Lipoprotein(a) as a cardiovascular risk factor: current status
Identifieur interne : 000F09 ( Istex/Corpus ); précédent : 000F08; suivant : 000F10Lipoprotein(a) as a cardiovascular risk factor: current status
Auteurs : Brge G. Nordestgaard ; M. John Chapman ; Kausik Ray ; Jan Born ; Felicita Andreotti ; Gerald F. Watts ; Henry Ginsberg ; Pierre Amarenco ; Alberico Catapano ; Olivier S. Descamps ; Edward Fisher ; Petri T. Kovanen ; Jan Albert Kuivenhoven ; Philippe Lesnik ; Luis Masana ; Zeljko Reiner ; Marja-Riitta Taskinen ; Lale Tokgzoglu ; Anne Tybjrg-HansenSource :
- European Heart Journal [ 0195-668X ] ; 2010-12.
Abstract
Aims The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. Methods and results The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, 3 10-year risk of fatal CVD according to European guidelines, and/or 10 10-year risk of fatal non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than 50 mg/dL). Treatment should primarily be niacin 13 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). Conclusion We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.
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DOI: 10.1093/eurheartj/ehq386
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John Chapman</name><affiliation><mods:affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</mods:affiliation></affiliation></author><author><name sortKey="Ray, Kausik" sort="Ray, Kausik" uniqKey="Ray K" first="Kausik" last="Ray">Kausik Ray</name><affiliation><mods:affiliation>St George's University of London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Born, Jan" sort="Born, Jan" uniqKey="Born J" first="Jan" last="Born">Jan Born</name><affiliation><mods:affiliation>University of Gothenburg, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Andreotti, Felicita" sort="Andreotti, Felicita" uniqKey="Andreotti F" first="Felicita" last="Andreotti">Felicita Andreotti</name><affiliation><mods:affiliation>Catholic University Medical School, Rome, Italy</mods:affiliation></affiliation></author><author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. 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Nordestgaard</name><affiliation><mods:affiliation>Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: brno@heh.regionh.dk</mods:affiliation></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name><affiliation><mods:affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</mods:affiliation></affiliation></author><author><name sortKey="Ray, Kausik" sort="Ray, Kausik" uniqKey="Ray K" first="Kausik" last="Ray">Kausik Ray</name><affiliation><mods:affiliation>St George's University of London, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Born, Jan" sort="Born, Jan" uniqKey="Born J" first="Jan" last="Born">Jan Born</name><affiliation><mods:affiliation>University of Gothenburg, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Andreotti, Felicita" sort="Andreotti, Felicita" uniqKey="Andreotti F" first="Felicita" last="Andreotti">Felicita Andreotti</name><affiliation><mods:affiliation>Catholic University Medical School, Rome, Italy</mods:affiliation></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><mods:affiliation>University of Western Australia, Perth, Australia</mods:affiliation></affiliation></author><author><name sortKey="Ginsberg, Henry" sort="Ginsberg, Henry" uniqKey="Ginsberg H" first="Henry" last="Ginsberg">Henry Ginsberg</name><affiliation><mods:affiliation>Columbia University, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Amarenco, Pierre" sort="Amarenco, Pierre" uniqKey="Amarenco P" first="Pierre" last="Amarenco">Pierre Amarenco</name><affiliation><mods:affiliation>Bichat University Hospital, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Catapano, Alberico" sort="Catapano, Alberico" uniqKey="Catapano A" first="Alberico" last="Catapano">Alberico Catapano</name><affiliation><mods:affiliation>University of Milan, Italy</mods:affiliation></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><mods:affiliation>Hopital de Jolimont, Haine Saint-Paul, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Fisher, Edward" sort="Fisher, Edward" uniqKey="Fisher E" first="Edward" last="Fisher">Edward Fisher</name><affiliation><mods:affiliation>New York University, New York, USA</mods:affiliation></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><mods:affiliation>Wihuri Research Institute, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Kuivenhoven, Jan Albert" sort="Kuivenhoven, Jan Albert" uniqKey="Kuivenhoven J" first="Jan Albert" last="Kuivenhoven">Jan Albert Kuivenhoven</name><affiliation><mods:affiliation>University of Amsterdam, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Lesnik, Philippe" sort="Lesnik, Philippe" uniqKey="Lesnik P" first="Philippe" last="Lesnik">Philippe Lesnik</name><affiliation><mods:affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</mods:affiliation></affiliation></author><author><name sortKey="Masana, Luis" sort="Masana, Luis" uniqKey="Masana L" first="Luis" last="Masana">Luis