Platelet Membrane Receptor Glycoprotein IIb/IIIa Antagonism in Unstable Angina

Théroux, Pierre; Kouz, Simon; Roy, Louis; Knudtson, Merril L.; Diodati, Jean G.; Marquis, Jean-François; Nasmith, James; Fung, A.; Boudreault, Jean-Roch; Delage, F; Dupuis, R.; Kells, Catherine; Bokslag, M.; Steiner, Beat; Rapold, Hans J.

doi:10.1161/01.cir.94.5.899

Cited by 168 publications

(65 citation statements)

References 22 publications

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“…Theroux and colleagues 14 did not report this outcome. As with other GPAs used for strategy 1, there is a suggestion of lower rates associated with treatment, but this is not statistically significant.…”

Section: Lamifibanmentioning

confidence: 87%

“…Where this was the case, RRRs at 30 days were used instead (four out of seven strategy 1 trials; 10,11,14,40 no strategy 2 trials; four out of 10 strategy 3 trials [42][43][44][45] ). If neither 30-day nor 6-month data were available the trial was excluded; this applied to one small trial only.…”

Section: Pooling Of Datamentioning

confidence: 99%

“…Unlike the latter two agents, lamifiban is not licensed for use in the UK and so was not included in the recent NICE update review. 34 However, for the purpose of the decision model it was decided (2000), 6,48 Akkerhuis (2000), 50 Dyke (2000), 51 Lincoff (2000), 52 Roe (2000), 53 Boersma (2000); 54 PRISM-PLUS: Theroux (2000); 55 The Phase II study 14 had a slightly lower validity assessment than the Phase II/III studies (PARAGON A 11 and PARAGON B 44 ). There was imbalance among the groups with regard to baseline characteristics and prognostically significant variables, which were not adjusted for in the analysis of end-points.…”

Section: Lamifibanmentioning

confidence: 99%

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Cost-effectiveness of alternative strategies for the initial medical management of non-ST elevation acute coronary syndrome: systematic review and decision-analytical modelling

Robinson

Palmer²,

Sculpher³

et al. 2005

Health Technol Assess

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Non-UK purchasers will have to pay a small fee for post and packing. For European countries the cost is £2 per monograph and for the rest of the world £3 per monograph.You can order HTA monographs from our Despatch Agents:-fax (with credit card or official purchase order) -post (with credit card or official purchase order or cheque) -phone during office hours (credit card only).Additionally the HTA website allows you either to pay securely by credit card or to print out your order and then post or fax it. NHS libraries can subscribe free of charge. Public libraries can subscribe at a very reduced cost of £100 for each volume (normally comprising 30-40 titles). The commercial subscription rate is £300 per volume. Please see our website for details. Subscriptions can only be purchased for the current or forthcoming volume. Contact details are as follows: Payment methods Paying by chequeIf you pay by cheque, the cheque must be in pounds sterling, made payable to Direct Mail Works Ltd and drawn on a bank with a UK address. Paying by credit cardThe following cards are accepted by phone, fax, post or via the website ordering pages: Delta, Eurocard, Mastercard, Solo, Switch and Visa. We advise against sending credit card details in a plain email. Paying by official purchase orderYou can post or fax these, but they must be from public bodies (i.e. NHS or universities) within the UK. We cannot at present accept purchase orders from commercial companies or from outside the UK. How do I get a copy of HTA on CD?Please use the form on the HTA website (www.hta.ac.uk/htacd.htm). Or contact Direct Mail Works (see contact details above) by email, post, fax or phone. HTA on CD is currently free of charge worldwide.The website also provides information about the HTA Programme and lists the membership of the various committees. HTA NHS R&D HTA ProgrammeT he research findings from the NHS R&D Health Technology Assessment (HTA) Programme directly influence key decision-making bodies such as the National Institute for Health and Clinical Excellence (NICE) and the National Screening Committee (NSC) who rely on HTA outputs to help raise standards of care. HTA findings also help to improve the quality of the service in the NHS indirectly in that they form a key component of the 'National Knowledge Service' that is being developed to improve the evidence of clinical practice throughout the NHS.The HTA Programme was set up in 1993. Its role is to ensure that high-quality research information on the costs, effectiveness and broader impact of health technologies is produced in the most efficient way for those who use, manage and provide care in the NHS. 'Health technologies' are broadly defined to include all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care, rather than settings of care.The HTA Programme commissions research only on topics where it has identified key gaps in the evidence needed by the NHS. Suggestions for topics are actively sought from people working in the NHS,...

