Effect of in-hospital evolocumab therapy on lipoprotein(a) in patients with acute myocardial infarction: a retrospective cohort study and a propensity score matching analysis.
Effect of in-hospital evolocumab therapy on lipoprotein(a) in patients with acute myocardial infarction: a retrospective cohort study and a propensity score matching analysis.
复制标题
DOI：
10.1097/cp9.0000000000000036
复制
发表时间：
2023-01
期刊：
影响因子：
--
通讯作者：
Chen, Tao
中科院分区：
文献类型：
--
作者：
Gao, Ge;Zheng, Tao;Lan, Beidi;Hui, Weiying;Chen, Shi;Yuan, Zuyi;Wu, Yue;Chiang, John Y L;Chen, Tao
脂蛋白(a)升高与动脉粥样硬化性心血管疾病的风险增加有关。Evolocumab是一种蛋白转化酶subtilisin/ keexin 9型抑制剂，已被证明可以降低脂蛋白(a)。然而，evolocumab对急性心肌梗死（AMI）患者脂蛋白(a)的影响研究甚少。本研究旨在探讨AMI患者在evolocumab治疗下脂蛋白(a)的变化。本回顾性队列分析共纳入467例入院时LDL-C水平为bb0 2.6 mmol/L的AMI患者，其中132例住院时接受evolocumab （140 mg / 2周）+他汀类药物（每天20 mg阿托伐他汀或10 mg瑞舒伐他汀），其余335例仅接受他汀类药物。比较两组患者随访1个月时的血脂水平。使用0.02卡尺，根据年龄、性别和基线脂蛋白(A)按1:1的比例进行倾向评分匹配分析。在1个月的随访中，evolocumab加他汀组的脂蛋白(a)水平从27.0 (17.5,50.6)mg/dL降至20.9 (9.4,52.5)mg/dL，而他汀单药组的脂蛋白(a)水平从24.5 (13.2,41.1)mg/dL上升至27.9 (14.8,58.6)mg/dL。倾向评分匹配分析纳入262例患者（每组131例）。在截断值为20和50 mg/dL的基线脂蛋白(a)分层的倾向评分匹配队列的亚组分析中，在evolocumab加他汀组的三个亚组中，脂蛋白(a)的绝对变化为- 4.9 (- 8.5,- 1.3),- 5.0 (- 13.9,1.9),- 0.2 (- 9.9,16.9)mg/dL，而在他汀单药组的三个亚组中，脂蛋白(a)的绝对变化为0.9 (- 1.7,5.5),10.7 (4.6,21.9),12.2 (2.9,35.6)mg/dL。与仅使用他汀类药物组相比，evolocumab联合他汀类药物组在1个月时所有亚组的脂蛋白(a)水平均较低（P < 0.05）。在AMI患者1个月的随访中，在他汀类药物治疗的背景下，在医院内开始使用evolocumab可降低脂蛋白(a)水平。Evolocumab联合他汀类药物治疗抑制了他汀类药物治疗中脂蛋白(a)的增加，无论基线脂蛋白(a)水平如何。
Elevated lipoprotein(a) is associated with an increased risk of atherosclerotic cardiovascular disease. Evolocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, has been shown to reduce lipoprotein(a). However, the effect of evolocumab on lipoprotein(a) in patients with acute myocardial infarction (AMI) is poorly studied. This study aims to investigate the change in lipoprotein(a) under evolocumab therapy in patients with AMI. This retrospective cohort analysis included a total of 467 AMI patients with LDL-C level >2.6 mmol/L upon admission, among whom 132 received in-hospital evolocumab (140 mg every 2 weeks) plus statin (20 mg atorvastatin or 10 mg rosuvastatin per day) and the remaining 335 received statin only. Lipid profiles at 1-month follow-up were compared between the two groups. A propensity score matching analysis was also conducted based on age, sex, and baseline lipoprotein(a) at a 1:1 ratio using a 0.02 caliper. At the 1-month follow-up, the lipoprotein(a) level decreased from 27.0 (17.5, 50.6) mg/dL to 20.9 (9.4, 52.5) mg/dL in evolocumab plus statin group, but increased from 24.5 (13.2, 41.1) mg/dL to 27.9 (14.8, 58.6) mg/dL in statin only group. The propensity score matching analysis included 262 patients (131 in each group). In subgroup analysis of the propensity score matching cohort stratified by the baseline lipoprotein(a) at cutoff values of 20 and 50 mg/dL, the absolute change in lipoprotein(a) was −4.9 (−8.5, −1.3), −5.0 (−13.9, 1.9), −0.2 (−9.9, 16.9) mg/dL in three subgroups in evolocumab plus statin group, and 0.9 (−1.7, 5.5), 10.7 (4.6, 21.9), 12.2 (2.9, 35.6) mg/dL in three subgroups in statin only group. In comparison to statin only group, evolocumab plus statin group had lower lipoprotein(a) level at 1 month in all subgroups (P < 0.05). In-hospital initiation of evolocumab on a background statin therapy reduced lipoprotein(a) level at 1-month follow-up in patients with AMI. Evolocumab plus statin therapy inhibited the increase in lipoprotein(a) in statin only therapy, regardless of the baseline lipoprotein(a) level.