Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL
Identifieur interne : 002014 ( PascalFrancis/Corpus ); précédent : 002013; suivant : 002015Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL
Auteurs : C. Ceconi ; S. B. Freedman ; J. C. Tardif ; P. Hildebrandt ; T. Mcdonagh ; P. Gueret ; G. Parrinello ; M. Robertson ; P. G. Steg ; M. Tendera ; I. Ford ; K. Fox ; R. FerrariSource :
- International journal of cardiology [ 0167-5273 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12 months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n=220 ivabradine; n = 206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, - 1.48 ± 13.00 mL/m2) versus an increase with placebo (1.85 ± 10.54 mL/m2) (P = 0.018). There was an increase in LV ejection fraction with ivabradine (2.00± 7.02%) versus no change with placebo (0.01 ± 6.20%) (P=0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r=0.18, P=0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
| pA |
|
|---|
Format Inist (serveur)
| NO : | PASCAL 11-0100745 INIST |
|---|---|
| ET : | Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL |
| AU : | CECONI (C.); FREEDMAN (S. B.); TARDIF (J. C.); HILDEBRANDT (P.); MCDONAGH (T.); GUERET (P.); PARRINELLO (G.); ROBERTSON (M.); STEG (P. G.); TENDERA (M.); FORD (I.); FOX (K.); FERRARI (R.) |
| AF : | University of Ferrara, S. Maugeri Foundation/Lumezzane/Italie (1 aut., 13 aut.); Concord Repatriation General Hospital, Sydney Medical School, University of Sydney/Australie (2 aut.); Montreal Heart Institute, Université de Montreal/Québec/Canada (3 aut.); Speciallaegecentret, University Hospital of Frederiksberg/Frederiksberg/Danemark (4 aut.); Royal Brompton Hospital, Sydney Street/London/Royaume-Uni (5 aut., 12 aut.); Hôpital Henri Mondor, Assistance Publique, Hôpitaux de Paris and INSERM U 955/Creteil/France (6 aut.); Medical Statistics Unit, University of Brescia/Italie (7 aut.); Robertson Centre for Biostatistics, University of Glasgow/Glasgow/Royaume-Uni (8 aut., 11 aut.); INSERM U-698, Hôpital Bichat-Claude Bernard, AP-HP, University Paris 7/Paris/France (9 aut.); Medial University of Silesia/Katowice/Pologne (10 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | International journal of cardiology; ISSN 0167-5273; Coden IJCDD5; Irlande; Da. 2011; Vol. 146; No. 3; Pp. 408-414; Bibl. 31 ref. |
| LA : | Anglais |
| EA : | Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12 months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n=220 ivabradine; n = 206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, - 1.48 ± 13.00 mL/m2) versus an increase with placebo (1.85 ± 10.54 mL/m2) (P = 0.018). There was an increase in LV ejection fraction with ivabradine (2.00± 7.02%) versus no change with placebo (0.01 ± 6.20%) (P=0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r=0.18, P=0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction. |
| CC : | 002B12; 002B24C01 |
| FD : | Pathologie de l'appareil circulatoire; Rythme cardiaque; Réduction; Ivabradine; Ventricule gauche; Remodelage vasculaire; Echocardiographie; Cardiologie |
| FG : | Exploration ultrason |
| ED : | Cardiovascular disease; Heart rate; Reduction; Ivabradine; Left ventricle; Vascular remodeling; Echocardiography; Cardiology |
| EG : | Sonography |
| SD : | Aparato circulatorio patología; Ritmo cardíaco; Reducción; Ivabradina; Ventrículo izquierdo; Remodelado vascular; Ecocardiografía; Cardiología |
| LO : | INIST-16457.354000193618650200 |
| ID : | 11-0100745 |
Links to Exploration step
