Lp(a) Lipoprotein/pre-β1-lipoprotein, serum lipids and atherosclerotic disease

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Abstract
With appropriate electrophoretic techniques and fresh serum samples, the Lp(a) lipoprotein/pre-.beta.1-lipoprotein is demonstrable as a distinct zone in the area between .beta.-lipoprotein and ordinary pre-.beta.-lipoprotein, when sera which are strongly positive with respect to the Lp(a) antigen are analyzed. The Lp(a) lipoprotein is a genetically determined normal serum component. The phenotype Lp(a+) was found significantly more frequently in 2 series of patients with coronary heart disease (CHD) than in appropriate controls. The frequency difference between patients and controls was particularly pronounced for the Finnish samples studied, 55% of the patients having the phenotype Lp(a+), as opposed to only 31% of the healthy controls. As judged from electrophoresis strips, high concentration of Lp(a) lipoprotein/pre-.beta.1-lipoprotein were positively correlated with coronary score as determined by angiography. This correlation was highly significant. Total serum cholesterol value was slightly higher in Lp(a+) than in Lp(a-) persons from 2 of the 4 population samples studied, but no statistically significant difference was found. Serum triglyceride levels exhibited a statistically insignificant trend towards higher values in Lp(a-) than in Lp(a+) individuals, in 3 of the 4 samples tested. The strong association between the phenotype Lp(a+) and CHD, as well as the correlation between high amounts of Lp(a) lipoprotein/pre-.beta.1-lipoprotein and coronary score, and the weak correlation between presence of Lp(a) lipoprotein/pre-.beta.1-lipoprotein and lipid values, make it highly unlikely that the increased frequency of the Lp(a+) phenotype in CHD patients merely reflects an over-all increase of the intravascular pool of LDL [low density lipoprotein] and/or VLDL [very low density lipoprotein] reflected in increased serum levels of cholesterol and/or triglycerides. It is unlikely that the insignificant effect on lipid values can, on its own, explain the correlation between Lp(a) phenotype and CHD.