Klingel Reinhard, Heigl Franz, Schettler Volker, Roeseler Eberhard, Grützmacher Peter, Hohenstein Bernd, Vogt Anja, Fassbender Cordula, Heibges Andreas, Julius Ulrich
Apheresis Research Institute, Cologne, Germany; First Department of Internal Medicine, University of Mainz, Mainz, Germany.
Medical Care Center Kempten-Allgäu, Kempten, Germany.
Atheroscler Suppl. 2019 Dec;40:17-22. doi: 10.1016/j.atherosclerosissup.2019.08.037.
Lipoprotein(a) (Lp(a)) consists of an LDL particle whose apolipoprotein B (apoB) is covalently bound to apolipoprotein(a) (apo[a]). An increased Lp(a) concentration is a causal, independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and a predictor of incident or recurrent cardiovascular events. Although Lp(a) was first described as early as 1963, only the more recent results of epidemiological, molecular, and genetic studies have led to this unequivocal conclusion. More than 20% of Western populations have elevated Lp(a) values. Lp(a) concentrations should be always part of the lipid profile when ASCVD risk is assessed. However, presence of other risk factors, laboratory findings, medical history and family history must be considered to conclude on its clinical relevance in an individual patient. Early or progressive ASCVD or a familial predisposition are key findings which can be associated with elevated Lp(a). The cholesterol portion contained in Lp(a) is also included in the various methods of LDL-C measurement. To assess proximity to the cardiovascular risk related target value for LDL-C, appropriate correction should be applied when high Lp(a) values are obtained to estimate the LDL-C that can actually be treated by lipid lowering drugs. Initial study data show that antisense oligonucleotides, which selectively decrease apolipoprotein(a), are promising as future treatment options. Currently, lipoprotein apheresis, which has a reimbursement guideline in Germany, is the therapy of choice for patients with Lp(a)-associated progressive ASCVD, with the aim of sustained prevention of further cardiovascular events.
脂蛋白(a)[Lp(a)]由一个低密度脂蛋白(LDL)颗粒组成,其载脂蛋白B(apoB)与载脂蛋白(a)[apo(a)]共价结合。Lp(a)浓度升高是动脉粥样硬化性心血管疾病(ASCVD)的一个因果性、独立危险因素,也是心血管事件发生或复发的预测指标。尽管Lp(a)早在1963年就被首次描述,但直到最近流行病学、分子和遗传学研究的结果才得出这一明确结论。超过20%的西方人群Lp(a)值升高。在评估ASCVD风险时,Lp(a)浓度应始终作为血脂谱的一部分。然而,在判断其对个体患者的临床相关性时,必须考虑其他危险因素的存在、实验室检查结果、病史和家族史。早期或进展性ASCVD或家族易感性是与Lp(a)升高相关的关键发现。Lp(a)中所含的胆固醇部分也包含在各种低密度脂蛋白胆固醇(LDL-C)测量方法中。为了评估与LDL-C心血管风险相关目标值的接近程度,当获得高Lp(a)值时,应进行适当校正,以估计实际上可通过降脂药物治疗的LDL-C。初步研究数据表明,选择性降低载脂蛋白(a)的反义寡核苷酸有望成为未来的治疗选择。目前,在德国有报销指南的脂蛋白分离术是Lp(a)相关进展性ASCVD患者的首选治疗方法,目的是持续预防进一步的心血管事件。