Abstract
Background and Aims : Lipoprotein(a) [Lp(a)] plasma concentrations are mainly regulated by the LPA gene. Besides the KIV-2 repeat (a complex copy number variation), multiple SNPs pronouncedly modify Lp(a) levels (e.g. the recently described KIV-2 variant 4925G>A). However, little is known about non-linear and/or epistatic mechanisms and SNP interactions. Thus, we investigated the impact of the interaction between the largely investigated LPA variant p.Thr3888Pro (rs41272110) and the KIV-2 variant 4925G>A on Lp(a) concentration and CAD risk.
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