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Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Cardiovascular Disease

CONTEXT Thrombus formation on disrupted atherosclerotic plaque is the major cause of acute coronary events. Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pa...

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Published in:JAMA : the journal of the American Medical Association 1999-04, Vol.281 (15), p.1407-1414
Main Authors: Vorchheimer, David A, Badimon, Juan Jose, Fuster, Valentin
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creator Vorchheimer, David A
Badimon, Juan Jose
Fuster, Valentin
description CONTEXT Thrombus formation on disrupted atherosclerotic plaque is the major cause of acute coronary events. Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway of platelet aggregation. OBJECTIVES To review mechanisms of platelet activation and aggregation and the role of the GP IIb/IIIa receptor in the acute coronary syndromes and to summarize completed clinical trials of GP IIb/IIIa receptor antagonists. DATA SOURCES English-language journal articles, reviews from a MEDLINE search from 1993 through 1998, as well as abstracts and presentations from major national or international cardiology meetings through November 1998. STUDY SELECTION/DATA EXTRACTION Randomized, placebo-controlled clinical trials testing intravenous GP IIb/IIIa receptor antagonists and having more than 500 subjects were included. Data quality and validity included publication or presentation venue. DATA SYNTHESIS/CONCLUSIONS The GP IIb/IIIa receptor is the final common pathway of platelet aggregation. Intravenous monoclonal antibody and peptide and nonpeptide antagonists of the GP IIb/IIIa receptor have been tested in randomized, placebo-controlled trials of the acute coronary syndromes and percutaneous coronary interventions. For patients undergoing percutaneous revascularization, these agents have demonstrated efficacy in reducing death, myocardial infarction, or urgent reintervention. Odds ratios of death or myocardial infarction at 30 days range from 0.42 to 0.84 for the drugs in these studies. More modest benefits have been seen in trials of IIb/IIIa receptor antagonists for patients with the acute coronary syndromes, with odds ratios for death or myocardial infarction at 30 days ranging from 0.70 to 0.89. The efficacy of oral agents for chronic GP IIb/IIIa receptor antagonism has not been sufficiently studied.
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Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway of platelet aggregation. OBJECTIVES To review mechanisms of platelet activation and aggregation and the role of the GP IIb/IIIa receptor in the acute coronary syndromes and to summarize completed clinical trials of GP IIb/IIIa receptor antagonists. DATA SOURCES English-language journal articles, reviews from a MEDLINE search from 1993 through 1998, as well as abstracts and presentations from major national or international cardiology meetings through November 1998. STUDY SELECTION/DATA EXTRACTION Randomized, placebo-controlled clinical trials testing intravenous GP IIb/IIIa receptor antagonists and having more than 500 subjects were included. Data quality and validity included publication or presentation venue. DATA SYNTHESIS/CONCLUSIONS The GP IIb/IIIa receptor is the final common pathway of platelet aggregation. Intravenous monoclonal antibody and peptide and nonpeptide antagonists of the GP IIb/IIIa receptor have been tested in randomized, placebo-controlled trials of the acute coronary syndromes and percutaneous coronary interventions. For patients undergoing percutaneous revascularization, these agents have demonstrated efficacy in reducing death, myocardial infarction, or urgent reintervention. Odds ratios of death or myocardial infarction at 30 days range from 0.42 to 0.84 for the drugs in these studies. More modest benefits have been seen in trials of IIb/IIIa receptor antagonists for patients with the acute coronary syndromes, with odds ratios for death or myocardial infarction at 30 days ranging from 0.70 to 0.89. The efficacy of oral agents for chronic GP IIb/IIIa receptor antagonism has not been sufficiently studied.