Pascal:11-0100745Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL</title><author><name sortKey="Ceconi, C" sort="Ceconi, C" uniqKey="Ceconi C" first="C." last="Ceconi">C. Ceconi</name><affiliation><inist:fA14 i1="01"><s1>University of Ferrara, S. Maugeri Foundation</s1><s2>Lumezzane</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Freedman, S B" sort="Freedman, S B" uniqKey="Freedman S" first="S. B." last="Freedman">S. B. Freedman</name><affiliation><inist:fA14 i1="02"><s1>Concord Repatriation General Hospital, Sydney Medical School, University of Sydney</s1><s3>AUS</s3><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tardif, J C" sort="Tardif, J C" uniqKey="Tardif J" first="J. C." last="Tardif">J. C. Tardif</name><affiliation><inist:fA14 i1="03"><s1>Montreal Heart Institute, Université de Montreal</s1><s2>Québec</s2><s3>CAN</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hildebrandt, P" sort="Hildebrandt, P" uniqKey="Hildebrandt P" first="P." last="Hildebrandt">P. Hildebrandt</name><affiliation><inist:fA14 i1="04"><s1>Speciallaegecentret, University Hospital of Frederiksberg</s1><s2>Frederiksberg</s2><s3>DNK</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Mcdonagh, T" sort="Mcdonagh, T" uniqKey="Mcdonagh T" first="T." last="Mcdonagh">T. Mcdonagh</name><affiliation><inist:fA14 i1="05"><s1>Royal Brompton Hospital, Sydney Street</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gueret, P" sort="Gueret, P" uniqKey="Gueret P" first="P." last="Gueret">P. Gueret</name><affiliation><inist:fA14 i1="06"><s1>Hôpital Henri Mondor, Assistance Publique, Hôpitaux de Paris and INSERM U 955</s1><s2>Creteil</s2><s3>FRA</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Parrinello, G" sort="Parrinello, G" uniqKey="Parrinello G" first="G." last="Parrinello">G. Parrinello</name><affiliation><inist:fA14 i1="07"><s1>Medical Statistics Unit, University of Brescia</s1><s3>ITA</s3><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Robertson, M" sort="Robertson, M" uniqKey="Robertson M" first="M." last="Robertson">M. Robertson</name><affiliation><inist:fA14 i1="08"><s1>Robertson Centre for Biostatistics, University of Glasgow</s1><s2>Glasgow</s2><s3>GBR</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Steg, P G" sort="Steg, P G" uniqKey="Steg P" first="P. G." last="Steg">P. G. Steg</name><affiliation><inist:fA14 i1="09"><s1>INSERM U-698, Hôpital Bichat-Claude Bernard, AP-HP, University Paris 7</s1><s2>Paris</s2><s3>FRA</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tendera, M" sort="Tendera, M" uniqKey="Tendera M" first="M." last="Tendera">M. Tendera</name><affiliation><inist:fA14 i1="10"><s1>Medial University of Silesia</s1><s2>Katowice</s2><s3>POL</s3><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ford, I" sort="Ford, I" uniqKey="Ford I" first="I." last="Ford">I. Ford</name><affiliation><inist:fA14 i1="08"><s1>Robertson Centre for Biostatistics, University of Glasgow</s1><s2>Glasgow</s2><s3>GBR</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fox, K" sort="Fox, K" uniqKey="Fox K" first="K." last="Fox">K. Fox</name><affiliation><inist:fA14 i1="05"><s1>Royal Brompton Hospital, Sydney Street</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ferrari, R" sort="Ferrari, R" uniqKey="Ferrari R" first="R." last="Ferrari">R. Ferrari</name><affiliation><inist:fA14 i1="01"><s1>University of Ferrara, S. Maugeri Foundation</s1><s2>Lumezzane</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0100745</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0100745 INIST</idno><idno type="RBID">Pascal:11-0100745</idno><idno type="wicri:Area/PascalFrancis/Corpus">002014</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL</title><author><name sortKey="Ceconi, C" sort="Ceconi, C" uniqKey="Ceconi C" first="C." last="Ceconi">C. Ceconi</name><affiliation><inist:fA14 i1="01"><s1>University of Ferrara, S. Maugeri Foundation</s1><s2>Lumezzane</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Freedman, S B" sort="Freedman, S B" uniqKey="Freedman S" first="S. B." last="Freedman">S. B. Freedman</name><affiliation><inist:fA14 i1="02"><s1>Concord Repatriation General Hospital, Sydney Medical School, University of Sydney</s1><s3>AUS</s3><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tardif, J C" sort="Tardif, J C" uniqKey="Tardif J" first="J. C." last="Tardif">J. C. Tardif</name><affiliation><inist:fA14 i1="03"><s1>Montreal Heart Institute, Université de Montreal</s1><s2>Québec</s2><s3>CAN</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hildebrandt, P" sort="Hildebrandt, P" uniqKey="Hildebrandt