Masana</name><affiliation><mods:affiliation>Universitat Rovira & Virgili, Reus, Spain</mods:affiliation></affiliation></author><author><name sortKey="Reiner, Zeljko" sort="Reiner, Zeljko" uniqKey="Reiner Z" first="Zeljko" last="Reiner">Zeljko Reiner</name><affiliation><mods:affiliation>University Hospital Center Zagreb, Croatia</mods:affiliation></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><mods:affiliation>Biomedicum, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Tokgzoglu, Lale" sort="Tokgzoglu, Lale" uniqKey="Tokgzoglu L" first="Lale" last="Tokgzoglu">Lale Tokgzoglu</name><affiliation><mods:affiliation>Hacettepe University, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Tybjrg Hansen, Anne" sort="Tybjrg Hansen, Anne" uniqKey="Tybjrg Hansen A" first="Anne" last="Tybjrg-Hansen">Anne Tybjrg-Hansen</name><affiliation><mods:affiliation>Rigshospitalet, University of Copenhagen, Denmark</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Heart Journal</title><idno type="ISSN">0195-668X</idno><idno type="eISSN">1522-9645</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-12">2010-12</date><biblScope unit="volume">31</biblScope><biblScope unit="issue">23</biblScope><biblScope unit="page" from="2844">2844</biblScope><biblScope unit="page" to="2853">2853</biblScope></imprint><idno type="ISSN">0195-668X</idno></series><idno type="istex">895558F69D4D2768A710408C3318A07B201733D7</idno><idno type="DOI">10.1093/eurheartj/ehq386</idno><idno type="href">ehq386.pdf</idno><idno type="ArticleID">ehq386</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0195-668X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Aims The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. Methods and results The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, 3 10-year risk of fatal CVD according to European guidelines, and/or 10 10-year risk of fatal non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than 50 mg/dL). Treatment should primarily be niacin 13 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). Conclusion We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Brge G. Nordestgaard</name><affiliations><json:string>Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark</json:string><json:string>E-mail: brno@heh.regionh.dk</json:string></affiliations></json:item><json:item><name>M. John Chapman</name><affiliations><json:string>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</json:string></affiliations></json:item><json:item><name>Kausik Ray</name><affiliations><json:string>St George's University of London, London, UK</json:string></affiliations></json:item><json:item><name>Jan Born</name><affiliations><json:string>University of Gothenburg, Sweden</json:string></affiliations></json:item><json:item><name>Felicita Andreotti</name><affiliations><json:string>Catholic University Medical School, Rome, Italy</json:string></affiliations></json:item><json:item><name>Gerald F. Watts</name><affiliations><json:string>University of Western Australia, Perth, Australia</json:string></affiliations></json:item><json:item><name>Henry Ginsberg</name><affiliations><json:string>Columbia University, New York, USA</json:string></affiliations></json:item><json:item><name>Pierre Amarenco</name><affiliations><json:string>Bichat University Hospital, Paris, France</json:string></affiliations></json:item><json:item><name>Alberico Catapano</name><affiliations><json:string>University of Milan, Italy</json:string></affiliations></json:item><json:item><name>Olivier S. Descamps</name><affiliations><json:string>Hopital de Jolimont, Haine Saint-Paul, Belgium</json:string></affiliations></json:item><json:item><name>Edward Fisher</name><affiliations><json:string>New York University, New York, USA</json:string></affiliations></json:item><json:item><name>Petri T. Kovanen</name><affiliations><json:string>Wihuri Research Institute, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Jan Albert Kuivenhoven</name><affiliations><json:string>University of Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Philippe Lesnik</name><affiliations><json:string>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</json:string></affiliations></json:item><json:item><name>Luis Masana</name><affiliations><json:string>Universitat Rovira & Virgili, Reus, Spain</json:string></affiliations></json:item><json:item><name>Zeljko Reiner</name><affiliations><json:string>University Hospital Center Zagreb, Croatia</json:string></affiliations></json:item><json:item><name>Marja-Riitta Taskinen</name><affiliations><json:string>Biomedicum, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Lale Tokgzoglu</name><affiliations><json:string>Hacettepe University, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Anne Tybjrg-Hansen</name><affiliations><json:string>Rigshospitalet, University of Copenhagen, Denmark</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Lipids</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Hyperlipidemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Prevention</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Myocardial