Bivalirudin for patients with acute coronary syndromes
Identifieur interne : 004041 ( PascalFrancis/Corpus ); précédent : 004040; suivant : 004042Bivalirudin for patients with acute coronary syndromes
Auteurs : Gregg W. Stone ; Brent T. Mclaurin ; David A. Cox ; Michel E. Bertrand ; A. Michael Lincoff ; Jeffrey W. Moses ; Harvey D. White ; Stuart J. Pocock ; James H. Ware ; Frederick Feit ; Antonio Colombo ; Philip E. Aylward ; Angel R. Cequier ; Harald Darius ; Walter Desmet ; Ramin Ebrahimi ; Martial Hamon ; Lars H. Rasmussen ; Hans-Jürgen Rupprecht ; James Hoekstra ; Roxana Mehran ; E. Magnus OhmanSource :
- The New England journal of medicine [ 0028-4793 ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
BACKGROUND Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. METHODS We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. RESULTS Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P=0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). CONCLUSIONS In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.
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Format Inist (serveur)
NO : | PASCAL 06-0540370 INIST |
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ET : | Bivalirudin for patients with acute coronary syndromes |
AU : | STONE (Gregg W.); MCLAURIN (Brent T.); COX (David A.); BERTRAND (Michel E.); LINCOFF (A. Michael); MOSES (Jeffrey W.); WHITE (Harvey D.); POCOCK (Stuart J.); WARE (James H.); FEIT (Frederick); COLOMBO (Antonio); AYLWARD (Philip E.); CEQUIER (Angel R.); DARIUS (Harald); DESMET (Walter); EBRAHIMI (Ramin); HAMON (Martial); RASMUSSEN (Lars H.); RUPPRECHT (Hans-Jürgen); HOEKSTRA (James); MEHRAN (Roxana); OHMAN (E. Magnus) |
AF : | Columbia University Medical Center and the Cardiovascular Research Foundation/New York/Etats-Unis (1 aut., 6 aut., 21 aut.); AnMed Health/Anderson, SC/Etats-Unis (2 aut.); Mid Carolina Cardiology/Charlotte, NC/Etats-Unis (3 aut.); Hôpital Cardiologique/Lille/France (4 aut.); Cleveland Clinic/Cleveland/Etats-Unis (5 aut.); Auckland City Hospital/Auckland/Nouvelle-Zélande (7 aut.); London School of Hygiene and Tropical Medicine/London/Royaume-Uni (8 aut.); Harvard University/Boston/Etats-Unis (9 aut.); New York University School of Medicine/New York/Etats-Unis (10 aut.); Ospedale San Raphael/Milan/Italie (11 aut.); Flinders Medical Center/Adelaide/Australie (12 aut.); Hospital Universitari de Bellvitge/Barcelona/Espagne (13 aut.); Krankenhaus Neukölln/Berlin/Allemagne (14 aut.); University Hospital/Gasthuisberg, Leuven/Belgique (15 aut.); UCLA and the Greater Los Angeles Veterans Affairs Medical Center/Los Angeles/Etats-Unis (16 aut.); University Hospital/Normandy/France (17 aut.); Aarhus University Hospital, Aalborg Hospital/Aalborg/Danemark (18 aut.); GPR Klinikum Rüsselsheim/Rüsselsheim/Allemagne (19 aut.); Wake Forest University/Winston-Salem, NC/Etats-Unis (20 aut.); Duke University Medical Center/Durham, NC/Etats-Unis (22 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | The New England journal of medicine; ISSN 0028-4793; Coden NEJMAG; Etats-Unis; Da. 2006; Vol. 355; No. 21; Pp. 2203-2216; Bibl. 26 ref. |
LA : | Anglais |
EA : | BACKGROUND Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. METHODS We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. RESULTS Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P=0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). CONCLUSIONS In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding. |
CC : | 002B01; 002B12A03 |
FD : | Cardiopathie coronaire; Bivalirudine; Homme; Malade; Aigu; Médecine; Anticoagulant |
FG : | Antithrombine; Inhibiteur enzyme; Peptide; Polypeptide; Thrombin; Serine endopeptidases; Peptidases; Hydrolases; Enzyme; Appareil circulatoire pathologie |
ED : | Coronary heart disease; Bivalirudin; Human; Patient; Acute; Medicine; Anticoagulant |
EG : | Antithrombin; Enzyme inhibitor; Peptides; Polypeptide; Thrombin; Serine endopeptidases; Peptidases; Hydrolases; Enzyme; Cardiovascular disease |
SD : | Cardiopatía coronaria; Bivalirudina; Hombre; Enfermo; Agudo; Medicina; Anticoagulante |
LO : | INIST-6013.354000143131430070 |
ID : | 06-0540370 |
Links to Exploration step
Pascal:06-0540370Le document en format XML
