Department of Internal Medicine, division of Vascular Medicine and Pharmacology, Division of Medical Psychology and Psychotherapy, Erasmus MC, Erasmus University Medical Center, Rotterdam, Netherlands.
Department of Internal Medicine, division of Vascular Medicine and Pharmacology, Division of Medical Psychology and Psychotherapy, Erasmus MC, Erasmus University Medical Center, Rotterdam, Netherlands; Department of Dietetics and Division of Medical Psychology and Psychotherapy, Erasmus MC, Erasmus University Medical Center, Rotterdam, Netherlands.
Atherosclerosis. 2019 Oct;289:201-205. doi: 10.1016/j.atherosclerosis.2019.07.001. Epub 2019 Jul 3.
We aimed to evaluate the effect of statin treatment initiation on lipoprotein(a) [Lp(a)] levels in patients with dyslipidemia, and the interactions with the apolipoprotein(a) [apo(a)] phenotype, LPA single nucleotide polymorphisms (SNPs) and change in LDL cholesterol.
The study population consisted of patients with dyslipidemia, predominantly familial hypercholesterolemia, who first initiated statin treatment (initiation group; n = 39) or were already on stable statin treatment for at least 4 months (control group; n = 42). Plasma Lp(a) levels were determined with a particle-enhanced immunoturbidimetric assay before and at least 2 months after start of statin treatment in individuals of the initiation group, and at two time points with an interval of at least 2 months in the control group. High and low molecular weight (HMW and LMW, respectively) apo(a) phenotype was determined by immunoblotting, and the common LPA SNPs rs10455872, rs3798220 and rs41272110 by Taqman assay.
Plasma Lp(a) levels did not increase significantly in the initiation group (median 20.5 (IQR 10.9-80.7) to 23.3 (10.8-71.8) mg/dL; p = 0.09) nor in the control group (30.9 (IQR 9.2-147.0) to 31.7 (IQR 10.9-164.0) mg/dL; p = 0.61). In patients with the LMW apo(a) phenotype, Lp(a) levels increased significantly from 66.4 (IQR 23.5-148.3) to 97.4 (IQR 24.9-160.4) mg/dL (p = 0.026) in the initiation group, but not in the control group and not in patients characterized by the HMW apo(a) phenotype. Interactions with common LPA SNPs and change in LDL cholesterol were not significant.
Statins affect Lp(a) levels differently in patients with dyslipidemia depending on the apo(a) phenotype. Statins increase Lp(a) levels exclusively in patients with the LMW apo(a) phenotype.
我们旨在评估他汀类药物治疗起始对血脂异常患者脂蛋白(a) [Lp(a)]水平的影响，并研究其与载脂蛋白(a) [apo(a)]表型、LPA 单核苷酸多态性 (SNP) 和 LDL 胆固醇变化的相互作用。
研究人群为血脂异常患者，主要为家族性高胆固醇血症，他们首次开始他汀类药物治疗（起始组；n=39）或已接受稳定的他汀类药物治疗至少 4 个月（对照组；n=42）。起始组的个体在开始他汀类药物治疗前和至少 2 个月后以及对照组至少 2 个月的两个时间点，使用颗粒增强免疫比浊法测定血浆 Lp(a)水平。通过免疫印迹法测定高和低分子量（HMW 和 LMW，分别）apo(a)表型，并通过 Taqman 法测定常见的 LPA SNP rs10455872、rs3798220 和 rs41272110。
起始组血浆 Lp(a)水平无显著升高（中位数 20.5（IQR 10.9-80.7）至 23.3（10.8-71.8）mg/dL；p=0.09），对照组也无显著升高（30.9（IQR 9.2-147.0）至 31.7（IQR 10.9-164.0）mg/dL；p=0.61）。在 LMW apo(a)表型患者中，起始组 Lp(a)水平从 66.4（IQR 23.5-148.3）显著升高至 97.4（IQR 24.9-160.4）mg/dL（p=0.026），但对照组和 HMW apo(a)表型患者无显著升高。与常见 LPA SNP 和 LDL 胆固醇变化的相互作用不显著。
他汀类药物在血脂异常患者中对 Lp(a)水平的影响取决于 apo(a)表型。他汀类药物仅增加 LMW apo(a)表型患者的 Lp(a)水平。
