Statins decrease the incidence of coronary heart disease (CHD) by reducing the levels of plasma LDL cholesterol (LDL-C), but some individuals still have CHD events despite receiving statin therapy. New research provides a genetic explanation to this inter-individual variability. Genotyping of 3,099 individuals with CHD events and 7,681 individuals without CHD events, both groups on statin therapy, identified seven single nucleotide polymorphisms (SNPs) that were associated with CHD and were located in the LPA gene, which encodes apolipoprotein(a) (Lp(a)). The SNP rs10455872 showed the strongest association with CHD, and individuals carrying this risk variant had a 58% increased risk of CHD events compared with non-carriers. This association was independent of LDL-C changes in response to statin therapy and persisted in individuals with LDL-C ≤70 mg/dl. A previous study also showed that rs10455872 is associated with increased plasma Lp(a) levels, an indicator of high risk of CHD. Thus, strategies to lower Lp(a) levels might reduce CHD incidence in patients receiving statin therapy.
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Wei, W.-Q. et al. LPA variants are associated with residual cardiovascular risk in patients receiving statins. Circulation https://doi.org/10.1161/CIRCULATIONAHA.117.031356 (2018)
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Le Bras, A. Genetic variation explains residual CHD risk with statin therapy. Nat Rev Cardiol 15, 440 (2018). https://doi.org/10.1038/s41569-018-0034-8
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DOI: https://doi.org/10.1038/s41569-018-0034-8