Lipoprotein(a) concentration does not differ between sexes in healthy offspring of patients with premature myocardial infarction

Aims: Although a family history of coronary artery disease (CAD) is an established factor influencing lipoprotein(a) [Lp(a)] levels, the effect of sex on Lp(a) concentration remains unclear. A potential cause of the conflicting findings regarding the effect of sex on this novel CAD risk factor is the limited ability of the studies, to date, to adequately control for the potential confounding effect of CAD familial predisposition. Our purpose was to evaluate the influence of sex on Lp(a) concentration in healthy young individuals by controlling for family history of CAD. In order to achieve our goal, we compared Lp(a) levels in pairs of brothers and sisters with a positive parental history of premature myocardial infarction (PHPMI). Methods: We measured Lp(a) concentration in 77 healthy brother-sister pairs with PHPMI (mean age: brothers: 18.4 ± 6.2 years and sisters: 18.1 ± 5.8 years). Total cholesterol, low-density lipoprotein (LDL)-cholesterol and high-density lipoprotein (HDL)-cholesterol, triglycerides, apolipoprotein (Apo) A-I and B were also measured. Results: Lp(a) levels did not differ between siblings of different sex (male vs. female sex: 0.994 ± 1.29 vs. 0.860 ± 0.82 μmol/l, P = 0.940); moreover, the prevalence of elevated (>1.071 μmol/l) Lp(a) concentrations between sexes was the same (29.9%). As expected, compared to female sex, male sex showed higher total/HDL-cholesterol ratio (3.642 ± 0.99 vs. 3.329 ± 0.89, P = 0.017) and lower HDL-cholesterol (1.221 ± 0.24 vs. 1.343 ± 0.28 μmol/l, P = 0.001), Apo A-I (1.390 ± 0.20 vs. 1.474 ± 0.23 g/l, P = 0.003) concentrations and Apo A-I/Apo B ratio (1.632 ± 0.49 vs. 1.830 ± 0.66, P = 0.016). Conclusion: Our results show that healthy young men with PHPMI have a similar Lp(a) levels but worse lipid profile than women.