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

Børge G Nordestgaard; M John Chapman; Kausik Ray; Jan Borén; 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 Tokgözoglu; Anne Tybjærg-Hansen; European Atherosclerosis Society Consensus Panel

doi:http://dx.doi.org/10.1093/eurheartj/ehq386

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

Børge G Nordestgaard, M John Chapman, Kausik Ray, Jan Borén, 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 Tokgözoglu, Anne Tybjærg-Hansen, European Atherosclerosis Society Consensus Panel

1025 Citations (Scopus)

Abstract

AimsThe 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 resultsThe 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). ConclusionWe 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.

Original language	English
Journal	European Heart Journal
Volume	31
Issue number	23
Pages (from-to)	2844-53
Number of pages	10
ISSN	0195-668X
DOIs	https://doi.org/10.1093/eurheartj/ehq386
Publication status	Published - 1 Dec 2010

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Nordestgaard, B. G., Chapman, M. J., Ray, K., Borén, J., Andreotti, F., Watts, G. F., Ginsberg, H., Amarenco, P., Catapano, A., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., Lesnik, P., Masana, L., Reiner, Z., Taskinen, M-R., Tokgözoglu, L., Tybjærg-Hansen, A., & European Atherosclerosis Society Consensus Panel (2010). Lipoprotein(a) as a cardiovascular risk factor: current status. European Heart Journal, 31(23), 2844-53. https://doi.org/10.1093/eurheartj/ehq386

Nordestgaard, BG, Chapman, MJ, Ray, K, Borén, J, Andreotti, F, Watts, GF, Ginsberg, H, Amarenco, P, Catapano, A, Descamps, OS, Fisher, E, Kovanen, PT, Kuivenhoven, JA, Lesnik, P, Masana, L, Reiner, Z, Taskinen, M-R, Tokgözoglu, L, Tybjærg-Hansen, A & European Atherosclerosis Society Consensus Panel 2010, 'Lipoprotein(a) as a cardiovascular risk factor: current status', European Heart Journal, vol. 31, no. 23, pp. 2844-53. https://doi.org/10.1093/eurheartj/ehq386

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title = "Lipoprotein(a) as a cardiovascular risk factor: current status",

abstract = "AimsThe 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 resultsThe 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). ConclusionWe 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.",

author = "Nordestgaard, {B{\o}rge G} and Chapman, {M John} and Kausik Ray and Jan Bor{\'e}n and Felicita Andreotti and Watts, {Gerald F} and Henry Ginsberg and Pierre Amarenco and Alberico Catapano and Descamps, {Olivier S} and Edward Fisher and Kovanen, {Petri T} and Kuivenhoven, {Jan Albert} and Philippe Lesnik and Luis Masana and Zeljko Reiner and Marja-Riitta Taskinen and Lale Tokg{\"o}zoglu and Anne Tybj{\ae}rg-Hansen and Anne Tybj{\ae}rg-Hansen",

year = "2010",

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doi = "http://dx.doi.org/10.1093/eurheartj/ehq386",

language = "English",

volume = "31",

pages = "2844--53",

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number = "23",

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T1 - Lipoprotein(a) as a cardiovascular risk factor: current status

AU - Nordestgaard, Børge G

AU - Chapman, M John

AU - Ray, Kausik

AU - Borén, Jan

AU - Andreotti, Felicita

AU - Watts, Gerald F

AU - Ginsberg, Henry

AU - Amarenco, Pierre

AU - Catapano, Alberico

AU - Descamps, Olivier S

AU - Fisher, Edward

AU - Kovanen, Petri T

AU - Kuivenhoven, Jan Albert

AU - Lesnik, Philippe

AU - Masana, Luis

AU - Reiner, Zeljko

AU - Taskinen, Marja-Riitta

AU - Tokgözoglu, Lale

AU - Tybjærg-Hansen, Anne

AU - European Atherosclerosis Society Consensus Panel

PY - 2010/12/1

Y1 - 2010/12/1

N2 - AimsThe 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 resultsThe 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). ConclusionWe 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.

AB - AimsThe 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 resultsThe 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). ConclusionWe 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.

U2 - http://dx.doi.org/10.1093/eurheartj/ehq386

DO - http://dx.doi.org/10.1093/eurheartj/ehq386

M3 - Journal article

SN - 0195-668X

VL - 31

SP - 2844

EP - 2853

JO - European Heart Journal

JF - European Heart Journal

IS - 23

ER -

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

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