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  • Nordestgaard, B. G. (author)

Lipoprotein(a) as a Cardiovascular Risk Factor: Current Status

  • Article/chapterEnglish2010

Publisher, publication year, extent ...

  • 2010-10-21
  • Oxford University Press (OUP),2010

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/133461
  • https://gup.ub.gu.se/publication/133461URI
  • https://doi.org/10.1093/eurheartj/ehq386DOI

Supplementary language notes

  • Language:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • 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 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.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Chapman, MJ (author)
  • Ray, K (author)
  • Borén, Jan,1963Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine(Swepub:gu)xborej (author)
  • Andreotti, F (author)
  • Watts, GF (author)
  • Ginsberg, Mark H (author)
  • Amarenco, P (author)
  • Descamps, OS (author)
  • Fisher, E (author)
  • Kovanen, PT (author)
  • Kuivenhoven, JA (author)
  • Lesnik, P (author)
  • Masana, L (author)
  • Reiner, Z (author)
  • Taskinen, Marja-Riitta (author)
  • Tokgözoglu, Lale (author)
  • Tybjaerg-Hansen, A. (author)
  • Göteborgs universitetInstitutionen för medicin, avdelningen för molekylär och klinisk medicin (creator_code:org_t)

Related titles

  • In:European Heart Journal: Oxford University Press (OUP)31:23, s. 2844-28530195-668X1522-9645

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