Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management
Identifieur interne : 004320 ( PascalFrancis/Curation ); précédent : 004319; suivant : 004321Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management
Auteurs : M. John Chapman [France] ; Henry N. Ginsberg [États-Unis] ; Pierre Amarenco [France] ; Felicita Andreotti [Italie] ; Jan Boren [Suède] ; Alberico L. Catapano [Italie] ; Olivier S. Descamps [Belgique] ; Edward Fisher [États-Unis] ; Petri T. Kovanen [Finlande] ; Jan Albert Kuivenhoven [Pays-Bas] ; Philippe Lesnik [France] ; Luis Masana [Espagne] ; Borge G. Nordestgaard [Danemark] ; Kausik K. Ray [Royaume-Uni] ; Zeljko Reiner [Croatie] ; Marja-Riitta Taskinen [Finlande] ; Lale Tokgözoglu [Turquie] ; Anne Tybjaerg-Hansen [Danemark] ; Gerald F. Watts [Australie]Source :
- European heart journal [ 0195-668X ] ; 2011.
Descripteurs français
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- Wicri :
- topic : Homme, Recommandation.
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Abstract
Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high- density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating trigtycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (>1.7mmol/L or 150mg/dL), a marker of TRL and their remnants, and/or low HDL-C (<1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</title><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital</s1><s2>Paris 75651</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Ginsberg, Henry N" sort="Ginsberg, Henry N" uniqKey="Ginsberg H" first="Henry N." last="Ginsberg">Henry N. 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Kovanen</name><affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Wihuri Research Institute</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>9 aut.</sZ></inist:fA14><country>Finlande</country></affiliation></author><author><name sortKey="Albert Kuivenhoven, Jan" sort="Albert Kuivenhoven, Jan" uniqKey="Albert Kuivenhoven J" first="Jan" last="Albert Kuivenhoven">Jan Albert Kuivenhoven</name><affiliation wicri:level="1"><inist:fA14 i1="10"><s1>University of Amsterdam</s1><s3>NLD</s3><sZ>10 aut.</sZ></inist:fA14><country>Pays-Bas</country></affiliation></author><author><name sortKey="Lesnik, Philippe" sort="Lesnik, Philippe" uniqKey="Lesnik P" first="Philippe" last="Lesnik">Philippe Lesnik</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital</s1><s2>Paris 75651</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Masana, Luis" sort="Masana, Luis" uniqKey="Masana L" first="Luis" last="Masana">Luis Masana</name><affiliation wicri:level="1"><inist:fA14 i1="11"><s1>Universitat Rovira & Virgili</s1><s2>Reus</s2><s3>ESP</s3><sZ>12 aut.</sZ></inist:fA14><country>Espagne</country></affiliation></author><author><name sortKey="Nordestgaard, Borge G" sort="Nordestgaard, Borge G" uniqKey="Nordestgaard B" first="Borge G." last="Nordestgaard">Borge G. Nordestgaard</name><affiliation wicri:level="1"><inist:fA14 i1="12"><s1>Heriev Hospital, Copenhagen University Hospital, University of Copenhagen</s1><s3>DNK</s3><sZ>13 aut.</sZ></inist:fA14><country>Danemark</country></affiliation></author><author><name sortKey="Ray, Kausik K" sort="Ray, Kausik K" uniqKey="Ray K" first="Kausik K." last="Ray">Kausik K. Ray</name><affiliation wicri:level="1"><inist:fA14 i1="13"><s1>St George's University of London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Reiner, Zeljko" sort="Reiner, Zeljko" uniqKey="Reiner Z" first="Zeljko" last="Reiner">Zeljko Reiner</name><affiliation wicri:level="1"><inist:fA14 i1="14"><s1>University Hospital Center Zagreb</s1><s3>HRV</s3><sZ>15 aut.</sZ></inist:fA14><country>Croatie</country></affiliation></author><author><name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name><affiliation wicri:level="1"><inist:fA14 i1="15"><s1>Biomedicum</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>16 aut.</sZ></inist:fA14><country>Finlande</country></affiliation></author><author><name sortKey="Tokgozoglu, Lale" sort="Tokgozoglu, Lale" uniqKey="Tokgozoglu L" first="Lale" last="Tokgözoglu">Lale Tokgözoglu</name><affiliation wicri:level="1"><inist:fA14 i1="16"><s1>Hacettepe University</s1><s2>Ankara</s2><s3>TUR</s3><sZ>17 aut.