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<author><name sortKey="Cequier, Angel R" sort="Cequier, Angel R" uniqKey="Cequier A" first="Angel R." last="Cequier">Angel R. Cequier</name>
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<author><name sortKey="Ebrahimi, Ramin" sort="Ebrahimi, Ramin" uniqKey="Ebrahimi R" first="Ramin" last="Ebrahimi">Ramin Ebrahimi</name>
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<author><name sortKey="Rasmussen, Lars H" sort="Rasmussen, Lars H" uniqKey="Rasmussen L" first="Lars H." last="Rasmussen">Lars H. Rasmussen</name>
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<author><name sortKey="Hoekstra, James" sort="Hoekstra, James" uniqKey="Hoekstra J" first="James" last="Hoekstra">James Hoekstra</name>
<affiliation><inist:fA14 i1="19"><s1>Wake Forest University</s1>
<s2>Winston-Salem, NC</s2>
<s3>USA</s3>
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</affiliation>
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<author><name sortKey="Mehran, Roxana" sort="Mehran, Roxana" uniqKey="Mehran R" first="Roxana" last="Mehran">Roxana Mehran</name>
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<s2>New York</s2>
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<author><name sortKey="Ohman, E Magnus" sort="Ohman, E Magnus" uniqKey="Ohman E" first="E. Magnus" last="Ohman">E. Magnus Ohman</name>
<affiliation><inist:fA14 i1="20"><s1>Duke University Medical Center</s1>
<s2>Durham, NC</s2>
<s3>USA</s3>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Bivalirudin for patients with acute coronary syndromes</title>
<author><name sortKey="Stone, Gregg W" sort="Stone, Gregg W" uniqKey="Stone G" first="Gregg W." last="Stone">Gregg W. Stone</name>
<affiliation><inist:fA14 i1="01"><s1>Columbia University Medical Center and the Cardiovascular Research Foundation</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>21 aut.</sZ>
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<author><name sortKey="Mclaurin, Brent T" sort="Mclaurin, Brent T" uniqKey="Mclaurin B" first="Brent T." last="Mclaurin">Brent T. Mclaurin</name>
<affiliation><inist:fA14 i1="02"><s1>AnMed Health</s1>
<s2>Anderson, SC</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cox, David A" sort="Cox, David A" uniqKey="Cox D" first="David A." last="Cox">David A. Cox</name>
<affiliation><inist:fA14 i1="03"><s1>Mid Carolina Cardiology</s1>
<s2>Charlotte, NC</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bertrand, Michel E" sort="Bertrand, Michel E" uniqKey="Bertrand M" first="Michel E." last="Bertrand">Michel E. Bertrand</name>
<affiliation><inist:fA14 i1="04"><s1>Hôpital Cardiologique</s1>
<s2>Lille</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lincoff, A Michael" sort="Lincoff, A Michael" uniqKey="Lincoff A" first="A. Michael" last="Lincoff">A. Michael Lincoff</name>
<affiliation><inist:fA14 i1="05"><s1>Cleveland Clinic</s1>
<s2>Cleveland</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Moses, Jeffrey W" sort="Moses, Jeffrey W" uniqKey="Moses J" first="Jeffrey W." last="Moses">Jeffrey W. Moses</name>
<affiliation><inist:fA14 i1="01"><s1>Columbia University Medical Center and the Cardiovascular Research Foundation</s1>
<s2>New York</s2>
<s3>USA</s3>
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<sZ>6 aut.</sZ>
<sZ>21 aut.</sZ>
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</author>
<author><name sortKey="White, Harvey D" sort="White, Harvey D" uniqKey="White H" first="Harvey D." last="White">Harvey D. White</name>
<affiliation><inist:fA14 i1="06"><s1>Auckland City Hospital</s1>
<s2>Auckland</s2>
<s3>NZL</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pocock, Stuart J" sort="Pocock, Stuart J" uniqKey="Pocock S" first="Stuart J." last="Pocock">Stuart J. Pocock</name>
<affiliation><inist:fA14 i1="07"><s1>London School of Hygiene and Tropical Medicine</s1>
<s2>London</s2>
<s3>GBR</s3>
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</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ware, James H" sort="Ware, James H" uniqKey="Ware J" first="James H." last="Ware">James H. Ware</name>
<affiliation><inist:fA14 i1="08"><s1>Harvard University</s1>
<s2>Boston</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Feit, Frederick" sort="Feit, Frederick" uniqKey="Feit F" first="Frederick" last="Feit">Frederick Feit</name>