infarction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Stroke</value></json:item></subject><articleId><json:string>ehq386</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Aims The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. Methods and results The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, 3 10-year risk of fatal CVD according to European guidelines, and/or 10 10-year risk of fatal non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) >80th percentile (less than 50 mg/dL). Treatment should primarily be niacin 13 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). Conclusion We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level >50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.</abstract><qualityIndicators><score>9</score><pdfVersion>1.5</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1935</abstractCharCount><pdfWordCount>6814</pdfWordCount><pdfCharCount>45911</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>271</abstractWordCount></qualityIndicators><title>Lipoprotein(a) as a cardiovascular risk factor: current status</title><genre><json:string>research-article</json:string></genre><host><volume>31</volume><publisherId><json:string>eurheartj</json:string></publisherId><pages><last>2853</last><first>2844</first></pages><issn><json:string>0195-668X</json:string></issn><issue>23</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1522-9645</json:string></eissn><title>European Heart Journal</title></host><categories><wos><json:string>CARDIAC & CARDIOVASCULAR SYSTEMS</json:string></wos></categories><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1093/eurheartj/ehq386</json:string></doi><id>895558F69D4D2768A710408C3318A07B201733D7</id><score>0.24773598</score><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/895558F69D4D2768A710408C3318A07B201733D7/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/895558F69D4D2768A710408C3318A07B201733D7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/895558F69D4D2768A710408C3318A07B201733D7/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Lipoprotein(a) as a cardiovascular risk factor: current status</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>Published on behalf of the European Society of Cardiology. All rights reserved. The Author 2010. For permissions please email: journals.permissionsoxfordjournals.org</p></availability><date>2010-10-21</date></publicationStmt><notesStmt><note>The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Lipoprotein(a) as a cardiovascular risk factor: current status</title><author xml:id="author-1"><persName><forename type="first">Brge G.</forename><surname>Nordestgaard</surname></persName><email>brno@heh.regionh.dk</email><affiliation>Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark</affiliation></author><author xml:id="author-2"><persName><forename type="first">M. John</forename><surname>Chapman</surname></persName><affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Kausik</forename><surname>Ray</surname></persName><affiliation>St George's University of London, London, UK</affiliation></author><author xml:id="author-4"><persName><forename type="first">Jan</forename><surname>Born</surname></persName><affiliation>University of Gothenburg, Sweden</affiliation></author><author xml:id="author-5"><persName><forename type="first">Felicita</forename><surname>Andreotti</surname></persName><affiliation>Catholic University Medical School, Rome, Italy</affiliation></author><author xml:id="author-6"><persName><forename type="first">Gerald F.</forename><surname>Watts</surname></persName><affiliation>University of Western Australia, Perth, Australia</affiliation></author><author xml:id="author-7"><persName><forename type="first">Henry</forename><surname>Ginsberg</surname></persName><affiliation>Columbia University, New York, USA</affiliation></author><author xml:id="author-8"><persName><forename type="first">Pierre</forename><surname>Amarenco</surname></persName><affiliation>Bichat University Hospital, Paris, France</affiliation></author><author xml:id="author-9"><persName><forename type="first">Alberico</forename><surname>Catapano</surname></persName><affiliation>University of Milan, Italy</affiliation></author><author xml:id="author-10"><persName><forename type="first">Olivier S.</forename><surname>Descamps</surname></persName><affiliation>Hopital de Jolimont, Haine Saint-Paul, Belgium</affiliation></author><author xml:id="author-11"><persName><forename type="first">Edward</forename><surname>Fisher</surname></persName><affiliation>New York University, New York, USA</affiliation></author><author xml:id="author-12"><persName><forename type="first">Petri T.