</sZ></inist:fA14><country>Turquie</country></affiliation></author><author><name sortKey="Tybjaerg Hansen, Anne" sort="Tybjaerg Hansen, Anne" uniqKey="Tybjaerg Hansen A" first="Anne" last="Tybjaerg-Hansen">Anne Tybjaerg-Hansen</name><affiliation wicri:level="1"><inist:fA14 i1="17"><s1>Rigshospitalet, University of Copenhagen</s1><s3>DNK</s3><sZ>18 aut.</sZ></inist:fA14><country>Danemark</country></affiliation></author><author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name><affiliation wicri:level="1"><inist:fA14 i1="18"><s1>University of Western Australia</s1><s2>Perth</s2><s3>AUS</s3><sZ>19 aut.</sZ></inist:fA14><country>Australie</country></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0287868</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0287868 INIST</idno><idno type="RBID">Pascal:11-0287868</idno><idno type="wicri:Area/PascalFrancis/Corpus">001C24</idno><idno type="wicri:Area/PascalFrancis/Curation">004320</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</title><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital</s1><s2>Paris 75651</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Ginsberg, Henry N" sort="Ginsberg, Henry N" uniqKey="Ginsberg H" first="Henry N." last="Ginsberg">Henry N. Ginsberg</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Irving Institute for Clinical and Translational Research Columbia University, PH 10-305 630 West 168th Street</s1><s2>NewYork, NY 10032</s2><s3>USA</s3><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Amarenco, Pierre" sort="Amarenco, Pierre" uniqKey="Amarenco P" first="Pierre" last="Amarenco">Pierre Amarenco</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Bichat University Hospital</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Andreotti, Felicita" sort="Andreotti, Felicita" uniqKey="Andreotti F" first="Felicita" last="Andreotti">Felicita Andreotti</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Catholic University Medical School</s1><s2>Rome</s2><s3>ITA</s3><sZ>4 aut.</sZ></inist:fA14><country>Italie</country></affiliation></author><author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>University of Gothenburg</s1><s3>SWE</s3><sZ>5 aut.</sZ></inist:fA14><country>Suède</country></affiliation></author><author><name sortKey="Catapano, Alberico L" sort="Catapano, Alberico L" uniqKey="Catapano A" first="Alberico L." last="Catapano">Alberico L. Catapano</name><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>University of Milan</s1><s3>ITA</s3><sZ>6 aut.</sZ></inist:fA14><country>Italie</country></affiliation></author><author><name sortKey="Descamps, Olivier S" sort="Descamps, Olivier S" uniqKey="Descamps O" first="Olivier S." last="Descamps">Olivier S. Descamps</name><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Hopital de Jolimont, Haine Saint-Paul</s1><s3>BEL</s3><sZ>7 aut.</sZ></inist:fA14><country>Belgique</country></affiliation></author><author><name sortKey="Fisher, Edward" sort="Fisher, Edward" uniqKey="Fisher E" first="Edward" last="Fisher">Edward Fisher</name><affiliation wicri:level="1"><inist:fA14 i1="08"><s1>New York University</s1><s2>New York</s2><s3>USA</s3><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Kovanen, Petri T" sort="Kovanen, Petri T" uniqKey="Kovanen P" first="Petri T." last="Kovanen">Petri T. Kovanen</name><affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Wihuri Research Institute</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>9 aut.</sZ></inist:fA14><country>Finlande</country></affiliation></author><author><name sortKey="Albert Kuivenhoven, Jan" sort="Albert Kuivenhoven, Jan" uniqKey="Albert Kuivenhoven J" first="Jan" last="Albert Kuivenhoven">Jan Albert Kuivenhoven</name><affiliation wicri:level="1"><inist:fA14 i1="10"><s1>University of Amsterdam</s1><s3>NLD</s3><sZ>10 aut.