Division of Cardiovascular Medicine, Department of Medicine, Cardiovascular Institute, UC San Diego Health, Sulpizio Cardiovascular Center, University of California San Diego, 9434 Medical Center Dr, MC 7241, La Jolla, CA, 92037, San Diego, USA.
Curr Cardiol Rep. 2023 Oct;25(10):1175-1187. doi: 10.1007/s11886-023-01937-z. Epub 2023 Aug 26.
Lipoprotein(a) is an independent risk factor for cardiovascular disease. We review the ongoing shifts in consensus guidelines for the testing and management of Lp(a) and provide insight into whether current evidence suggests that awareness and testing of Lp(a) is clinically actionable.
GWAS and Mendelian randomization studies have established causal links between elevated Lp(a) and forms of CVD, including CAD and calcific aortic valve disease. Testing of Lp(a) identifies patients with similar risk to that of heterozygous FH, enhances risk stratification in patients with borderline/intermediate risk as determined through traditional factors, and facilitates the assessment of inherited CVD risk through cascade screening in patients with known family history of elevated Lp(a). Reductions in Lp(a) through non-targeted therapies including PCSK9 inhibition and lipoprotein apheresis have demonstrated reductions in ASCVD risk that are likely attributable to lowering Lp(a). Targeted therapies to potently lower Lp(a) are in clinical development. Lp(a) is actionable, and can be used to identify high risk patients for primary prevention and their family members through cascade screening, and to guide intensification of therapy in primary and secondary prevention of ASCVD.
脂蛋白（a）是心血管疾病的独立危险因素。我们回顾了脂蛋白（a）检测和管理的共识指南的最新变化，并深入探讨了当前的证据是否表明，脂蛋白（a）的检测具有临床意义。
全基因组关联研究和孟德尔随机化研究已经确立了脂蛋白（a）升高与心血管疾病（包括 CAD 和钙化性主动脉瓣疾病）之间的因果关系。脂蛋白（a）检测可识别出与杂合子 FH 风险相似的患者，通过传统因素确定的边缘/中间风险患者的风险分层得到增强，并且通过已知脂蛋白（a）升高家族史的患者的级联筛查来评估遗传性 CVD 风险。通过非靶向治疗（包括 PCSK9 抑制和脂蛋白吸附）降低脂蛋白（a），已经证明降低 ASCVD 风险可能归因于降低脂蛋白（a）。强有力地降低脂蛋白（a）的靶向治疗正在临床开发中。脂蛋白（a）是可操作的，可以通过级联筛查来识别高危患者及其家庭成员进行一级预防，以及指导 ASCVD 一级和二级预防的治疗强化。
