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Lipoprotein(a) as a cardiovascular risk factor: current status

Identifieur interne : 002292 ( PascalFrancis/Checkpoint ); précédent : 002291; suivant : 002293

Lipoprotein(a) as a cardiovascular risk factor: current status

Auteurs : B Rge G. Nordestgaard [Danemark] ; M. John Chapman [France] ; Kausik Ray [Royaume-Uni] ; Jan Boren [Suède] ; Felicita Andreotti [Italie] ; Gerald F. Watts [Australie] ; Henry Ginsberg [États-Unis] ; Pierre Amarenco [France] ; Alberico 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] ; Zeljko Reiner [Croatie] ; Marja-Riitta Taskinen [Finlande] ; Lale Tokgözoglu [Turquie] ; Anne Tybjaerg-Hansen [Danemark]

Source :

RBID : Pascal:11-0028076

Descripteurs français

English descriptors

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 The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/cor-and results onary 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 hyperchotesterolaemia, 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). 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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Pascal:11-0028076

Le document en format XML

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<name sortKey="Masana, Luis" sort="Masana, Luis" uniqKey="Masana L" first="Luis" last="Masana">Luis Masana</name>
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<name sortKey="Reiner, Zeljko" sort="Reiner, Zeljko" uniqKey="Reiner Z" first="Zeljko" last="Reiner">Zeljko Reiner</name>
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<title xml:lang="en" level="a">Lipoprotein(a) as a cardiovascular risk factor: current status</title>
<author>
<name sortKey="Nordestgaard, B Rge G" sort="Nordestgaard, B Rge G" uniqKey="Nordestgaard B" first="B Rge G." last="Nordestgaard">B Rge G. Nordestgaard</name>
<affiliation wicri:level="1">
<inist:fA14 i1="01">
<s1>Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen</s1>
<s2>2730 Herlev</s2>
<s3>DNK</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Danemark</country>
<wicri:noRegion>2730 Herlev</wicri:noRegion>
</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 wicri:level="1">
<inist:fA14 i1="02">
<s1>European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital</s1>
<s2>Paris 75651</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>75651</wicri:noRegion>
<placeName>
<settlement type="city">Paris</settlement>
<region type="région" nuts="2">Île-de-France</region>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Ray, Kausik" sort="Ray, Kausik" uniqKey="Ray K" first="Kausik" last="Ray">Kausik Ray</name>
<affiliation wicri:level="4">
<inist:fA14 i1="03">
<s1>St George's University of London</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
<country>Royaume-Uni</country>
<placeName>
<settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
<settlement type="city">Londres</settlement>
</placeName>
<orgName type="university">Université de Londres</orgName>
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<name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name>
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<inist:fA14 i1="04">
<s1>University of Gothenburg</s1>
<s3>SWE</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Suède</country>
<wicri:noRegion>University of Gothenburg</wicri:noRegion>
</affiliation>
</author>
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<name sortKey="Andreotti, Felicita" sort="Andreotti, Felicita" uniqKey="Andreotti F" first="Felicita" last="Andreotti">Felicita Andreotti</name>
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<name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name>
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<s1>University of Western Australia</s1>
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<name sortKey="Ginsberg, Henry" sort="Ginsberg, Henry" uniqKey="Ginsberg H" first="Henry" last="Ginsberg">Henry Ginsberg</name>
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</inist:fA14>
<country>États-Unis</country>
<placeName>
<region type="state">État de New York</region>
<settlement type="city">New York</settlement>
</placeName>
<orgName type="university">Université Columbia</orgName>
</affiliation>
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<name sortKey="Amarenco, Pierre" sort="Amarenco, Pierre" uniqKey="Amarenco P" first="Pierre" last="Amarenco">Pierre Amarenco</name>
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<name sortKey="Catapano, Alberico" sort="Catapano, Alberico" uniqKey="Catapano A" first="Alberico" last="Catapano">Alberico Catapano</name>
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<s1>University of Milan</s1>
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</inist:fA14>
<country>Italie</country>
<wicri:noRegion>University of Milan</wicri:noRegion>
</affiliation>
</author>
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<name sortKey="Descamps, Olivier S" sort="Descamps, Olivier S" uniqKey="Descamps O" first="Olivier S." last="Descamps">Olivier S. Descamps</name>
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<s1>Hopital de Jolimont</s1>
<s2>Haine Saint-Paul</s2>
<s3>BEL</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
<country>Belgique</country>
<wicri:noRegion>Hopital de Jolimont</wicri:noRegion>
</affiliation>
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<name sortKey="Fisher, Edward" sort="Fisher, Edward" uniqKey="Fisher E" first="Edward" last="Fisher">Edward Fisher</name>
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<s1>New York University</s1>
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<country>États-Unis</country>
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<region type="state">État de New York</region>
</placeName>
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<name sortKey="Kovanen, Petri T" sort="Kovanen, Petri T" uniqKey="Kovanen P" first="Petri T." last="Kovanen">Petri T. Kovanen</name>
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<inist:fA14 i1="12">
<s1>Wihuri Research Institute</s1>
<s2>Helsinki</s2>
<s3>FIN</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
<wicri:noRegion>Wihuri Research Institute</wicri:noRegion>
</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 wicri:level="4">
<inist:fA14 i1="13">
<s1>University of Amsterdam</s1>
<s3>NLD</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
<country>Pays-Bas</country>
<placeName>
<settlement type="city">Amsterdam</settlement>
<region>Hollande-Septentrionale</region>
</placeName>
<orgName type="university">Université d'Amsterdam</orgName>
</affiliation>
</author>
<author>
<name sortKey="Lesnik, Philippe" sort="Lesnik, Philippe" uniqKey="Lesnik P" first="Philippe" last="Lesnik">Philippe Lesnik</name>
<affiliation wicri:level="3">
<inist:fA14 i1="02">
<s1>European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital</s1>