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Section: Lamifibanmentioning

confidence: 87%

Section: Pooling Of Datamentioning

confidence: 99%

Section: Lamifibanmentioning

confidence: 99%

See 1 more Smart Citation

Cost-effectiveness of alternative strategies for the initial medical management of non-ST elevation acute coronary syndrome: systematic review and decision-analytical modelling

Robinson

Palmer²,

Sculpher³

et al. 2005

Health Technol Assess

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“…Thrombocytopenia occurred in patients also receiving heparin. 126 Other oral agents, such as sibrafiban and xemilofiban, are in de~elopment. '~', 12 * The safety and optimal administration of oral GP IIb-IXIa inhibitors are as yet unknown.…”

Section: Individual Antiplatelet Agentsmentioning

confidence: 99%

Platelet‐endothelial interactions in atherothrombotic disease: Therapeutic implications

Wilson

Ferguson

1999

Clinical Cardiology

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The role of the platelet and the endothelium in the pathogenesis of atherosclerosis and subsequent ischemic events has been the subject of extensive investigation. Arterial sites where endothelial function is severely impaired are often the sites of atheroma development. Lesion evolution impairs endothelial function, leading to a self‐perpetuating cycle of growth. During early lesion development, overt thrombotic events are rare. However, rupture of an advanced, necrotic plaque or intimal ulceration triggers arterial thrombosis, at which point the importance of platelet function may be seen clearly. The Antiplatelet Trialists' Collaboration meta‐analysis demonstrated the benefit of antiplatelet therapy to patients with atherosclerotic disease. Aspirin is the most widely studied agent and is considered the standard of antiplatelet therapy. Newer agents that intervene at different stages of the platelet activation pathway have been developed. Clopidogrel, a new adenosine diphosphate receptor antagonist, is more effective than aspirin in reducing vascular events in patients with prior myocardial infarction, stroke, or established peripheral arterial disease. The glycoprotein IIb‐IIIa antagonists such as abciximab have proven effective in the setting of active arterial thrombosis and percutaneous revascularization, but their value in secondary prevention remains unknown. All patients with atherosclerosis should be treated with an antiplatelet drug. Current evidence suggests that either aspirin or clopidogrel are appropriate first‐line agents. There is urgent need for an analysis of the risk/benefit ratio in various populations and clinical settings to determine the most appropriate type and intensity of therapy for a given patient.

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“…O anticorpo monoclonal contra a GP IIb/IIIa, ou abciximab, tem sido extensivamente estudado em pacientes submetidos a intervenções coroná-rias [5][6][7][8][9][10][11] , sendo o primeiro de uma série de agentes a ser introduzido para o uso clínico. Um número expressivo de outros bloqueadores peptídicos e não peptídicos do receptor plaquetário GP IIb/IIIa também estão sendo avaliados em estudos clínicos de fase II e III [12][13][14][15][16][17][18][19] . Esta atualização tem por finalidade descrever como estes potentes agentes antiplaquetários atuam e discutir as situações clínicas em que há benefí-cio potencial ou demonstrado com o seu uso, baseado nos resultados de estudos clínicos randomizados.…”

unclassified

Inibição do receptor plaquetário glicoproteína (GP) IIb/IIIa em síndromes isquêmicas agudas e intervenções coronárias

Caramori¹,

J²,

Zago³

et al. 1998

Arq. Bras. Cardiol.