</description><identifier>ISSN: 0098-7484</identifier><identifier>EISSN: 1538-3598</identifier><identifier>DOI: 10.1001/jama.281.15.1407</identifier><identifier>PMID: 10217057</identifier><identifier>CODEN: JAMAAP</identifier><language>eng</language><publisher>Chicago, IL: American Medical Association</publisher><subject>Acute Disease ; Angioplasty, Balloon, Coronary ; Anticoagulants - therapeutic use ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Cardiovascular disease ; Cardiovascular Diseases - blood ; Cardiovascular Diseases - drug therapy ; Cardiovascular Diseases - therapy ; Cerebral Hemorrhage - chemically induced ; Clinical trials ; Drug therapy ; Heart ; Heparin - therapeutic use ; Humans ; Medical sciences ; Myocardial Infarction - drug therapy ; Peptides ; Pharmacology. Drug treatments ; Platelet Activation ; Platelet Aggregation ; Platelet Aggregation Inhibitors - adverse effects ; Platelet Aggregation Inhibitors - therapeutic use ; Platelet Glycoprotein GPIIb-IIIa Complex - antagonists &amp; inhibitors ; Randomized Controlled Trials as Topic ; Thrombocytopenia - chemically induced</subject><ispartof>JAMA : the journal of the American Medical Association, 1999-04, Vol.281 (15), p.1407-1414</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Medical Association Apr 21, 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a436t-94e6ec293c8f7e9d576a1a8744b3d1aa1feca81884303e40fb0d2fdca0a897c63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1757912$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10217057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vorchheimer, David A</creatorcontrib><creatorcontrib>Badimon, Juan Jose</creatorcontrib><creatorcontrib>Fuster, Valentin</creatorcontrib><title>Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Cardiovascular Disease</title><title>JAMA : the journal of the American Medical Association</title><addtitle>JAMA</addtitle><description>CONTEXT Thrombus formation on disrupted atherosclerotic plaque is the major cause of acute coronary events. Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway of platelet aggregation. OBJECTIVES To review mechanisms of platelet activation and aggregation and the role of the GP IIb/IIIa receptor in the acute coronary syndromes and to summarize completed clinical trials of GP IIb/IIIa receptor antagonists. DATA SOURCES English-language journal articles, reviews from a MEDLINE search from 1993 through 1998, as well as abstracts and presentations from major national or international cardiology meetings through November 1998. STUDY SELECTION/DATA EXTRACTION Randomized, placebo-controlled clinical trials testing intravenous GP IIb/IIIa receptor antagonists and having more than 500 subjects were included. Data quality and validity included publication or presentation venue. DATA SYNTHESIS/CONCLUSIONS The GP IIb/IIIa receptor is the final common pathway of platelet aggregation. Intravenous monoclonal antibody and peptide and nonpeptide antagonists of the GP IIb/IIIa receptor have been tested in randomized, placebo-controlled trials of the acute coronary syndromes and percutaneous coronary interventions. For patients undergoing percutaneous revascularization, these agents have demonstrated efficacy in reducing death, myocardial infarction, or urgent reintervention. Odds ratios of death or myocardial infarction at 30 days range from 0.42 to 0.84 for the drugs in these studies. More modest benefits have been seen in trials of IIb/IIIa receptor antagonists for patients with the acute coronary syndromes, with odds ratios for death or myocardial infarction at 30 days ranging from 0.70 to 0.89. The efficacy of oral agents for chronic GP IIb/IIIa receptor antagonism has not been sufficiently studied.</description><subject>Acute Disease</subject><subject>Angioplasty, Balloon, Coronary</subject><subject>Anticoagulants - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Diseases - blood</subject><subject>Cardiovascular Diseases - drug therapy</subject><subject>Cardiovascular Diseases - therapy</subject><subject>Cerebral Hemorrhage - chemically induced</subject><subject>Clinical trials</subject><subject>Drug therapy</subject><subject>Heart</subject><subject>Heparin - therapeutic use</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Peptides</subject><subject>Pharmacology. Drug treatments</subject><subject>Platelet Activation</subject><subject>Platelet Aggregation</subject><subject>Platelet Aggregation Inhibitors - adverse effects</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Platelet Glycoprotein GPIIb-IIIa Complex - antagonists &amp; inhibitors</subject><subject>Randomized Controlled Trials as Topic</subject><subject>Thrombocytopenia - chemically induced</subject><issn>0098-7484</issn><issn>1538-3598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNpF0M1LwzAUAPAgipvTu16kiNd2eU3aJMcxdRYmiui5vKapdHTtTFJh_72BTXyXd3g_3hch10AToBTmG9xikkpIIEuAU3FCppAxGbNMyVMypVTJWHDJJ-TCuQ0NAUyckwnQFATNxJS8vHXoTWd8tOr2etjZwZu2j4qimhdFgdG70WbnBxsteo9fQ98676IAlmjrdvhBp8cObfTQOoPOXJKzBjtnro55Rj6fHj-Wz_H6dVUsF-sYOct9rLjJjU4V07IRRtWZyBFQCs4rVgMiNEajBCk5o8xw2lS0TptaI0WphM7ZjNwd-oZ9v0fjfLkZRtuHkWUKkCqRZRDQ7RGN1dbU5c62W7T78u_4AO6PIJyBXWOx1637dyITCtLAbg4sPPu_KBXPJfsF6axwwg</recordid><startdate>19990421</startdate><enddate>19990421</enddate><creator>Vorchheimer, David A</creator><creator>Badimon, Juan Jose</creator><creator>Fuster, Valentin</creator><general>American