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. 2016 Feb 20;30:87–100. doi: 10.1007/s10557-016-6648-3

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© The Author(s) 2016

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 3 — Mendelian Randomization approach to demonstrate a causal association between Lp(a) concentrations and coronary heart disease (CHD). Panel a shows the association between elevated Lp(a) concentrations and cardiovascular disease (CVD) as shown in the Copenhagen City Heart Study [53]. Panel b shows the association between the number of K-IV repeats in the LPA gene and Lp(a) concentrations: individuals with small apo(a) isoform have markedly higher median Lp(a) concentrations than individuals with large apo(a) isoforms. Data are derived from [107]. Panel c shows the preponderance of small apo(a) isoforms in patients with CVD when compared to controls. Data are taken from a case–control study in multiple populations [56]. Since a low number of KIV copies (11–22 copies) is associated with high Lp(a) levels and high Lp(a) levels are associated with CHD, it follows that a low number of KIV copies has to be associated with CVD if the association of Lp(a) with CVD is causal