<affiliation><inist:fA14 i1="09"><s1>New York University School of Medicine</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Colombo, Antonio" sort="Colombo, Antonio" uniqKey="Colombo A" first="Antonio" last="Colombo">Antonio Colombo</name>
<affiliation><inist:fA14 i1="10"><s1>Ospedale San Raphael</s1>
<s2>Milan</s2>
<s3>ITA</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Aylward, Philip E" sort="Aylward, Philip E" uniqKey="Aylward P" first="Philip E." last="Aylward">Philip E. Aylward</name>
<affiliation><inist:fA14 i1="11"><s1>Flinders Medical Center</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cequier, Angel R" sort="Cequier, Angel R" uniqKey="Cequier A" first="Angel R." last="Cequier">Angel R. Cequier</name>
<affiliation><inist:fA14 i1="12"><s1>Hospital Universitari de Bellvitge</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Darius, Harald" sort="Darius, Harald" uniqKey="Darius H" first="Harald" last="Darius">Harald Darius</name>
<affiliation><inist:fA14 i1="13"><s1>Krankenhaus Neukölln</s1>
<s2>Berlin</s2>
<s3>DEU</s3>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Desmet, Walter" sort="Desmet, Walter" uniqKey="Desmet W" first="Walter" last="Desmet">Walter Desmet</name>
<affiliation><inist:fA14 i1="14"><s1>University Hospital</s1>
<s2>Gasthuisberg, Leuven</s2>
<s3>BEL</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ebrahimi, Ramin" sort="Ebrahimi, Ramin" uniqKey="Ebrahimi R" first="Ramin" last="Ebrahimi">Ramin Ebrahimi</name>
<affiliation><inist:fA14 i1="15"><s1>UCLA and the Greater Los Angeles Veterans Affairs Medical Center</s1>
<s2>Los Angeles</s2>
<s3>USA</s3>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hamon, Martial" sort="Hamon, Martial" uniqKey="Hamon M" first="Martial" last="Hamon">Martial Hamon</name>
<affiliation><inist:fA14 i1="16"><s1>University Hospital</s1>
<s2>Normandy</s2>
<s3>FRA</s3>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rasmussen, Lars H" sort="Rasmussen, Lars H" uniqKey="Rasmussen L" first="Lars H." last="Rasmussen">Lars H. Rasmussen</name>
<affiliation><inist:fA14 i1="17"><s1>Aarhus University Hospital, Aalborg Hospital</s1>
<s2>Aalborg</s2>
<s3>DNK</s3>
<sZ>18 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rupprecht, Hans Jurgen" sort="Rupprecht, Hans Jurgen" uniqKey="Rupprecht H" first="Hans-Jürgen" last="Rupprecht">Hans-Jürgen Rupprecht</name>
<affiliation><inist:fA14 i1="18"><s1>GPR Klinikum Rüsselsheim</s1>
<s2>Rüsselsheim</s2>
<s3>DEU</s3>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hoekstra, James" sort="Hoekstra, James" uniqKey="Hoekstra J" first="James" last="Hoekstra">James Hoekstra</name>
<affiliation><inist:fA14 i1="19"><s1>Wake Forest University</s1>
<s2>Winston-Salem, NC</s2>
<s3>USA</s3>
<sZ>20 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Mehran, Roxana" sort="Mehran, Roxana" uniqKey="Mehran R" first="Roxana" last="Mehran">Roxana Mehran</name>
<affiliation><inist:fA14 i1="01"><s1>Columbia University Medical Center and the Cardiovascular Research Foundation</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ohman, E Magnus" sort="Ohman, E Magnus" uniqKey="Ohman E" first="E. Magnus" last="Ohman">E. Magnus Ohman</name>
<affiliation><inist:fA14 i1="20"><s1>Duke University Medical Center</s1>
<s2>Durham, NC</s2>
<s3>USA</s3>
<sZ>22 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">The New England journal of medicine</title>
<title level="j" type="abbreviated">N. Engl. j. med.</title>
<idno type="ISSN">0028-4793</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">The New England journal of medicine</title>
<title level="j" type="abbreviated">N. Engl. j. med.</title>
<idno type="ISSN">0028-4793</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute</term>
<term>Anticoagulant</term>
<term>Bivalirudin</term>
<term>Coronary heart disease</term>
<term>Human</term>
<term>Medicine</term>
<term>Patient</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Cardiopathie coronaire</term>
<term>Bivalirudine</term>
<term>Homme</term>
<term>Malade</term>
<term>Aigu</term>
<term>Médecine</term>
