LIPOPROTEIN(A) - LEVELS IN A SWEDISH POPULATION IN RELATION TO OTHER LIPID PARAMETERS AND IN COMPARISON WITH A MALE SRI-LANKAN POPULATION

Objective: To evaluate differences in Lipoprotein (a) [Lp(a)] concentrations between a Swedish and Sri Lankan population. Methods: The distribution of Lp(a) and its relation to other lipid parameters, measured with an automated turbidimetric method, in 4646 Swedes (1944 females and 2702 males) undergoing health screening and 757 randomly selected Sri Lankan males (667 non-CHD and 80 CHD subjects) was evaluated. Results: The distribution was highly skewed towards low values in both the Swedish population and the Sri Lankan male population. The Swedish population had a median of 0.16 g/L (reported as total mass) whereas the Sri Lankan population median of 0.06 g/L was much lower. For the Swedes, there was a small significant difference of 0.03 g/L between the sexes (F < M; p < 0.001) and Lp(a) was significantly higher in subjects >50 years of age in both sexes (p < 0.002(F); p < 0.02(M)). 29% had Lp(a) values >0.30 g/L. In the Sri Lankan males population Lp(a) was also significantly higher in subjects >50 years of age (p < 0.009) but only 7% had an Lp(a) concentration of >0.30 g/L. In the CHD subgroup, though not significant, subjects >50 years of age had a lower Lp(a) concentration, indicating that Lp(a) may be a more significant risk factor in younger subjects. Both the Swedish female and male hypercholesterolemic subgroups had significantly higher Lp(a) concentrations than normolipemic subgroups and the male hypertriglyceridemic subgroups significantly lower Lp(a) concentrations than normolipemic. Great differences in Lp(a) levels are thus found between the two populations. The differences are similar in normolipemic subjects and probably they reflect mainly genetic differences. Lipid/lipoprotein concentrations were also found to differ. It is being investigated ii this reflects differences in CHD prevalence. Conclusion: Our data support the importance of including Lp(a) measurements when assessing the risk profile for premature development of CHD in the individual patient.