Department of Physiology & Pharmacology and Robarts Research Institute, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada (Drs Koschinsky, Boffa).
Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA (Drs Bajaj, Soffer).
J Clin Lipidol. 2024 May-Jun;18(3):e308-e319. doi: 10.1016/j.jacl.2024.03.001. Epub 2024 Apr 1.
Since the 2019 National Lipid Association (NLA) Scientific Statement on Use of Lipoprotein(a) in Clinical Practice was issued, accumulating epidemiological data have clarified the relationship between lipoprotein(a) [Lp(a)] level and cardiovascular disease risk and risk reduction. Therefore, the NLA developed this focused update to guide clinicians in applying this emerging evidence in clinical practice. We now have sufficient evidence to support the recommendation to measure Lp(a) levels at least once in every adult for risk stratification. Individuals with Lp(a) levels <75 nmol/L (30 mg/dL) are considered low risk, individuals with Lp(a) levels ≥125 nmol/L (50 mg/dL) are considered high risk, and individuals with Lp(a) levels between 75 and 125 nmol/L (30-50 mg/dL) are at intermediate risk. Cascade screening of first-degree relatives of patients with elevated Lp(a) can identify additional individuals at risk who require intervention. Patients with elevated Lp(a) should receive early, more-intensive risk factor management, including lifestyle modification and lipid-lowering drug therapy in high-risk individuals, primarily to reduce low-density lipoprotein cholesterol (LDL-C) levels. The U.S. Food and Drug Administration approved an indication for lipoprotein apheresis (which reduces both Lp(a) and LDL-C) in high-risk patients with familial hypercholesterolemia and documented coronary or peripheral artery disease whose Lp(a) level remains ≥60 mg/dL [∼150 nmol/L)] and LDL-C ≥ 100 mg/dL on maximally tolerated lipid-lowering therapy. Although Lp(a) is an established independent causal risk factor for cardiovascular disease, and despite the high prevalence of Lp(a) elevation (∼1 of 5 individuals), measurement rates are low, warranting improved screening strategies for cardiovascular disease prevention.
自 2019 年美国脂质协会(NLA)发布关于脂蛋白(a)在临床实践中的应用科学声明以来,不断积累的流行病学数据阐明了脂蛋白(a)[Lp(a)]水平与心血管疾病风险及其降低之间的关系。因此,NLA 制定了本重点更新内容,以指导临床医生将这一新兴证据应用于临床实践。我们现在有足够的证据支持建议至少对每个成年人进行一次脂蛋白(a)水平检测,以进行风险分层。Lp(a)水平<75 nmol/L(30 mg/dL)的个体被认为是低风险,Lp(a)水平≥125 nmol/L(50 mg/dL)的个体被认为是高风险,Lp(a)水平在 75 至 125 nmol/L(30-50 mg/dL)之间的个体被认为是中风险。对 Lp(a)升高患者的一级亲属进行级联筛查,可以发现需要干预的其他风险个体。升高的 Lp(a)患者应接受早期、更强化的危险因素管理,包括生活方式改变和高风险个体的降脂药物治疗,主要是降低低密度脂蛋白胆固醇(LDL-C)水平。美国食品和药物管理局批准了脂蛋白吸附术(可降低 Lp(a)和 LDL-C)的适应证,用于家族性高胆固醇血症的高危患者和有记录的冠心病或外周动脉疾病患者,其 Lp(a)水平仍≥60 mg/dL[~150 nmol/L],且最大耐受降脂治疗后 LDL-C≥100 mg/dL。尽管 Lp(a)是心血管疾病的既定独立因果风险因素,而且 Lp(a)升高的患病率很高(约 1/5 的个体),但其检测率较低,需要改进心血管疾病预防的筛查策略。