<term>Anticoagulant</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">BACKGROUND Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. METHODS We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. RESULTS Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P=0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). CONCLUSIONS In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.</div>
</front>
</TEI>
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</fA01>
<fA02 i1="01"><s0>NEJMAG</s0>
</fA02>
<fA03 i2="1"><s0>N. Engl. j. med.</s0>
</fA03>
<fA05><s2>355</s2>
</fA05>
<fA06><s2>21</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Bivalirudin for patients with acute coronary syndromes</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>STONE (Gregg W.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>MCLAURIN (Brent T.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>COX (David A.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>BERTRAND (Michel E.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>LINCOFF (A. Michael)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>MOSES (Jeffrey W.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>WHITE (Harvey D.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>POCOCK (Stuart J.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>WARE (James H.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>FEIT (Frederick)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>COLOMBO (Antonio)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>AYLWARD (Philip E.)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>CEQUIER (Angel R.)</s1>
</fA11>
<fA11 i1="14" i2="1"><s1>DARIUS (Harald)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>DESMET (Walter)</s1>
</fA11>
<fA11 i1="16" i2="1"><s1>EBRAHIMI (Ramin)</s1>
</fA11>
<fA11 i1="17" i2="1"><s1>HAMON (Martial)</s1>
</fA11>
<fA11 i1="18" i2="1"><s1>RASMUSSEN (Lars H.)</s1>
</fA11>
<fA11 i1="19" i2="1"><s1>RUPPRECHT (Hans-Jürgen)</s1>
</fA11>
<fA11 i1="20" i2="1"><s1>HOEKSTRA (James)</s1>
</fA11>
<fA11 i1="21" i2="1"><s1>MEHRAN (Roxana)</s1>
</fA11>
<fA11 i1="22" i2="1"><s1>OHMAN (E. Magnus)</s1>
</fA11>
<fA14 i1="01"><s1>Columbia University Medical Center and the Cardiovascular Research Foundation</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>21 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>AnMed Health</s1>
<s2>Anderson, SC</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Mid Carolina Cardiology</s1>
<s2>Charlotte, NC</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Hôpital Cardiologique</s1>
<s2>Lille</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Cleveland Clinic</s1>
<s2>Cleveland</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Auckland City Hospital</s1>
<s2>Auckland</s2>
<s3>NZL</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>London School of Hygiene and Tropical Medicine</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Harvard University</s1>
<s2>Boston</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>New York University School of Medicine</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>Ospedale San Raphael</s1>
<s2>Milan</s2>
<s3>ITA</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="11"><s1>Flinders Medical Center</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="12"><s1>Hospital Universitari de Bellvitge</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="13"><s1>Krankenhaus Neukölln</s1>
<s2>Berlin</s2>
<s3>DEU</s3>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="14"><s1>University Hospital</s1>
<s2>Gasthuisberg, Leuven</s2>
<s3>BEL</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="15"><s1>UCLA and the Greater Los Angeles Veterans Affairs Medical Center</s1>
<s2>Los Angeles</s2>
<s3>USA</s3>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="16"><s1>University Hospital</s1>
<s2>Normandy</s2>
<s3>FRA</s3>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="17"><s1>Aarhus University Hospital, Aalborg Hospital</s1>
<s2>Aalborg</s2>
<s3>DNK</s3>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="18"><s1>GPR Klinikum Rüsselsheim</s1>
<s2>Rüsselsheim</s2>
<s3>DEU</s3>
<sZ>19 aut.</sZ>
</fA14>
<fA14 i1="19"><s1>Wake Forest University</s1>
<s2>Winston-Salem, NC</s2>
<s3>USA</s3>
<sZ>20 aut.</sZ>
</fA14>
<fA14 i1="20"><s1>Duke University Medical Center</s1>
<s2>Durham, NC</s2>
<s3>USA</s3>
<sZ>22 aut.</sZ>