P" first="P." last="Hildebrandt">P. Hildebrandt</name><affiliation><inist:fA14 i1="04"><s1>Speciallaegecentret, University Hospital of Frederiksberg</s1><s2>Frederiksberg</s2><s3>DNK</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Mcdonagh, T" sort="Mcdonagh, T" uniqKey="Mcdonagh T" first="T." last="Mcdonagh">T. Mcdonagh</name><affiliation><inist:fA14 i1="05"><s1>Royal Brompton Hospital, Sydney Street</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gueret, P" sort="Gueret, P" uniqKey="Gueret P" first="P." last="Gueret">P. Gueret</name><affiliation><inist:fA14 i1="06"><s1>Hôpital Henri Mondor, Assistance Publique, Hôpitaux de Paris and INSERM U 955</s1><s2>Creteil</s2><s3>FRA</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Parrinello, G" sort="Parrinello, G" uniqKey="Parrinello G" first="G." last="Parrinello">G. Parrinello</name><affiliation><inist:fA14 i1="07"><s1>Medical Statistics Unit, University of Brescia</s1><s3>ITA</s3><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Robertson, M" sort="Robertson, M" uniqKey="Robertson M" first="M." last="Robertson">M. Robertson</name><affiliation><inist:fA14 i1="08"><s1>Robertson Centre for Biostatistics, University of Glasgow</s1><s2>Glasgow</s2><s3>GBR</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Steg, P G" sort="Steg, P G" uniqKey="Steg P" first="P. G." last="Steg">P. G. Steg</name><affiliation><inist:fA14 i1="09"><s1>INSERM U-698, Hôpital Bichat-Claude Bernard, AP-HP, University Paris 7</s1><s2>Paris</s2><s3>FRA</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tendera, M" sort="Tendera, M" uniqKey="Tendera M" first="M." last="Tendera">M. Tendera</name><affiliation><inist:fA14 i1="10"><s1>Medial University of Silesia</s1><s2>Katowice</s2><s3>POL</s3><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ford, I" sort="Ford, I" uniqKey="Ford I" first="I." last="Ford">I. Ford</name><affiliation><inist:fA14 i1="08"><s1>Robertson Centre for Biostatistics, University of Glasgow</s1><s2>Glasgow</s2><s3>GBR</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fox, K" sort="Fox, K" uniqKey="Fox K" first="K." last="Fox">K. Fox</name><affiliation><inist:fA14 i1="05"><s1>Royal Brompton Hospital, Sydney Street</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ferrari, R" sort="Ferrari, R" uniqKey="Ferrari R" first="R." last="Ferrari">R. Ferrari</name><affiliation><inist:fA14 i1="01"><s1>University of Ferrara, S. Maugeri Foundation</s1><s2>Lumezzane</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">International journal of cardiology</title><title level="j" type="abbreviated">Int. j. cardiol.</title><idno type="ISSN">0167-5273</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">International journal of cardiology</title><title level="j" type="abbreviated">Int. j. cardiol.</title><idno type="ISSN">0167-5273</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cardiology</term><term>Cardiovascular disease</term><term>Echocardiography</term><term>Heart rate</term><term>Ivabradine</term><term>Left ventricle</term><term>Reduction</term><term>Vascular remodeling</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Pathologie de l'appareil circulatoire</term><term>Rythme cardiaque</term><term>Réduction</term><term>Ivabradine</term><term>Ventricule gauche</term><term>Remodelage vasculaire</term><term>Echocardiographie</term><term>Cardiologie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12 months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n=220 ivabradine; n = 206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, - 1.48 ± 13.00 mL/m<sup>2</sup>) versus an increase with placebo (1.85 ± 10.54 mL/m<sup>2</sup>) (P = 0.018). There was an increase in LV ejection fraction with ivabradine (2.00± 7.02%) versus no change with placebo (0.01 ± 6.20%) (P=0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r=0.18, P=0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0167-5273</s0></fA01><fA02 i1="01"><s0>IJCDD5</s0></fA02><fA03 i2="1"><s0>Int. j. cardiol.