</forename><surname>Kovanen</surname></persName><affiliation>Wihuri Research Institute, Helsinki, Finland</affiliation></author><author xml:id="author-13"><persName><forename type="first">Jan Albert</forename><surname>Kuivenhoven</surname></persName><affiliation>University of Amsterdam, The Netherlands</affiliation></author><author xml:id="author-14"><persName><forename type="first">Philippe</forename><surname>Lesnik</surname></persName><affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</affiliation></author><author xml:id="author-15"><persName><forename type="first">Luis</forename><surname>Masana</surname></persName><affiliation>Universitat Rovira & Virgili, Reus, Spain</affiliation></author><author xml:id="author-16"><persName><forename type="first">Zeljko</forename><surname>Reiner</surname></persName><affiliation>University Hospital Center Zagreb, Croatia</affiliation></author><author xml:id="author-17"><persName><forename type="first">Marja-Riitta</forename><surname>Taskinen</surname></persName><affiliation>Biomedicum, Helsinki, Finland</affiliation></author><author xml:id="author-18"><persName><forename type="first">Lale</forename><surname>Tokgzoglu</surname></persName><affiliation>Hacettepe University, Ankara, Turkey</affiliation></author><author xml:id="author-19"><persName><forename type="first">Anne</forename><surname>Tybjrg-Hansen</surname></persName><affiliation>Rigshospitalet, University of Copenhagen, Denmark</affiliation></author></analytic><monogr><title level="j">European Heart Journal</title><idno type="pISSN">0195-668X</idno><idno type="eISSN">1522-9645</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-12"></date><biblScope unit="volume">31</biblScope><biblScope unit="issue">23</biblScope><biblScope unit="page" from="2844">2844</biblScope><biblScope unit="page" to="2853">2853</biblScope></imprint></monogr><idno type="istex">895558F69D4D2768A710408C3318A07B201733D7</idno><idno type="DOI">10.1093/eurheartj/ehq386</idno><idno type="href">ehq386.pdf</idno><idno type="ArticleID">ehq386</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010-10-21</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Aims The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. Methods and results The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, 3 10-year risk of fatal CVD according to European guidelines, and/or 10 10-year risk of fatal non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than 50 mg/dL). Treatment should primarily be niacin 13 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). Conclusion We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.</p></abstract><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>Lipids</term></item><item><term>Hyperlipidemia</term></item><item><term>Prevention</term></item><item><term>Myocardial infarction</term></item><item><term>Stroke</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-10-21">Created</change><change when="2010-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/895558F69D4D2768A710408C3318A07B201733D7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">ehj</journal-id><journal-id journal-id-type="publisher-id">eurheartj</journal-id><journal-title>European Heart Journal</journal-title><issn pub-type="ppub">0195-668X</issn><issn pub-type="epub">1522-9645</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/eurheartj/ehq386</article-id><article-id pub-id-type="publisher-id">ehq386</article-id><article-categories><subj-group subj-group-type="heading"><subject>CURRENT OPINION</subject></subj-group></article-categories><title-group><article-title>Lipoprotein(a) as a cardiovascular risk factor: current status</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Nordestgaard</surname><given-names>Børge G.</given-names></name><xref ref-type="aff" rid="af1">1</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Chapman</surname><given-names>M. John</given-names></name><xref ref-type="aff" rid="af2">2</xref></contrib><contrib contrib-type="author"><name><surname>Ray</surname><given-names>Kausik</given-names></name><xref ref-type="aff" rid="af3">3</xref></contrib><contrib contrib-type="author"><name><surname>Borén</surname><given-names>Jan</given-names></name><xref ref-type="aff" rid="af4">4</xref></contrib><contrib contrib-type="author"><name><surname>Andreotti</surname><given-names>Felicita</given-names></name><xref ref-type="aff" rid="af5">5</xref></contrib><contrib contrib-type="author"><name><surname>Watts</surname><given-names>Gerald F.</given-names></name><xref ref-type="aff" rid="af6">6</xref></contrib><contrib contrib-type="author"><name><surname>Ginsberg</surname><given-names>Henry</given-names></name><xref ref-type="aff" rid="af7">7</xref></contrib><contrib contrib-type="author"><name><surname>Amarenco</surname><given-names>Pierre</given-names></name><xref ref-type="aff" rid="af8">8</xref></contrib><contrib contrib-type="author"><name><surname>Catapano</surname><given-names>Alberico</given-names></name><xref ref-type="aff" rid="af9">9</xref></contrib><contrib contrib-type="author"><name><surname>Descamps</surname><given-names>Olivier S.</given-names></name><xref ref-type="aff" rid="af10">10</xref></contrib><contrib contrib-type="author"><name><surname>Fisher</surname><given-names>Edward</given-names></name><xref ref-type="aff" rid="af11">11</xref></contrib><contrib contrib-type="author"><name><surname>Kovanen</surname><given-names>Petri T.