</fA14>
<fA17 i1="01" i2="1"><s1>ACUITY Investigators</s1>
<s3>INC</s3>
</fA17>
<fA20><s1>2203-2216</s1>
</fA20>
<fA21><s1>2006</s1>
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<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>6013</s2>
<s5>354000143131430070</s5>
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<fA44><s0>0000</s0>
<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>26 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>06-0540370</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>The New England journal of medicine</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>BACKGROUND Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. METHODS We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. RESULTS Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P=0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). CONCLUSIONS In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B01</s0>
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<fC02 i1="02" i2="X"><s0>002B12A03</s0>
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<fC03 i1="02" i2="X" l="SPA"><s0>Bivalirudina</s0>
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</standard>
<server><NO>PASCAL 06-0540370 INIST</NO>
<ET>Bivalirudin for patients with acute coronary syndromes</ET>
<AU>STONE (Gregg W.); MCLAURIN (Brent T.); COX (David A.); BERTRAND (Michel E.); LINCOFF (A. Michael); MOSES (Jeffrey W.); WHITE (Harvey D.); POCOCK (Stuart J.); WARE (James H.); FEIT (Frederick); COLOMBO (Antonio); AYLWARD (Philip E.); CEQUIER (Angel R.); DARIUS (Harald); DESMET (Walter); EBRAHIMI (Ramin); HAMON (Martial); RASMUSSEN (Lars H.); RUPPRECHT (Hans-Jürgen); HOEKSTRA (James); MEHRAN (Roxana); OHMAN (E. Magnus)</AU>
<AF>Columbia University Medical Center and the Cardiovascular Research Foundation/New York/Etats-Unis (1 aut., 6 aut., 21 aut.); AnMed Health/Anderson, SC/Etats-Unis (2 aut.); Mid Carolina Cardiology/Charlotte, NC/Etats-Unis (3 aut.); Hôpital Cardiologique/Lille/France (4 aut.); Cleveland Clinic/Cleveland/Etats-Unis (5 aut.); Auckland City Hospital/Auckland/Nouvelle-Zélande (7 aut.); London School of Hygiene and Tropical Medicine/London/Royaume-Uni (8 aut.); Harvard University/Boston/Etats-Unis (9 aut.); New York University School of Medicine/New York/Etats-Unis (10 aut.); Ospedale San Raphael/Milan/Italie (11 aut.); Flinders Medical Center/Adelaide/Australie (12 aut.); Hospital Universitari de Bellvitge/Barcelona/Espagne (13 aut.); Krankenhaus Neukölln/Berlin/Allemagne (14 aut.); University Hospital/Gasthuisberg, Leuven/Belgique (15 aut.); UCLA and the Greater Los Angeles Veterans Affairs Medical Center/Los Angeles/Etats-Unis (16 aut.); University Hospital/Normandy/France (17 aut.); Aarhus University Hospital, Aalborg Hospital/Aalborg/Danemark (18 aut.); GPR Klinikum Rüsselsheim/Rüsselsheim/Allemagne (19 aut.); Wake Forest University/Winston-Salem, NC/Etats-Unis (20 aut.); Duke University Medical Center/Durham, NC/Etats-Unis (22 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>The New England journal of medicine; ISSN 0028-4793; Coden NEJMAG; Etats-Unis; Da. 2006; Vol. 355; No. 21; Pp. 2203-2216; Bibl. 26 ref.</SO>
<LA>Anglais</LA>
<EA>BACKGROUND Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. METHODS We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. RESULTS Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P=0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). CONCLUSIONS In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.</EA>
<CC>002B01; 002B12A03</CC>
<FD>Cardiopathie coronaire; Bivalirudine; Homme; Malade; Aigu; Médecine; Anticoagulant</FD>
<FG>Antithrombine; Inhibiteur enzyme; Peptide; Polypeptide; Thrombin; Serine endopeptidases; Peptidases; Hydrolases; Enzyme; Appareil circulatoire pathologie</FG>
<ED>Coronary heart disease; Bivalirudin; Human; Patient; Acute; Medicine; Anticoagulant</ED>
<EG>Antithrombin; Enzyme inhibitor; Peptides; Polypeptide; Thrombin; Serine endopeptidases; Peptidases; Hydrolases; Enzyme; Cardiovascular disease</EG>
<SD>Cardiopatía coronaria; Bivalirudina; Hombre; Enfermo; Agudo; Medicina; Anticoagulante</SD>
<LO>INIST-6013.354000143131430070</LO>
<ID>06-0540370</ID>
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