( 13,700 to 16,500 per year of life added), (3-blockers (less than 5,000 to 15,000 cost per year of life saved), ACE inhibitors ( 3,000 to 5,000 cost per year of life saved), eplerenone ( 15,300 to 32,400 per year of life gained), statins ( 4,500 to 9,500 per year of life saved) and gemfibrozil ( 17,000 per year of life saved).49-58 Because cost-effectiveness ratios of less than 50,000 per added life-year are considered economically attractive from a societal perspective,49 pharmacotherapy described above for ACS and secondary prevention are standards of care because of their efficacy and cost attractiveness to payors. [Pg.101]

Lefkovits J., Plow E. F., Topol E. Platelet glycoprotein Ilb/IIIa receptors in cardiovascular medicine. N Engl J Med 1995 332, 1553-9. [Pg.163]

Fig. 9.1. A dysfunctional or injured endothelium is at the basis for initiation of and progression to atherosclerosis. Several mechanisms, such as adhesion molecules or liberation of von Willebrand factor (vWf, upper panel), determine a series of phenomena, including platelet activation and aggregation. This participation of platelets involves the implication of molecules like glycoprotein Ilb/IIIa, fibrinogen, and von Willebrand factor. The endothelium also acts as a source of signals that regulate local functions, including VSMCs (lower panel). A list of the most relevant messengers produced by a functional and a dysfunctonal endothelium is presented in the lower panel... Fig. 9.1. A dysfunctional or injured endothelium is at the basis for initiation of and progression to atherosclerosis. Several mechanisms, such as adhesion molecules or liberation of von Willebrand factor (vWf, upper panel), determine a series of phenomena, including platelet activation and aggregation. This participation of platelets involves the implication of molecules like glycoprotein Ilb/IIIa, fibrinogen, and von Willebrand factor. The endothelium also acts as a source of signals that regulate local functions, including VSMCs (lower panel). A list of the most relevant messengers produced by a functional and a dysfunctonal endothelium is presented in the lower panel...
Badawy, S.I., Williams, R.C., and Gilbert, D.L., Chemical stability of an ester prodrug of a glycoprotein Ilb/IIIa receptor antagonist in solid dosage forms,. Pharm. Sci., 88, 428,1999. [Pg.48]

Lincoff AM, Bittl JA, Harrington RA, Feit F, Kleiman NS, Jackman JD, Sarembock IJ, Cohen DJ, Spriggs D, Ebrahimi R, Keren G Carr J, Cohen EA, Betriu A, Desmet W, Kereiakes DJ, Rutsch W, Wilcox RG de Feyter PJ, Vahanian A, Topol EJ. (2003) Bivalirudin and provisional glycoprotein Ilb/IIIa blockade compared with heparin and planned glycoprotein Ilb/nia blockade during percutaneous coronary intervention REPLACE-2 randomized trial. J Am Med Assoc (JAMA) 289 853-863. [Pg.154]

Novel inhibitors of glycoprotein Ilb/IIIa and fibrinogen/van WiUebrand interaction include injectable peptides (e.g. integrilin, 175) and orally active peptidomimetics that act as competitive inhibitors and a monoclonal antibody c7E3 (abciximab) that irreversibly binds to GP Ilb/ Ilia. [Pg.56]

Wang W, Borchardt RT, Wang B. Orally active peptidomimetic analogues that are glycoprotein Ilb/IIIa antagonists. Curr Med Chem 2000 7 437-53. [Pg.82]

Cannon C, Weintraub W, Demopoulos L, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with Glycoprotein Ilb/IIIa inhibitor Tirofiban. N Engl J of Med 2001 344 1879-1887. [Pg.82]


See other pages where Glycoprotein Ilb/IIIa is mentioned: [Pg.1493]    [Pg.145]    [Pg.145]    [Pg.145]    [Pg.282]    [Pg.24]    [Pg.84]    [Pg.85]    [Pg.97]    [Pg.98]    [Pg.98]    [Pg.99]    [Pg.100]    [Pg.136]    [Pg.136]    [Pg.156]    [Pg.568]    [Pg.600]    [Pg.184]    [Pg.243]    [Pg.65]    [Pg.405]    [Pg.319]    [Pg.56]    [Pg.150]    [Pg.73]    [Pg.75]   
See also in sourсe #XX -- [ Pg.56 ]

See also in sourсe #XX -- [ Pg.367 ]




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Glycoprotein Ilb/IIIa (GpIIb

Glycoprotein Ilb/IIIa Receptor Antagonists

Glycoprotein Ilb/IIIa antagonists

Glycoprotein Ilb/IIIa inhibitors

Glycoprotein Ilb/IIIa receptor

Glycoprotein Ilb/IIIa receptor inhibitors

Platelet glycoprotein Ilb/IIIa

Platelet glycoprotein Ilb/IIIa receptor

Platelet glycoprotein Ilb/IIIa receptor antagonists

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