</sZ></inist:fA14><country>Pays-Bas</country></affiliation></author><author><name sortKey="Lesnik, Philippe" sort="Lesnik, Philippe" uniqKey="Lesnik P" first="Philippe" last="Lesnik">Philippe Lesnik</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital</s1><s2>Paris 75651</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Masana, Luis" sort="Masana, Luis" uniqKey="Masana L" first="Luis" last="Masana">Luis Masana</name><affiliation wicri:level="1"><inist:fA14 i1="11"><s1>Universitat Rovira & Virgili</s1><s2>Reus</s2><s3>ESP</s3><sZ>12 aut.</sZ></inist:fA14><country>Espagne</country></affiliation></author><author><name sortKey="Nordestgaard, Borge G" sort="Nordestgaard, Borge G" uniqKey="Nordestgaard B" first="Borge G." last="Nordestgaard">Borge G. Nordestgaard</name><affiliation wicri:level="1"><inist:fA14 i1="12"><s1>Heriev Hospital, Copenhagen University Hospital, University of Copenhagen</s1><s3>DNK</s3><sZ>13 aut.</sZ></inist:fA14><country>Danemark</country></affiliation></author><author><name sortKey="Ray, Kausik K" sort="Ray, Kausik K" uniqKey="Ray K" first="Kausik K." last="Ray">Kausik K. Ray</name><affiliation wicri:level="1"><inist:fA14 i1="13"><s1>St George's University of London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Reiner, Zeljko" sort="Reiner, Zeljko" uniqKey="Reiner Z" first="Zeljko" last="Reiner">Zeljko Reiner</name><affiliation wicri:level="1"><inist:fA14 i1="14"><s1>University Hospital Center Zagreb</s1><s3>HRV</s3><sZ>15 aut.</sZ></inist:fA14><country>Croatie</country></affiliation></author><author><name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name><affiliation wicri:level="1"><inist:fA14 i1="15"><s1>Biomedicum</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>16 aut.</sZ></inist:fA14><country>Finlande</country></affiliation></author><author><name sortKey="Tokgozoglu, Lale" sort="Tokgozoglu, Lale" uniqKey="Tokgozoglu L" first="Lale" last="Tokgözoglu">Lale Tokgözoglu</name><affiliation wicri:level="1"><inist:fA14 i1="16"><s1>Hacettepe University</s1><s2>Ankara</s2><s3>TUR</s3><sZ>17 aut.</sZ></inist:fA14><country>Turquie</country></affiliation></author><author><name sortKey="Tybjaerg Hansen, Anne" sort="Tybjaerg Hansen, Anne" uniqKey="Tybjaerg Hansen A" first="Anne" last="Tybjaerg-Hansen">Anne Tybjaerg-Hansen</name><affiliation wicri:level="1"><inist:fA14 i1="17"><s1>Rigshospitalet, University of Copenhagen</s1><s3>DNK</s3><sZ>18 aut.</sZ></inist:fA14><country>Danemark</country></affiliation></author><author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name><affiliation wicri:level="1"><inist:fA14 i1="18"><s1>University of Western Australia</s1><s2>Perth</s2><s3>AUS</s3><sZ>19 aut.</sZ></inist:fA14><country>Australie</country></affiliation></author></analytic><series><title level="j" type="main">European heart journal</title><title level="j" type="abbreviated">Eur. heart j.</title><idno type="ISSN">0195-668X</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">European heart journal</title><title level="j" type="abbreviated">Eur. heart j.</title><idno type="ISSN">0195-668X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atherosclerosis</term><term>Cardiology</term><term>Cardiovascular disease</term><term>Cholesterol</term><term>Circulatory system</term><term>Clinical management</term><term>Dyslipemia</term><term>Guidance</term><term>High risk</term><term>Human</term><term>Lipids</term><term>Lipoprotein HDL</term><term>Patient</term><term>Recommendation</term><term>Triglyceride</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dyslipémie</term><term>Athérosclérose</term><term>Triglycéride</term><term>Lipoprotéine HDL</term><term>Cholestérol</term><term>Homme</term><term>Malade</term><term>Risque élevé</term><term>Pathologie de l'appareil circulatoire</term><term>Guidage</term><term>Conduite à tenir</term><term>Recommandation</term><term>Appareil circulatoire</term><term>Cardiologie</term><term>Lipide</term><term>Maladie cardiovasculaire</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term><term>Recommandation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high- density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating trigtycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (>1.7mmol/L or 150mg/dL), a marker of TRL and their remnants, and/or low HDL-C (<1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0195-668X</s0></fA01><fA03 i2="1"><s0>Eur. heart j.