Lipoprotein(a) is a genetically regulated trait, and its concentration in serum seems to be independent from that of other lipoprotein classes. It can be detected by ultracentrifugation in the d = 1.05-1.12 g/ml density range. Based on epidemiological observations Lp(a) is an independent risk factor for coronary heart disease. Its structure resembles LDL, but contains, in addition to apolipoprotein B 100, the disulphide-linked apoprotein(a). Apoprotein(a) shares a striking homology with plasminogen, consisting multiple repeating domains similar to kringle IV, a single kringle V and an inactive protease segment. The heterogeneity of Lp(a) complex is determined by the apoprotein(a) moiety. It seems so, that atherogenic properties of Lp(a) can be explained by its binding to glycosaminoglycans and inhibition of fibrinolysis. This latter effect is carried out by the kringle domains, which can interact with the plasminogen activators and plasmin binding sites on endothelial surface. The atherogenic properties of Lp(a) are expressed over 30 mg/dL serum concentration. Well-known antilipidemic drugs do not affect its serum level and genetically determined phenotype. Diseases leading to secondary hyperlipoproteinemia may influence the lipoprotein(a) level, too.