</s0></fA03><fA05><s2>146</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL</s1></fA08><fA11 i1="01" i2="1"><s1>CECONI (C.)</s1></fA11><fA11 i1="02" i2="1"><s1>FREEDMAN (S. B.)</s1></fA11><fA11 i1="03" i2="1"><s1>TARDIF (J. C.)</s1></fA11><fA11 i1="04" i2="1"><s1>HILDEBRANDT (P.)</s1></fA11><fA11 i1="05" i2="1"><s1>MCDONAGH (T.)</s1></fA11><fA11 i1="06" i2="1"><s1>GUERET (P.)</s1></fA11><fA11 i1="07" i2="1"><s1>PARRINELLO (G.)</s1></fA11><fA11 i1="08" i2="1"><s1>ROBERTSON (M.)</s1></fA11><fA11 i1="09" i2="1"><s1>STEG (P. G.)</s1></fA11><fA11 i1="10" i2="1"><s1>TENDERA (M.)</s1></fA11><fA11 i1="11" i2="1"><s1>FORD (I.)</s1></fA11><fA11 i1="12" i2="1"><s1>FOX (K.)</s1></fA11><fA11 i1="13" i2="1"><s1>FERRARI (R.)</s1></fA11><fA14 i1="01"><s1>University of Ferrara, S. Maugeri Foundation</s1><s2>Lumezzane</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="02"><s1>Concord Repatriation General Hospital, Sydney Medical School, University of Sydney</s1><s3>AUS</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Montreal Heart Institute, Université de Montreal</s1><s2>Québec</s2><s3>CAN</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>Speciallaegecentret, University Hospital of Frederiksberg</s1><s2>Frederiksberg</s2><s3>DNK</s3><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>Royal Brompton Hospital, Sydney Street</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="06"><s1>Hôpital Henri Mondor, Assistance Publique, Hôpitaux de Paris and INSERM U 955</s1><s2>Creteil</s2><s3>FRA</s3><sZ>6 aut.</sZ></fA14><fA14 i1="07"><s1>Medical Statistics Unit, University of Brescia</s1><s3>ITA</s3><sZ>7 aut.</sZ></fA14><fA14 i1="08"><s1>Robertson Centre for Biostatistics, University of Glasgow</s1><s2>Glasgow</s2><s3>GBR</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="09"><s1>INSERM U-698, Hôpital Bichat-Claude Bernard, AP-HP, University Paris 7</s1><s2>Paris</s2><s3>FRA</s3><sZ>9 aut.</sZ></fA14><fA14 i1="10"><s1>Medial University of Silesia</s1><s2>Katowice</s2><s3>POL</s3><sZ>10 aut.</sZ></fA14><fA20><s1>408-414</s1></fA20><fA21><s1>2011</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>16457</s2><s5>354000193618650200</s5></fA43><fA44><s0>0000</s0><s1>© 2011 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>31 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>11-0100745</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>International journal of cardiology</s0></fA64><fA66 i1="01"><s0>IRL</s0></fA66><fC01 i1="01" l="ENG"><s0>Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12 months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n=220 ivabradine; n = 206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, - 1.48 ± 13.00 mL/m<sup>2</sup>) versus an increase with placebo (1.85 ± 10.54 mL/m<sup>2</sup>) (P = 0.018). There was an increase in LV ejection fraction with ivabradine (2.00± 7.02%) versus no change with placebo (0.01 ± 6.20%) (P=0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r=0.18, P=0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction.</s0></fC01><fC02 i1="01" i2="X"><s0>002B12</s0></fC02><fC02 i1="02" i2="X"><s0>002B24C01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Pathologie de l'appareil circulatoire</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Cardiovascular disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Rythme cardiaque</s0><s5>09</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Heart rate</s0><s5>09</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Ritmo cardíaco</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Réduction</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Reduction</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Reducción</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Ivabradine</s0><s2>NK</s2><s2>FR</s2><s5>11</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Ivabradine</s0><s2>NK</s2><s2>FR</s2><s5>11</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Ivabradina</s0><s2>NK</s2><s2>FR</s2><s5>11</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Ventricule gauche</s0><s5>12</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Left