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Two hundred and ninety four pairs of Swedish twins reared apart and twins reared together were used to evaluate the importance of genetic and environmental influences on lipoprotein(a) (Lp(a)) levels. Lp(a) levels ranged from10 mg/l to 926 mg/l with 7.9% of the sample having undetectable Lp(a) levels (i.e.10 mg/l). A substantial genetic component in Lp(a) variation was indicated by a heritability estimate of approximately 90%. No difference in heritability was found across age groups. Quantitative genetic analyses also suggest correlated environmental effects most likely composed of maternal, neonatal and postnatal environmental influences. However, these effects did not reach statistical significance, partly due to a lack of power. Results from analyses of co-twin differences in Lp(a) levels for monozygotic twins indicate that sex hormone use may be of importance for Lp(a) variation in women. There was no evidence of potential influences of alcohol consumption, beta-blocker and diuretic administration on Lp(a) levels in either men or women.

Pig aorta glycerol ester hydrolase activity has been measured against a glyceryl tripalmitate hydrosol. The pattern of fatty acid release and the effect of some reagents known to modify lipase activity suggest that the glycerol ester hydrolase present in the pig aorta wall is a lipoprotein lipase.

The Lp(a) lipoprotein was originally suggested to be a qualitative autosomal dominant genetic marker confined to about 35% of Caucasian populations, when these were screened by a gel-diffusion technique. Using a more sensitive and quantitative immunochemical technique, the Lp(a) lipoprotein is found to be detectable in 75% of a random British population and to show quantitative variation in concentration between individuals. In hyperlipidaemic subjects (with the exception of subjects with the Type V abnormality) there is an overall increase in Lp(a) reactivity with a tendency for higher individual values to occur, regardless of the type of hyperlipidaemia. In individuals with coronary heart disease, hypertriglyceridaemia and the presence of a pre-beta-lipoprotein band on electrophoresis, no evidence was obtained to suggest that the electrophoretic abnormality was directly due to the increased frequency of Lp(a) reactivity found in such subjects. Using the immunofluorescent technique, the Lp(a) antigen has been demonstrated in the arterial atherosclerotic lesions of Lp(a) reactors in a topographic distribution closely similar to that of LDL.