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      Lipoprotein(a) Levels and the Risk of Myocardial Infarction Among 7 Ethnic Groups

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          Abstract

          Lipoprotein(a) [Lp(a)] levels predict the risk of myocardial infarction (MI) in populations of European ancestry; however, few data are available for other ethnic groups. Furthermore, differences in isoform size distribution and the associated Lp(a) concentrations have not fully been characterized between ethnic groups.

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          Antisense oligonucleotides targeting apolipoprotein(a) in people with raised lipoprotein(a): two randomised, double-blind, placebo-controlled, dose-ranging trials.

          Nicholas Viney, Julian C van Capelleveen, Richard S Geary … (2016)
          Elevated lipoprotein(a) (Lp[a]) is a highly prevalent (around 20% of people) genetic risk factor for cardiovascular disease and calcific aortic valve stenosis, but no approved specific therapy exists to substantially lower Lp(a) concentrations. We aimed to assess the efficacy, safety, and tolerability of two unique antisense oligonucleotides designed to lower Lp(a) concentrations.
          Article 0 comments Cited 244 times – based on 0 reviews     Review now
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            Lipoprotein(a): resurrected by genetics.

            G Utermann, F Kronenberg (2012)
            Plasma lipoprotein(a) [Lp(a)] is a quantitative genetic trait with a very broad and skewed distribution, which is largely controlled by genetic variants at the LPA locus on chromosome 6q27. Based on genetic evidence provided by studies conducted over the last two decades, Lp(a) is currently considered to be the strongest genetic risk factor for coronary heart disease (CHD). The copy number variation of kringle IV in the LPA gene has been strongly associated with both Lp(a) levels in plasma and risk of CHD, thereby fulfilling the main criterion for causality in a Mendelian randomization approach. Alleles with a low kringle IV copy number that together have a population frequency of 25-35% are associated with a doubling of the relative risk for outcomes, which is exceptional in the field of complex genetic phenotypes. The recently identified binding of oxidized phospholipids to Lp(a) is considered as one of the possible mechanisms that may explain the pathogenicity of Lp(a). Drugs that have been shown to lower Lp(a) have pleiotropic effects on other CHD risk factors, and an improvement of cardiovascular endpoints is up to now lacking. However, it has been established in a proof of principle study that lowering of very high Lp(a) by apheresis in high-risk patients with already maximally reduced low-density lipoprotein cholesterol levels can dramatically reduce major coronary events. © 2012 The Association for the Publication of the Journal of Internal Medicine.
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              Extreme lipoprotein(a) levels and risk of myocardial infarction in the general population: the Copenhagen City Heart Study.

              Maria Kamstrup, Marianne Benn, Borge Nordestgaard … (2008)
              Elevated lipoprotein(a) levels are associated with myocardial infarction (MI) in some but not all studies. Limitations of previous studies include lack of risk estimates for extreme lipoprotein(a) levels, measurements in long-term frozen samples, no correction for regression dilution bias, and lack of absolute risk estimates in the general population. We tested the hypothesis that extreme lipoprotein(a) levels predict MI in the general population, measuring levels shortly after sampling, correcting for regression dilution bias, and calculating hazard ratios and absolute risk estimates. We examined 9330 men and women from the general population in the Copenhagen City Heart Study. During 10 years of follow-up, 498 participants developed MI. In women, multifactorially adjusted hazard ratios for MI for elevated lipoprotein(a) levels were 1.1 (95% CI, 0.6 to 1.9) for 5 to 29 mg/dL (22nd to 66th percentile), 1.7 (1.0 to 3.1) for 30 to 84 mg/dL (67th to 89th percentile), 2.6 (1.2 to 5.9) for 85 to 119 mg/dL (90th to 95th percentile), and 3.6 (1.7 to 7.7) for > or =120 mg/dL (>95th percentile) versus levels 60 years with lipoprotein(a) levels of or =120 mg/dL, respectively. Equivalent values in men were 19% and 35%. We observed a stepwise increase in risk of MI with increasing levels of lipoprotein(a), with no evidence of a threshold effect. Extreme lipoprotein(a) levels predict a 3- to 4-fold increase in risk of MI in the general population and absolute 10-year risks of 20% and 35% in high-risk women and men.
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                Author and article information

                Journal
                Title: Circulation
                Abbreviated Title: Circulation
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 0009-7322
                ISSN (Electronic): 1524-4539
                Publication date Created: March 19 2019
                Publication date (Print): March 19 2019
                Volume: 139
                Issue: 12
                Pages: 1472-1482
                Affiliations
                [1 ]Population Health Research Institute, Hamilton, Canada (G.P., M.M., S.S.A., S.Y.).
                [2 ]Genetic & Molecular Epidemiology Laboratory, Department of Pathology and Molecular Medicine (G.P.), McMaster University, Hamilton, Canada.
                [3 ]Department of Biochemistry, University of Sherbrooke, Canada (A.C.).
                [4 ]Department of Pathology and Molecular Medicine (M.M.), McMaster University, Hamilton, Canada.
                [5 ]Clinical Research Laboratory and Biobank, Hamilton Health Sciences, Canada (M.M.).
                [6 ]Department of Medicine (S.S.A.), McMaster University, Hamilton, Canada.
                [7 ]Coronary Artery Disease Among Asian Indians Research Foundation, Advanced Heart and Lipid Clinic Ltd, Downers Grove, IL (E.E.).
                [8 ]Nuffield Department of Population Health, University of Oxford, UK (R.C.).
                [9 ]Department of Biochemistry (M.B.B.), Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Canada.
                [10 ]Department of Physiology and Pharmacology (M.K.), Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Canada.
                [11 ]Beijing Hypertension League Institute, China (X.W.).
                Article
                DOI: 10.1161/CIRCULATIONAHA.118.034311
                PubMed ID: 30667276
                SO-VID: 4b67256b-abe4-4147-b127-58894191882c
                Copyright © © 2019
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