Relationship of plasma lipoprotein Lp(a) levels to race and to apolipoprotein B.

Abstract

Lipoprotein Lp(a) is an atherogenic subfraction of plasma lipoproteins which has been studied predominantly in white populations. We quantified Lp(a) by electroimmunoassay in plasma from 105 black and 134 white healthy men and women. Results were correlated with clinical variables and plasma levels of lipids, other lipoproteins, and apolipoprotein (apo) B determined by radioimmunoassay. Black subjects had levels of Lp(a) that averaged twice those of whites (p < 0.001). Among blacks, Lp(a) levels showed a bell-shaped frequency distribution, while among whites the distribution was strongly skewed, with the highest frequencies at low levels. Contrary to previously published results, the apo B levels in our study correlated significantly, though weakly, with Lp L ipoprotein Lp(a) is a cholesterol-rich lipoprotein that can be identified by its characteristic Lp(a) antigenic activity in human plasma.12 The apoproteins of lipoprotein Lp(a) include apolipoprotein (apo) B and apo (a), the antigenic determinant.2 Lipoprotein Lp(a) migrates as a distinct prebeta, band on agarose gel electrophoresis 1 and shows an apparent hydrated density in the range of 1.05 to 1.12 g/ml on ultracentrifugation.2 It is identical to the "prebeta," or the "sinking-prebeta" lipoprotein. 34 Catabolic rates and pathways of lipoprotein Lp(a) resemble those of iow density iipoprotein (LDL). 56 Other metabolic aspects are obscure but appear to be distinct from those of LDL 7 - Despite the fact that lipoprotein Lp(a) typically carries less than 15% of the cholesterol in plasma, levels of this lipoprotein are strongly and positively associated with coronary heart disease.3 ' A i a " Plasma levels of apo B also are strongly associated with the risk for coronary heart disease, and in certain situations, apo B appears to impart risk independently of total plasma cholesterol or LDL cholesterol.12 " 15However, there are few prevalence data in which both Lp(a) and apo B have been measured in the same group of individuals. 4 Such data are needed to clarify the interactive roles of Lp(a) and apo B in iipid metabolism and atherogenesis.Further understanding may be gained by measuring these putatively atherogenic entities within population groups that differ in their average risk of cardiovascular disease. As measured at autopsy, blacks showed less propensity for atherosclerosis than whites, 16 -17 and black men have relatively low mortality from coronary heart disease.1819 Thus far, the comparison of atherogenic apolipoprotein levels in black versus white individuals is limited to qualitative Lp(a) determinations;

Factors contributing to variation in lipoprotein (a) in Melbourne Anglo-Celtic population

“…These results agree with those of Cobbaert and Kesteloot (1992), Guyton et al, (1985), Kostner et al, (1981) and Parra et al, (1987). Also, the lack of a relationship of Lp(a) concentration with age is in agreement with the findings of Heinrich et al, (1991) and Steinmetz et al (1993).…”

Metabolic and anthropometric determinants of serum Lp(a) concentrations and Apo(a) polymorphism in a healthy Arab population

“…26 These levels are lower than reported values in native Africans and African Americans, in whom the distribution is also different, being more bell-shaped with a tendency to higher values. 18,25,28,31 There was, however, a tendency towards higher Lp(a) values in the women we studied (P 0.069), as in Koreans 20 and Nigerians. 25 In our women, there was also a positive correlation with age raising the possibility of the in¯uence of menopause, as previously described.…”

Genetic control of lipoprotein(a) concentrations is different in Africans and Caucasians

“…Despite this similarity there exist also significant differences between human populations. Several studies have documented significantly higher average Lp(a) levels in Black populations as compared to Caucasians, 20,[35][36][37] but the underlying mechanism(s) remained unclear. Differences in the frequency distribution of K IV VNTR alleles certainly do not explain Lp(a) level differences among populations.…”