ventricle</s0><s5>12</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Ventrículo izquierdo</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Remodelage vasculaire</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Vascular remodeling</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Remodelado vascular</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Echocardiographie</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Echocardiography</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Ecocardiografía</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Cardiologie</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Cardiology</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Cardiología</s0><s5>15</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Exploration ultrason</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Sonography</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Exploración ultrasonido</s0><s5>37</s5></fC07><fN21><s1>066</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 11-0100745 INIST</NO><ET>Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL</ET><AU>CECONI (C.); FREEDMAN (S. B.); TARDIF (J. C.); HILDEBRANDT (P.); MCDONAGH (T.); GUERET (P.); PARRINELLO (G.); ROBERTSON (M.); STEG (P. G.); TENDERA (M.); FORD (I.); FOX (K.); FERRARI (R.)</AU><AF>University of Ferrara, S. Maugeri Foundation/Lumezzane/Italie (1 aut., 13 aut.); Concord Repatriation General Hospital, Sydney Medical School, University of Sydney/Australie (2 aut.); Montreal Heart Institute, Université de Montreal/Québec/Canada (3 aut.); Speciallaegecentret, University Hospital of Frederiksberg/Frederiksberg/Danemark (4 aut.); Royal Brompton Hospital, Sydney Street/London/Royaume-Uni (5 aut., 12 aut.); Hôpital Henri Mondor, Assistance Publique, Hôpitaux de Paris and INSERM U 955/Creteil/France (6 aut.); Medical Statistics Unit, University of Brescia/Italie (7 aut.); Robertson Centre for Biostatistics, University of Glasgow/Glasgow/Royaume-Uni (8 aut., 11 aut.); INSERM U-698, Hôpital Bichat-Claude Bernard, AP-HP, University Paris 7/Paris/France (9 aut.); Medial University of Silesia/Katowice/Pologne (10 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>International journal of cardiology; ISSN 0167-5273; Coden IJCDD5; Irlande; Da. 2011; Vol. 146; No. 3; Pp. 408-414; Bibl. 31 ref.</SO><LA>Anglais</LA><EA>Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12 months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n=220 ivabradine; n = 206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, - 1.48 ± 13.00 mL/m<sup>2</sup>) versus an increase with placebo (1.85 ± 10.54 mL/m<sup>2</sup>) (P = 0.018). There was an increase in LV ejection fraction with ivabradine (2.00± 7.02%) versus no change with placebo (0.01 ± 6.20%) (P=0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r=0.18, P=0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction.</EA><CC>002B12; 002B24C01</CC><FD>Pathologie de l'appareil circulatoire; Rythme cardiaque; Réduction; Ivabradine; Ventricule gauche; Remodelage vasculaire; Echocardiographie; Cardiologie</FD><FG>Exploration ultrason</FG><ED>Cardiovascular disease; Heart rate; Reduction; Ivabradine; Left ventricle; Vascular remodeling; Echocardiography; Cardiology</ED><EG>Sonography</EG><SD>Aparato circulatorio patología; Ritmo cardíaco; Reducción; Ivabradina; Ventrículo izquierdo; Remodelado vascular; Ecocardiografía; Cardiología</SD><LO>INIST-16457.354000193618650200</LO><ID>11-0100745</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Asie/explor/AustralieFrV1/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002014 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 002014 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Asie
|area= AustralieFrV1
|flux= PascalFrancis
|étape= Corpus
|type= RBID
|clé= Pascal:11-0100745
|texte= Effect of heart rate reduction by ivabradine on left ventricular remodeling in the echocardiographic substudy of BEAUTIFUL
}}
| This area was generated with Dilib version V0.6.33. |  |