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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 |
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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. |
doi_str_mv | 10.1001/jama.281.15.1407 |
format | article |
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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><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 & 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&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 & 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 & 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 & 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 & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & 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. The efficacy of oral agents for chronic GP IIb/IIIa receptor
antagonism has not been sufficiently studied.</abstract><cop>Chicago, IL</cop><pub>American Medical Association</pub><pmid>10217057</pmid><doi>10.1001/jama.281.15.1407</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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ispartof | JAMA : the journal of the American Medical Association, 1999-04, Vol.281 (15), p.1407-1414 |
issn | 0098-7484 1538-3598 |
language | eng |
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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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