Clinical investigation of Lp(a) is largely hampered by the fact that Lp(a)-hyperlipidemia (Lp(a)-HLP) frequently co-incides with other genetic factors for hyperlipidemia and risk of CVD, such as familial hypercholesterolemia (FH) or apolipoprotein E4-allele [3, 4]. Here, LPA is linked to familial hyperaldosteronism.