</given-names></name><xref ref-type="aff" rid="af12">12</xref></contrib><contrib contrib-type="author"><name><surname>Kuivenhoven</surname><given-names>Jan Albert</given-names></name><xref ref-type="aff" rid="af13">13</xref></contrib><contrib contrib-type="author"><name><surname>Lesnik</surname><given-names>Philippe</given-names></name><xref ref-type="aff" rid="af2">2</xref></contrib><contrib contrib-type="author"><name><surname>Masana</surname><given-names>Luis</given-names></name><xref ref-type="aff" rid="af14">14</xref></contrib><contrib contrib-type="author"><name><surname>Reiner</surname><given-names>Zeljko</given-names></name><xref ref-type="aff" rid="af15">15</xref></contrib><contrib contrib-type="author"><name><surname>Taskinen</surname><given-names>Marja-Riitta</given-names></name><xref ref-type="aff" rid="af16">16</xref></contrib><contrib contrib-type="author"><name><surname>Tokgözoglu</surname><given-names>Lale</given-names></name><xref ref-type="aff" rid="af17">17</xref></contrib><contrib contrib-type="author"><name><surname>Tybjærg-Hansen</surname><given-names>Anne</given-names></name><xref ref-type="aff" rid="af18">18</xref></contrib><contrib contrib-type="contributor"><on-behalf-of>for the European Atherosclerosis Society Consensus Panel</on-behalf-of><xref ref-type="fn" rid="AN1">†</xref></contrib></contrib-group><aff id="af1"><label>1</label><addr-line>Department of Clinical Biochemistry</addr-line>, <institution>Herlev Hospital, Copenhagen University Hospital</institution>, <addr-line>University of Copenhagen, DK-2730 Herlev</addr-line>, <country>Denmark</country></aff><aff id="af2"><label>2</label><institution>European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital</institution>, <addr-line>Paris 75651</addr-line>, <country>France</country></aff><aff id="af3"><label>3</label>St George's University of London, London, UK</aff><aff id="af4"><label>4</label>University of Gothenburg, Sweden</aff><aff id="af5"><label>5</label>Catholic University Medical School, Rome, Italy</aff><aff id="af6"><label>6</label>University of Western Australia, Perth, Australia</aff><aff id="af7"><label>7</label>Columbia University, New York, USA</aff><aff id="af8"><label>8</label>Bichat University Hospital, Paris, France</aff><aff id="af9"><label>9</label>University of Milan, Italy</aff><aff id="af10"><label>10</label>Hopital de Jolimont, Haine Saint-Paul, Belgium</aff><aff id="af11"><label>11</label>New York University, New York, USA</aff><aff id="af12"><label>12</label>Wihuri Research Institute, Helsinki, Finland</aff><aff id="af13"><label>13</label>University of Amsterdam, The Netherlands</aff><aff id="af14"><label>14</label>Universitat Rovira & Virgili, Reus, Spain</aff><aff id="af15"><label>15</label>University Hospital Center Zagreb, Croatia</aff><aff id="af16"><label>16</label>Biomedicum, Helsinki, Finland</aff><aff id="af17"><label>17</label>Hacettepe University, Ankara, Turkey</aff><aff id="af18"><label>18</label>Rigshospitalet, University of Copenhagen, Denmark</aff><author-notes><corresp id="cor1"><label>*</label>Correspondence author. Tel: +45 44883297, Fax: +45 44883311, Email: <email>brno@heh.regionh.dk</email> (B.G.N.); Tel: +33 1 42177878, Email: <email>john.chapman@upmc.fr</email> (M.J.C.)</corresp><fn><p>The opinions expressed in this article are not necessarily those of the Editors of the <italic>European Heart Journal</italic> or of the European Society of Cardiology.</p></fn><fn fn-type="con" id="AN1"><label>†</label><p>Writing Committee Members, Co-Chairs, and Consensus Panel members are listed in the Author contribution section.</p></fn></author-notes><pub-date pub-type="ppub"><month>12</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>21</day><month>10</month><year>2010</year></pub-date><volume>31</volume><issue>23</issue><fpage>2844</fpage><lpage>2853</lpage><history><date date-type="received"><day>11</day><month>6</month><year>2010</year></date><date date-type="rev-recd"><day>17</day><month>8</month><year>2010</year></date><date date-type="accepted"><day>24</day><month>9</month><year>2010</year></date></history><permissions><copyright-statement>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2010</copyright-year><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by-nc/2.5/"><p>The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.</p></license></permissions><self-uri content-type="pdf" xlink:href="ehq386.pdf"></self-uri><abstract><sec><title>Aims</title><p>The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies.</p></sec><sec><title>Methods and results</title><p>The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, ≥3% 10-year risk of fatal CVD according to European guidelines, and/or ≥10% 10-year risk of fatal + non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than ∼50 mg/dL). Treatment should primarily be niacin 1–3 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a).</p></sec><sec><title>Conclusion</title><p>We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.