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. Author manuscript; available in PMC: 2023 Dec 1.
Published in final edited form as: Curr Opin Lipidol. 2022 Oct 14;33(6):342–352. doi: 10.1097/MOL.0000000000000855

Figure 2:

Figure 2:

Principle of Mendelian randomization studies demonstrating that a lifelong genetic exposure to high or low Lp(a) concentrations supports causality between Lp(a) concentrations and atherosclerotic cardiovascular disease (ASCVD). Panel A shows Lp(a)-increasing variants such as small apo(a) isoforms characterized by a low number of K-IV repeats [11, 12], or a low sum of K-IV repeats of both alleles [13] or single nucleotide polymorphisms such as rs10455872 and rs3798220 [14] which show a pronounced association with high Lp(a) concentrations are also significantly associated with ASCVD outcomes. In this case the association between Lp(a) concentrations and ASCVD is strongly supported to be causal. Panel B illustrates the Lp(a)-decreasing variants such as large apo(a) isoforms or the splice site variants 4733G>A [22**] and 4925G>A [21] within the kringle-IV type 2 or the missense variant rs41267813 are associated with low Lp(a) and concentrations and a lower ASCVD risk supporting a protective role of low Lp(a) concentrations against ASCVD.