<s2>Paris 75651</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
<country>France</country>
<placeName>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
</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="14">
<s1>Universitat Rovira & Virgili</s1>
<s2>Reus</s2>
<s3>ESP</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
<country>Espagne</country>
<wicri:noRegion>Universitat Rovira & Virgili</wicri:noRegion>
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<name sortKey="Reiner, Zeljko" sort="Reiner, Zeljko" uniqKey="Reiner Z" first="Zeljko" last="Reiner">Zeljko Reiner</name>
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<s1>University Hospital Center Zagreb</s1>
<s3>HRV</s3>
<sZ>16 aut.</sZ>
</inist:fA14>
<country>Croatie</country>
<wicri:noRegion>University Hospital Center Zagreb</wicri:noRegion>
</affiliation>
</author>
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<name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
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<inist:fA14 i1="16">
<s1>Biomedicum</s1>
<s2>Helsinki</s2>
<s3>FIN</s3>
<sZ>17 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
<wicri:noRegion>Biomedicum</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Tokgozoglu, Lale" sort="Tokgozoglu, Lale" uniqKey="Tokgozoglu L" first="Lale" last="Tokgözoglu">Lale Tokgözoglu</name>
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<s1>Hacettepe University</s1>
<s2>Ankara</s2>
<s3>TUR</s3>
<sZ>18 aut.</sZ>
</inist:fA14>
<country>Turquie</country>
<wicri:noRegion>Hacettepe University</wicri:noRegion>
</affiliation>
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<name sortKey="Tybjaerg Hansen, Anne" sort="Tybjaerg Hansen, Anne" uniqKey="Tybjaerg Hansen A" first="Anne" last="Tybjaerg-Hansen">Anne Tybjaerg-Hansen</name>
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<inist:fA14 i1="18">
<s1>Rigshospitalet. University of Copenhagen</s1>
<s3>DNK</s3>
<sZ>19 aut.</sZ>
</inist:fA14>
<country>Danemark</country>
<wicri:noRegion>Rigshospitalet. University of Copenhagen</wicri:noRegion>
</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="2010">2010</date>
</imprint>
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<title level="j" type="main">European heart journal</title>
<title level="j" type="abbreviated">Eur. heart j.</title>
<idno type="ISSN">0195-668X</idno>
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<term>Atherosclerosis</term>
<term>Cardiology</term>
<term>Cardiovascular disease</term>
<term>Circulatory system</term>
<term>Current</term>
<term>Lipids</term>
<term>Lipoprotein a</term>
<term>Myocardial infarction</term>
<term>Prevention</term>
<term>Risk factor</term>
<term>Stroke</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Athérosclérose</term>
<term>Pathologie de l'appareil circulatoire</term>
<term>Infarctus du myocarde</term>
<term>Accident cérébrovasculaire</term>
<term>Lipoprotéine a</term>
<term>Facteur risque</term>
<term>Courant</term>
<term>Lipide</term>
<term>Prévention</term>
<term>Appareil circulatoire</term>
<term>Cardiologie</term>
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<front>
<div type="abstract" xml:lang="en">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 The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/cor-and results onary 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 hyperchotesterolaemia, 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). 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>
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<s1>NORDESTGAARD (Børge G.)</s1>
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<s1>CATAPANO (Alberico)</s1>
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<s1>DESCAMPS (Olivier S.)</s1>
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<s1>FISHER (Edward)</s1>
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<s1>KOVANEN (Petri T.)</s1>
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<s1>KUIVENHOVEN (Jan Albert)</s1>
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<s1>LESNIK (Philippe)</s1>
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<s1>MASANA (Luis)</s1>
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<sZ>2 aut.</sZ>
<sZ>14 aut.</sZ>
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<s1>St George's University of London</s1>
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<sZ>3 aut.</sZ>
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<fA14 i1="04">
<s1>University of Gothenburg</s1>
<s3>SWE</s3>
<sZ>4 aut.</sZ>
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<s1>Catholic University Medical School</s1>
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<fA14 i1="06">
<s1>University of Western Australia</s1>
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<sZ>6 aut.</sZ>
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<fA14 i1="07">
<s1>Columbia University</s1>
<s2>New York</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
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<fA14 i1="08">
<s1>Bichat University Hospital</s1>
<s2>Paris</s2>
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<sZ>8 aut.</sZ>
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<fA14 i1="09">
<s1>University of Milan</s1>
<s3>ITA</s3>
<sZ>9 aut.</sZ>
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<fA14 i1="10">
<s1>Hopital de Jolimont</s1>
<s2>Haine Saint-Paul</s2>
<s3>BEL</s3>
<sZ>10 aut.</sZ>
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<s1>New York University</s1>
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<sZ>11 aut.</sZ>
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<s1>Wihuri Research Institute</s1>
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<sZ>12 aut.</sZ>
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<fA14 i1="13">
<s1>University of Amsterdam</s1>
<s3>NLD</s3>
<sZ>13 aut.</sZ>
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<fA14 i1="14">
<s1>Universitat Rovira & Virgili</s1>
<s2>Reus</s2>
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<fA14 i1="15">
<s1>University Hospital Center Zagreb</s1>
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<s1>Rigshospitalet. University of Copenhagen</s1>
<s3>DNK</s3>
<sZ>19 aut.</sZ>
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<s1>European Atherosclerosis Society Consensus Panel</s1>
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<s1>2844-2853</s1>
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<s0>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 The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/cor-and results onary 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 hyperchotesterolaemia, 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). 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.</s0>
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