</p></sec></abstract><kwd-group><kwd>Lipids</kwd><kwd>Hyperlipidemia</kwd><kwd>Prevention</kwd><kwd>Myocardial infarction</kwd><kwd>Stroke</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Lipoprotein(a) as a cardiovascular risk factor: current status</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Lipoprotein(a) as a cardiovascular risk factor: current status</title></titleInfo><name type="personal"><namePart type="given">Brge G.</namePart><namePart type="family">Nordestgaard</namePart><affiliation>Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark</affiliation><affiliation>E-mail: brno@heh.regionh.dk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. John</namePart><namePart type="family">Chapman</namePart><affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kausik</namePart><namePart type="family">Ray</namePart><affiliation>St George's University of London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Born</namePart><affiliation>University of Gothenburg, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Felicita</namePart><namePart type="family">Andreotti</namePart><affiliation>Catholic University Medical School, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerald F.</namePart><namePart type="family">Watts</namePart><affiliation>University of Western Australia, Perth, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Henry</namePart><namePart type="family">Ginsberg</namePart><affiliation>Columbia University, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Amarenco</namePart><affiliation>Bichat University Hospital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberico</namePart><namePart type="family">Catapano</namePart><affiliation>University of Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olivier S.</namePart><namePart type="family">Descamps</namePart><affiliation>Hopital de Jolimont, Haine Saint-Paul, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edward</namePart><namePart type="family">Fisher</namePart><affiliation>New York University, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Petri T.</namePart><namePart type="family">Kovanen</namePart><affiliation>Wihuri Research Institute, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan Albert</namePart><namePart type="family">Kuivenhoven</namePart><affiliation>University of Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Lesnik</namePart><affiliation>European Atherosclerosis Society, INSERM UMR-S939, Piti-Salpetriere University Hospital, Paris 75651, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luis</namePart><namePart type="family">Masana</namePart><affiliation>Universitat Rovira & Virgili, Reus, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zeljko</namePart><namePart type="family">Reiner</namePart><affiliation>University Hospital Center Zagreb, Croatia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marja-Riitta</namePart><namePart type="family">Taskinen</namePart><affiliation>Biomedicum, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lale</namePart><namePart type="family">Tokgzoglu</namePart><affiliation>Hacettepe University, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anne</namePart><namePart type="family">Tybjrg-Hansen</namePart><affiliation>Rigshospitalet, University of Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2010-12</dateIssued><dateCreated encoding="w3cdtf">2010-10-21</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Aims The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. Methods and results The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, 3 10-year risk of fatal CVD according to European guidelines, and/or 10 10-year risk of fatal non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than 50 mg/dL). Treatment should primarily be niacin 13 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). Conclusion We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.</abstract><note type="footnotes">The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.</note><subject><genre>keywords</genre><topic>Lipids</topic><topic>Hyperlipidemia</topic><topic>Prevention</topic><topic>Myocardial infarction</topic><topic>Stroke</topic></subject><relatedItem type="host"><titleInfo><title>European Heart Journal</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0195-668X</identifier><identifier type="eISSN">1522-9645</identifier><identifier type="PublisherID">eurheartj</identifier><identifier type="PublisherID-hwp">ehj</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>31</number></detail><detail type="issue"><caption>no.</caption><number>23</number></detail><extent unit="pages"><start>2844</start><end>2853</end></extent></part></relatedItem><identifier type="istex">895558F69D4D2768A710408C3318A07B201733D7</identifier><identifier type="DOI">10.1093/eurheartj/ehq386</identifier><identifier type="href">ehq386.pdf</identifier><identifier type="ArticleID">ehq386</identifier><accessCondition type="use and reproduction" contentType="copyright">Published on behalf of the European Society of Cardiology. 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