In the middle of the 1990s the interest in Lp(a) vanished after a few badly performed studies almost erased Lp(a) from the map of biological targets. However, since roughly 10 years the interest has begun to grow again mainly for two reasons: first, genetic studies using easily accessible and high-throughput techniques for genotyping of single-nucleotide polymorphisms (SNPs) have allowed large studies in patients with cardiovascular disease and controls to be performed. This strengthened the earlier findings on a copy number variation in the LPA gene and its association with cardiovascular outcomes. Second, new therapies are on the horizon raising strong and justified hope that in a few years drugs will become available which tremendously lower Lp(a) concentrations. This review article should provide an introduction to the genetic determination of Lp(a) concentrations and considerations whether Lp(a) concentrations or genetic variants are important for the prediction of cardiovascular risk.
Keywords: Apolipoprotein(a); Association study; Cardiovascular disease; Copy number variation; Lipoprotein(a); Mendelian randomization.