Abstract
Lipoprotein(a) [Lp(a)] levels are an independent risk factor for coronary artery disease (CAD). Two single-nucleotide polymorphisms (rs10455872, rs3798220) and number of KIV-2 repeats in the gene encoding Lp(a) (LPA) are associated with Lp(a) and CAD. Our aim was to investigate whether in patients with stable CAD and high Lp(a) levels these genetic variants are associated with increased Lp(a) and arterial wall properties. Blood samples underwent biochemical and genetic analyses. Ultrasound measurements for the functional and morphological properties of arterial wall were performed. Genotypes of rs10455872 and haplotypes AT and GT showed significant association with Lp(a) levels. Patients with GG showed significantly higher Lp(a) levels compared with those with AG genotype (2180 vs. 1391 mg/L, p = 0.045). Patients with no AT haplotype had significantly higher Lp(a) compared to carriers of one AT haplotype (2158 vs. 1478 mg/L, p = 0.023) or two AT haplotypes (2158 vs. 1487 mg/L, p = 0.044). There were no significant associations with the properties of the arterial wall. Lp(a) levels significantly correlated also with number of KIV-2 repeats (r = −0.601; p < 0.0001). In our patients, these two LPA polymorphisms and number of KIV-2 repeats are associated with Lp(a), but not arterial wall properties.
Highlights
Lipoprotein(a) [Lp(a)] has been shown to be an independent risk factor for cardiovascular diseases [1]
Clarke et al identified two single-nucleotide polymorphisms (SNPs; rs10455872, rs3798220) in the LPA gene that were strongly associated with both increased Lp(a) levels and increased risk of coronary diseases [4]
All of the patients were receiving statins at the highest tolerated dose without/with ezetimibe, their low-density lipoprotein (LDL) cholesterol was not within target levels according to recent guidelines [22]
Summary
Lipoprotein(a) [Lp(a)] has been shown to be an independent risk factor for cardiovascular diseases [1]. Clarke et al identified two single-nucleotide polymorphisms (SNPs; rs10455872, rs3798220) in the LPA gene that were strongly associated with both increased Lp(a) levels and increased risk of coronary diseases [4]. These two SNPs explained 36% of the variation in Lp(a) levels. Kamstrup et al explained 21% and 27% of the total interindividual variation in Lp(a) levels in two independent samples of the general population according to copy-number variations of the kringle IV type 2 (KIV-2) repeat [5] They showed that the risk of myocardial infarction (MI) increased with decreasing numbers of KIV-2 repeats, and is associated with high Lp(a) levels.
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