Lp(a) or pre-beta 1-lipoprotein or Sinking pre-beta LP (SPB) is a special LP. Its very high density (1050 to 1120) means that it can be extracted from LDL and HDL. In common with the LDL, it possesses apo B and a similar size. It is characterized by the presence of specific apoproteins, non-immunoreactive albumin and a carbohydrate chain rich in sialic acid. Its transmission is hereditary; there is a major locus transmitted by autosomal dominant inheritance. Another hypothesis suggests that it is transmitted autosomally according to a polygenic mechanism for 75 p. cent of the molecule with superimposition of non-genetic elements for the rest. Lp(a) is not a product of Lp(b) metabolism; it is not transformed into any other LP and it does not exchange its apoproteins. Its synthesis is constant over time and its function is not yet known. Its assay depends on the antigenicity of the specific determinants of the apo Lp(a). Only radio-immunoassay is able to give values for any sample size especially for levels of less than 50 to 80 mg/l (respective limits of the EID and IDR techniques). It appears that a high Lp(a) level could constitute an additional risk to developing coronary heart disease and the limit beyond which this risk exists could be 300 mg/l in normolipidaemic subjects. The in vitro binding of LP to glycoaminoglycanes (GAG) could be a model for studying LP binding in vivo. It has been seen that, by the intermediary of a low concentration of Ca++ ions, the reactivity of Lp(a) to GAG was selective.