Medical Association</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19990421</creationdate><title>Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Cardiovascular Disease</title><author>Vorchheimer, David A ; Badimon, Juan Jose ; Fuster, Valentin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a436t-94e6ec293c8f7e9d576a1a8744b3d1aa1feca81884303e40fb0d2fdca0a897c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Acute Disease</topic><topic>Angioplasty, Balloon, Coronary</topic><topic>Anticoagulants - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Diseases - blood</topic><topic>Cardiovascular Diseases - drug therapy</topic><topic>Cardiovascular Diseases - therapy</topic><topic>Cerebral Hemorrhage - chemically induced</topic><topic>Clinical trials</topic><topic>Drug therapy</topic><topic>Heart</topic><topic>Heparin - therapeutic use</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Peptides</topic><topic>Pharmacology. Drug treatments</topic><topic>Platelet Activation</topic><topic>Platelet Aggregation</topic><topic>Platelet Aggregation Inhibitors - adverse effects</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Platelet Glycoprotein GPIIb-IIIa Complex - antagonists &amp; inhibitors</topic><topic>Randomized Controlled Trials as Topic</topic><topic>Thrombocytopenia - chemically induced</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vorchheimer, David A</creatorcontrib><creatorcontrib>Badimon, Juan Jose</creatorcontrib><creatorcontrib>Fuster, Valentin</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>JAMA : the journal of the American Medical Association</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vorchheimer, David A</au><au>Badimon, Juan Jose</au><au>Fuster, Valentin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Cardiovascular Disease</atitle><jtitle>JAMA : the journal of the American Medical Association</jtitle><addtitle>JAMA</addtitle><date>1999-04-21</date><risdate>1999</risdate><volume>281</volume><issue>15</issue><spage>1407</spage><epage>1414</epage><pages>1407-1414</pages><issn>0098-7484</issn><eissn>1538-3598</eissn><coden>JAMAAP</coden><abstract>CONTEXT Thrombus formation on disrupted atherosclerotic plaque is the major cause of acute coronary events. Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway of platelet aggregation. OBJECTIVES To review mechanisms of platelet activation and aggregation and the role of the GP IIb/IIIa receptor in the acute coronary syndromes and to summarize completed clinical trials of GP IIb/IIIa receptor antagonists. DATA SOURCES English-language journal articles, reviews from a MEDLINE search from 1993 through 1998, as well as abstracts and presentations from major national or international cardiology meetings through November 1998. STUDY SELECTION/DATA EXTRACTION Randomized, placebo-controlled clinical trials testing intravenous GP IIb/IIIa receptor antagonists and having more than 500 subjects were included. Data quality and validity included publication or presentation venue. DATA SYNTHESIS/CONCLUSIONS The GP IIb/IIIa receptor is the final common pathway of platelet aggregation. Intravenous monoclonal antibody and peptide and nonpeptide antagonists of the GP IIb/IIIa receptor have been tested in randomized, placebo-controlled trials of the acute coronary syndromes and percutaneous coronary interventions. For patients undergoing percutaneous revascularization, these agents have demonstrated efficacy in reducing death, myocardial infarction, or urgent reintervention. Odds ratios of death or myocardial infarction at 30 days range from 0.42 to 0.84 for the drugs in these studies. More modest benefits have been seen in trials of IIb/IIIa receptor antagonists for patients with the acute coronary syndromes, with odds ratios for death or myocardial infarction at 30 days ranging from 0.70 to 0.89. 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source AMA Current Titles
subjects Acute Disease
Angioplasty, Balloon, Coronary
Anticoagulants - therapeutic use
Biological and medical sciences
Blood. Blood coagulation. Reticuloendothelial system
Cardiovascular disease
Cardiovascular Diseases - blood
Cardiovascular Diseases - drug therapy
Cardiovascular Diseases - therapy
Cerebral Hemorrhage - chemically induced
Clinical trials
Drug therapy
Heart
Heparin - therapeutic use
Humans
Medical sciences
Myocardial Infarction - drug therapy
Peptides
Pharmacology. Drug treatments
Platelet Activation
Platelet Aggregation
Platelet Aggregation Inhibitors - adverse effects
Platelet Aggregation Inhibitors - therapeutic use
Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors
Randomized Controlled Trials as Topic
Thrombocytopenia - chemically induced
title Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Cardiovascular Disease
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