Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Mar-Apr;71(2):99-112.
doi: 10.1016/j.ihj.2019.03.004. Epub 2019 Mar 20.

Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction

Enas A Enas  1 , Basil Varkey  2 , T S Dharmarajan  3 , Guillaume Pare  4 , Vinay K Bahl  5
Affiliations
Review

Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction

Enas A Enas et al. Indian Heart J. 2019 Mar-Apr.

Abstract

Lipoprotein(a) [Lp(a)] is a circulating lipoprotein, and its level is largely determined by variation in the Lp(a) gene (LPA) locus encoding apo(a). Genetic variation in the LPA gene that increases Lp(a) level also increases coronary artery disease (CAD) risk, suggesting that Lp(a) is a causal factor for CAD risk. Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), a proatherogenic and proinflammatory biomarker. Lp(a) adversely affects endothelial function, inflammation, oxidative stress, fibrinolysis, and plaque stability, leading to accelerated atherothrombosis and premature CAD. The INTER-HEART Study has established the usefulness of Lp(a) in assessing the risk of acute myocardial infarction in ethnically diverse populations with South Asians having the highest risk and population attributable risk. The 2018 Cholesterol Clinical Practice Guideline have recognized elevated Lp(a) as an atherosclerotic cardiovascular disease risk enhancer for initiating or intensifying statin therapy.

Keywords: Acute myocardial infarction; Cardiovascular disease; Genetic risk factor; Genome-wide association studies; Indians; Isoforms; Kringles; Lipoprotein(a); Mendelian randomization; Oxidized phospholipids; Premature coronary artery disease; Single nucleotide polymorphism; meta-analysis.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Lp(a) particles: One containing large apo(a) isoform and the other containg small apo(a) isoform.
Fig. 2
Fig. 2
Mendelian randomization approach to demonstrate causal association between Lp(a) concentrations and CVD (Ref 12,37).
See this image and copyright information in PMC

References

    1. Tsimikas S., Fazio S., Ferdinand K.C. NHLBI working group recommendations to reduce lipoprotein(a)-mediated risk of cardiovascular disease and aortic stenosis. J Am Coll Cardiol. 2018;71(2):177–192. - PMC - PubMed
    1. Tsimikas S. A test in context: lipoprotein(a): diagnosis, prognosis, controversies, and emerging therapies. J Am Coll Cardiol. 2017;69(6):692–711. - PubMed
    1. Capoulade R., Chan K.L., Yeang C. Oxidized phospholipids, lipoprotein(a), and progression of calcific aortic valve stenosis. J Am Coll Cardiol. 2015;66(11):1236–1246. - PubMed
    1. Varvel S., McConnell J.P., Tsimikas S. Prevalence of elevated lp(a) mass levels and patient thresholds in 532 359 patients in the United States. Arterioscler Thromb Vasc Biol. 2016;36(11):2239–2245. - PubMed
    1. Nordestgaard B.G., Chapman M.J., Ray K. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010 - PMC - PubMed