T he Lp(a) lipoprotein was first described by Berg 1 as a genetic variant of low density lipoprotein (LDL), and it was believed that this lipoprotein is inherited as an autosomal, dominant trait. After the introduction of quantitative Lp(a) measurement, it was shown that the Lp(a) lipoprotein represents a quantitative trait and that Lp(a) concentration is under polygenic control, probably with a major gene effect for high Lp(a) concentration.2 " 5 The interest in this unusual lipoprotein was greatly stimulated by reports of an association of high levels of Lp(a) lipoprotein with atherosclerosis.6 "
11The Lp(a) lipoprotein is an LDL-like particle that floats in a density range of about 1.05 to 1.10 g/ml. The lipid composition is similar to that of the LDL particle, but its protein moiety contains, in addition to apo B-100, the Lp(a)-specific glycoprotein, which is linked to apo B by disulfide bonds.
12-13> u The Lp(a) lipoprotein exhibits a density heterogeneity within and between individuals, as well as a size heterogeneity of the Lp(a)-specific glycoprotein. 1315 Recently, six different types of this Lp(a)-specific glycoprotein were resolved in our laboratory by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) followed by immunoblotting. 16 Preliminary evidence suggests that Lp(a) phenotypes are genetically controlled and, moreover, are associated with Lp(a) lipoprotein concentration in plasma. 16 Hence, the interesting possibility arose that the observed association of Lp(a) lipoprotein levels with atherosclerosis might be due to differences in Lp(a) glycoprotein species, rather than to differences in the concentration of the lipoprotein. To answer this and related questions, a method that allows convenient phenotyping of a large number of samples in epidemiologic studies is needed. In this paper, we describe an improved method for