</s0></fA03><fA05><s2>32</s2></fA05><fA06><s2>11</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</s1></fA08><fA11 i1="01" i2="1"><s1>CHAPMAN (M. John)</s1></fA11><fA11 i1="02" i2="1"><s1>GINSBERG (Henry N.)</s1></fA11><fA11 i1="03" i2="1"><s1>AMARENCO (Pierre)</s1></fA11><fA11 i1="04" i2="1"><s1>ANDREOTTI (Felicita)</s1></fA11><fA11 i1="05" i2="1"><s1>BOREN (Jan)</s1></fA11><fA11 i1="06" i2="1"><s1>CATAPANO (Alberico L.)</s1></fA11><fA11 i1="07" i2="1"><s1>DESCAMPS (Olivier S.)</s1></fA11><fA11 i1="08" i2="1"><s1>FISHER (Edward)</s1></fA11><fA11 i1="09" i2="1"><s1>KOVANEN (Petri T.)</s1></fA11><fA11 i1="10" i2="1"><s1>ALBERT KUIVENHOVEN (Jan)</s1></fA11><fA11 i1="11" i2="1"><s1>LESNIK (Philippe)</s1></fA11><fA11 i1="12" i2="1"><s1>MASANA (Luis)</s1></fA11><fA11 i1="13" i2="1"><s1>NORDESTGAARD (Borge G.)</s1></fA11><fA11 i1="14" i2="1"><s1>RAY (Kausik K.)</s1></fA11><fA11 i1="15" i2="1"><s1>REINER (Zeljko)</s1></fA11><fA11 i1="16" i2="1"><s1>TASKINEN (Marja-Riitta)</s1></fA11><fA11 i1="17" i2="1"><s1>TOKGÖZOGLU (Lale)</s1></fA11><fA11 i1="18" i2="1"><s1>TYBJAERG-HANSEN (Anne)</s1></fA11><fA11 i1="19" i2="1"><s1>WATTS (Gerald F.)</s1></fA11><fA14 i1="01"><s1>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital</s1><s2>Paris 75651</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="02"><s1>Irving Institute for Clinical and Translational Research Columbia University, PH 10-305 630 West 168th Street</s1><s2>NewYork, NY 10032</s2><s3>USA</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Bichat University Hospital</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>Catholic University Medical School</s1><s2>Rome</s2><s3>ITA</s3><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>University of Gothenburg</s1><s3>SWE</s3><sZ>5 aut.</sZ></fA14><fA14 i1="06"><s1>University of Milan</s1><s3>ITA</s3><sZ>6 aut.</sZ></fA14><fA14 i1="07"><s1>Hopital de Jolimont, Haine Saint-Paul</s1><s3>BEL</s3><sZ>7 aut.</sZ></fA14><fA14 i1="08"><s1>New York University</s1><s2>New York</s2><s3>USA</s3><sZ>8 aut.</sZ></fA14><fA14 i1="09"><s1>Wihuri Research Institute</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>9 aut.</sZ></fA14><fA14 i1="10"><s1>University of Amsterdam</s1><s3>NLD</s3><sZ>10 aut.</sZ></fA14><fA14 i1="11"><s1>Universitat Rovira & Virgili</s1><s2>Reus</s2><s3>ESP</s3><sZ>12 aut.</sZ></fA14><fA14 i1="12"><s1>Heriev Hospital, Copenhagen University Hospital, University of Copenhagen</s1><s3>DNK</s3><sZ>13 aut.</sZ></fA14><fA14 i1="13"><s1>St George's University of London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></fA14><fA14 i1="14"><s1>University Hospital Center Zagreb</s1><s3>HRV</s3><sZ>15 aut.</sZ></fA14><fA14 i1="15"><s1>Biomedicum</s1><s2>Helsinki</s2><s3>FIN</s3><sZ>16 aut.</sZ></fA14><fA14 i1="16"><s1>Hacettepe University</s1><s2>Ankara</s2><s3>TUR</s3><sZ>17 aut.</sZ></fA14><fA14 i1="17"><s1>Rigshospitalet, University of Copenhagen</s1><s3>DNK</s3><sZ>18 aut.</sZ></fA14><fA14 i1="18"><s1>University of Western Australia</s1><s2>Perth</s2><s3>AUS</s3><sZ>19 aut.</sZ></fA14><fA17 i1="01" i2="1"><s1>European Atherosclerosis Society Consensus Panel</s1><s3>INC</s3></fA17><fA20><s1>1345-1361</s1></fA20><fA21><s1>2011</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>18785</s2><s5>354000192171820060</s5></fA43><fA44><s0>0000</s0><s1>© 2011 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1/4 p.</s0></fA45><fA47 i1="01" i2="1"><s0>11-0287868</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>European heart journal</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high- density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating trigtycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (>1.7mmol/L or 150mg/dL), a marker of TRL and their remnants, and/or low HDL-C (<1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.