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)] concentr ations between a Swedish and Sri Lankan population. Methods: The distr ibution of Lp(a) and its relation to other lipid parameters, measured with an automated turbidimetric method, in 4646 Swedes (1944 females a nd 2702 males) undergoing health screening and 757 randomly selected S ri Lankan males (667 non-CHD and 80 CHD subjects) was evaluated. Resul ts: The distribution was highly skewed towards low values in both the Swedish population and the Sri Lankan male population. The Swedish pop ulation 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 Swede s, there was a small significant difference of 0.03 g/L between the se xes (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 als o significantly higher in subjects >50 years of age (p < 0.009) but on ly 7% had an Lp(a) concentration of >0.30 g/L. In the CHD subgroup, th ough not significant, subjects >50 years of age had a lower Lp(a) conc entration, indicating that Lp(a) may be a more significant risk factor in younger subjects. Both the Swedish female and male hypercholestero lemic subgroups had significantly higher Lp(a) concentrations than nor molipemic subgroups and the male hypertriglyceridemic subgroups signif icantly lower Lp(a) concentrations than normolipemic. Great difference s in Lp(a) levels are thus found between the two populations. The diff erences are similar in normolipemic subjects and probably they reflect mainly genetic differences. Lipid/lipoprotein concentrations were als o found to differ. It is being investigated ii this reflects differenc es in CHD prevalence. Conclusion: Our data support the importance of i ncluding Lp(a) measurements when assessing the risk profile for premat ure development of CHD in the individual patient.