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前蛋白转化酶枯草溶菌素9抑制剂对心血管疾病高风险和极高风险患者血脂水平的影响:一项系统评价和荟萃分析

Effect of PCSK9 Inhibitor on Blood Lipid Levels in Patients with High and Very-High CVD Risk: A Systematic Review and Meta-Analysis.

作者信息

Zhang Yue, Suo Yanrong, Yang Lin, Zhang Xiaolu, Yu Qun, Zeng Miao, Zhang Wenlan, Jiang Xijuan, Wang Yijing

机构信息

School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Traditional Chinese Medicine Department, Ganzhou People's Hospital, Ganzhou, China.

出版信息

Cardiol Res Pract. 2022 Apr 26;2022:8729003. doi: 10.1155/2022/8729003. eCollection 2022.

DOI:10.1155/2022/8729003
PMID:35529059
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9072011/
Abstract

OBJECTIVES

We aimed to investigate the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor on blood lipid levels in patients with high and very-high cardiovascular risk.

DESIGN

14 trials ( = 52,586 patients) comparing treatment with or without PCSK9 inhibitors were retrieved from PubMed and Embase updated to 1st Jun 2021. The data quality of included studies was assessed by two independent researchers using the Cochrane systematic review method. All-cause mortality, cardiovascular mortality, and changes in serum low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglyceride (TG), apolipoprotein B (ApoB), lipoprotein (a) (LP (a)), non-high-density lipoprotein cholesterol (non-HDL-C), high-density lipoprotein cholesterol (HDL-C), and apolipoprotein A1 (ApoA1) from baseline were analyzed using Rev Man 5.1.0 software.

RESULTS

Compared with treatments without PCSK9 inhibitor, addition of PCSK9 inhibitors (evolocumab and alirocumab) had obvious decreasing effects on the levels of LDL-C [MD = -46.86, 95% CI (-54.99 to -38.72), < 0.00001], TC [MD = -31.92, 95% CI (-39.47 to -24.38), < 0.00001], TG [MD = -8.13, 95% CI (-10.48 to -5.79), < 0.00001], LP(a) [MD = -26.69, 95% CI (-27.93 to -25.44), < 0.00001], non-HDL-C [MD = -42.86, 95% CI (-45.81 to -39.92), < 0.00001], and ApoB [MD = -38.44, 95% CI (-42.23 to -34.65), < 0.00001] in high CVD risk patients. Conversely, changes of HDL-C [MD = 6.27, CI (5.17 to 7.36), < 0.00001] and ApoA1 [MD = 4.33, 95% CI (3.53 to 5.13), < 0.00001] from baseline were significantly more in high cardiovascular disease risk patients who received PCSK9 inhibitors treatment.

CONCLUSION

Addition of PCSK9 inhibitors to standard therapy resulted in definite improvement in blood lipid levels compared with therapies that did not include them.

摘要

目的

我们旨在研究前蛋白转化酶枯草溶菌素/克新9型(PCSK9)抑制剂对心血管风险高和非常高的患者血脂水平的影响。

设计

从截至2021年6月1日更新的PubMed和Embase中检索了14项试验(n = 52,586例患者),这些试验比较了使用或不使用PCSK9抑制剂的治疗。两名独立研究人员采用Cochrane系统评价方法评估纳入研究的数据质量。使用Rev Man 5.1.0软件分析全因死亡率、心血管死亡率以及血清低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)、甘油三酯(TG)、载脂蛋白B(ApoB)、脂蛋白(a)[LP(a)]、非高密度脂蛋白胆固醇(非HDL-C)、高密度脂蛋白胆固醇(HDL-C)和载脂蛋白A-1(ApoA1)相对于基线的变化。

结果

与不使用PCSK9抑制剂的治疗相比,添加PCSK9抑制剂(依洛尤单抗和阿利西尤单抗)对心血管疾病高风险患者的LDL-C水平[MD = -46.86,95%CI(-54.99至-38.72),P < 0.00001]、TC水平[MD = -31.92,95%CI(-39.47至-24.38),P < 0.00001]、TG水平[MD = -8.13,95%CI(-10.48至-5.79),P < 0.00001]、LP(a)水平[MD = -26.69,95%CI(-27.93至-25.44),P < 0.00001]、非HDL-C水平[MD = -42.86,95%CI(-45.81至-39.92),P < 0.00001]和ApoB水平[MD = -38.44,95%CI(-42.23至-34.65),P < 0.00001]有明显降低作用。相反,接受PCSK9抑制剂治疗的心血管疾病高风险患者中,HDL-C相对于基线的变化[MD = 6.27,CI(5.17至7.36),P < 0.00001]和ApoA1相对于基线的变化[MD = 4.33,95%CI(3.53至5.13),P < 0.

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/7cb573fde76a/CRP2022-8729003.011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/9ae7db9f8142/CRP2022-8729003.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/768fed81fff0/CRP2022-8729003.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/ca06775472a3/CRP2022-8729003.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/8c58d695e3ae/CRP2022-8729003.009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/7cb573fde76a/CRP2022-8729003.011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/a0518af8af0b/CRP2022-8729003.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/9ae7db9f8142/CRP2022-8729003.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/a7db59f7bca4/CRP2022-8729003.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/de618b54d1b0/CRP2022-8729003.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/1c42699b09be/CRP2022-8729003.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/768fed81fff0/CRP2022-8729003.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/ca06775472a3/CRP2022-8729003.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/8c58d695e3ae/CRP2022-8729003.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/e248b7e933c3/CRP2022-8729003.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d03/9072011/7cb573fde76a/CRP2022-8729003.011.jpg

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