</s0></fC01><fC02 i1="01" i2="X"><s0>002B12B01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Dyslipémie</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Dyslipemia</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Dislipemia</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Athérosclérose</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Atherosclerosis</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Ateroesclerosis</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Triglycéride</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Triglyceride</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Triglicérido</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Lipoprotéine HDL</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Lipoprotein HDL</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Lipoproteina HDL</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Cholestérol</s0><s2>NK</s2><s5>11</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Cholesterol</s0><s2>NK</s2><s5>11</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Colesterol</s0><s2>NK</s2><s5>11</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Human</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Malade</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Patient</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Enfermo</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Risque élevé</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>High risk</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Riesgo alto</s0><s5>14</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Pathologie de l'appareil circulatoire</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Cardiovascular disease</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0><s5>15</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Guidage</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Guidance</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Guiado</s0><s5>16</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Conduite à tenir</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Clinical management</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Actitud médica</s0><s5>17</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Recommandation</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Recommendation</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Recomendación</s0><s5>18</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Appareil circulatoire</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Circulatory system</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Aparato circulatorio</s0><s5>19</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Cardiologie</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Cardiology</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Cardiología</s0><s5>20</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Lipide</s0><s5>78</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Lipids</s0><s5>78</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Lípido</s0><s5>78</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Maladie cardiovasculaire</s0><s4>CD</s4><s5>96</s5></fC03><fC03 i1="16" i2="X" l="ENG"><s0>Cardiovascular disease</s0><s4>CD</s4><s5>96</s5></fC03><fC03 i1="16" i2="X" l="SPA"><s0>Cardiovascular enfermedad</s0><s4>CD</s4><s5>96</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Maladie métabolique</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Metabolic diseases</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Metabolismo patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Pathologie des vaisseaux sanguins</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Vascular disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Vaso sanguíneo patología</s0><s5>38</s5></fC07><fN21><s1>192</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist></record>Pour manipuler ce document sous Unix (Dilib)
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