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A progressiva compreensão do papel primordial que as plaquetas desempenham na doença cardiovascular, particularmente em síndromes isquêmicas agudas, tem aberto grandes oportunidades terapêuticas em cardiologia [1][2][3][4] . Os bloqueadores do receptor plaquetário glicoproteína (GP) IIb/IIIa, que inibem a via comum da agregação plaquetária, possuem um grande potencial terapêutico em pacientes submetidos a intervenções coronárias e no manejo de síndromes coronárias agudas. O anticorpo monoclonal contra a GP IIb/IIIa, ou abciximab, tem sido extensivamente estudado em pacientes submetidos a intervenções coroná-rias 5-11 , sendo o primeiro de uma série de agentes a ser introduzido para o uso clínico. Um número expressivo de outros bloqueadores peptídicos e não peptídicos do receptor plaquetário GP IIb/IIIa também estão sendo avaliados em estudos clínicos de fase II e III [12][13][14][15][16][17][18][19] . Esta atualização tem por finalidade descrever como estes potentes agentes antiplaquetários atuam e discutir as situações clínicas em que há benefí-cio potencial ou demonstrado com o seu uso, baseado nos resultados de estudos clínicos randomizados. Adicionalmente, discutiremos o uso dos bloqueadores do receptor GP IIb/ IIIa em associação com stents em intervenções coronárias. Síndromes isquêmicas agudas e os receptores GP IIb/IIIaA ruptura do endotélio sobre uma placa arteroscleróti-ca é responsável pela maioria das síndromes coronárias agudas. A exposição dos componentes subendoteliais inicia a cascata da coagulação e provê as condições para ativação plaquetária 20 . As plaquetas possuem receptores que interagem com glicoproteínas subendoteliais, como o colágeno e o fator von Willebrand, aderindo ao tecido vascular desprovido de endotélio. A adesão estimula a ativação plaquetária. As plaquetas ativadas sofrem modificações conformacionais com aumento da sua superfície e liberam agonistas como o tromboxano A 2 , a adenosina difosfato e a serotonina 21 . Estes agonistas, por sua vez, ativam outras plaquetas. As alterações conformacionais secundá-rias a ativação levam à exteriorização dos receptores GP IIb/ IIIa na superfície da membrana plaquetária [22][23][24] . Os receptores GP IIb/IIIa ligam-se a proteínas plasmáticas, como o fibrinogênio e o fator von Willebrand, determinando a agregação plaquetária 25 .A cascata da coagulação ativada leva a conversão do fibrinogênio à fibrina. A fibrina estabiliza as pontes que ligam as plaquetas, criando uma rede de plaquetas e fibrina. Paralelamente, a cascata da coagulação forma trombina, que é um potente ativador plaquetário, e amplifica o processo de agregação 26 . A trombina liga-se a hemá-cias e ao agregado plaquetário, formando um coágulo rico em plaquetas. Isto causa obstrução total ou parcial do fluxo sangüíneo através da artéria coronária acometida, causando isquemia miocárdica 27,28 .O receptores GP IIb/IIIa são os receptores mais abundantes na superfície plaquetária 29 . Eles pertencem a uma grande família de receptores, comumente denominados, "integrinas" 30,31 , qu...

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Platelet Membrane Receptor Glycoprotein IIb/IIIa Antagonism in Unstable Angina

Abstract: The nonpeptide GP IIb/IIIa antagonist lamifiban protected patients with unstable angina from severe ischemic events during a 3- to 5-day infusion and reduced the incidence of death and infarction at 1 month, suggesting considerable promise for this new therapeutic approach.

Cited by 168 publications

References 22 publications

Cost-effectiveness of alternative strategies for the initial medical management of non-ST elevation acute coronary syndrome: systematic review and decision-analytical modelling

Cost-effectiveness of alternative strategies for the initial medical management of non-ST elevation acute coronary syndrome: systematic review and decision-analytical modelling

Platelet‐endothelial interactions in atherothrombotic disease: Therapeutic implications

Inibição do receptor plaquetário glicoproteína (GP) IIb/IIIa em síndromes isquêmicas agudas e intervenções coronárias

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