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

Identifieur interne : 000106 ( France/Analysis ); précédent : 000105; suivant : 000107

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

Auteurs : Brge G. Nordestgaard [Danemark] ; M. John Chapman [France] ; Kausik Ray [Royaume-Uni] ; Jan Born [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 Tokgzoglu [Turquie] ; Anne Tybjrg-Hansen [Danemark]

Source :

RBID : ISTEX:895558F69D4D2768A710408C3318A07B201733D7

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.

Url:
DOI: 10.1093/eurheartj/ehq386


Affiliations:


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ISTEX:895558F69D4D2768A710408C3318A07B201733D7

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<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>
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   |area=    OpenAccessBelV2
   |flux=    France
   |étape=   Analysis
   |type=    RBID
   |clé=     ISTEX:895558F69D4D2768A710408C3318A07B201733D7
   |texte=   Lipoprotein(a) as a cardiovascular risk factor: current status
}}

Wicri

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Data generation: Thu Dec 1 00:43:49 2016. Site generation: Wed Mar 6 14:51:30 2024