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急性心肌梗死患者的脂蛋白(a)浓度不能预示六个月随访时的水平。

Lipoprotein(a) concentrations in acute myocardial infarction patients are not indicative of levels at six month follow-up.

作者信息

Ziogos Efthymios, Vavuranakis Michael A, Harb Tarek, Foran Palmer L, Blaha Michael J, Jones Steven R, Lai Shenghan, Gerstenblith Gary, Leucker Thorsten M

机构信息

Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

出版信息

Eur Heart J Open. 2023 Apr 5;3(2):oead035. doi: 10.1093/ehjopen/oead035. eCollection 2023 Mar.


DOI:10.1093/ehjopen/oead035
PMID:37095769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10122422/
Abstract

AIMS: Lipoprotein(a) [Lp(a)] levels are generally constant throughout an individual's lifetime, and current guidelines recommend that a single measurement is sufficient to assess the risk of coronary artery disease (CAD). However, it is unclear whether a single measurement of Lp(a) in individuals with acute myocardial infarction (MI) is indicative of the Lp(a) level six months following the event. METHODS AND RESULTS: Lp(a) levels were obtained from individuals with non-ST-elevation myocardial infarction (NSTEMI) or ST-elevation myocardial infarction (STEMI) ( = 99) within 24 h of hospital admission and after six months, who were enrolled in two randomized trials of evolocumab and placebo, and in individuals with NSTEMI or STEMI ( = 9) who enrolled in a small observation arm of the two protocols and did not receive study drug, but whose levels were obtained at the same time points. Median Lp(a) levels increased from 53.5 nmol/L (19, 165) during hospital admission to 58.0 nmol/L (14.8, 176.8) six months after the acute infarction ( = 0.02). Subgroup analysis demonstrated no difference in the baseline, six-month, or change between the baseline and six-month Lp(a) values between the STEMI and NSTEMI groups and between the group which received evolocumab and the group that did not. CONCLUSION: This study demonstrated that Lp(a) levels in individuals with acute MI are significantly higher six months after the initial event. Therefore, a single measurement of Lp(a) in the peri-infarction setting is not sufficient to predict the Lp(a)-associated CAD risk in the post-infarction period. REGISTRATION: Evolocumab in Acute Coronary Syndrome Trial [EVACS I] NCT03515304, Evolocumab in Patients with Acute Myocardial Infarction [EVACS II], NCT04082442.

摘要

目的:脂蛋白(a)[Lp(a)]水平在个体一生中通常保持恒定,当前指南建议单次测量足以评估冠状动脉疾病(CAD)风险。然而,急性心肌梗死(MI)患者单次测量Lp(a)是否能代表事件发生六个月后的Lp(a)水平尚不清楚。 方法与结果:从因非ST段抬高型心肌梗死(NSTEMI)或ST段抬高型心肌梗死(STEMI)入院24小时内及六个月后的患者(n = 99)中获取Lp(a)水平,这些患者参与了两项关于依洛尤单抗和安慰剂的随机试验,以及参与两项试验小观察臂、未接受研究药物但在相同时间点测量Lp(a)水平的NSTEMI或STEMI患者(n = 9)。急性梗死入院时Lp(a)水平中位数为53.5 nmol/L(19,165),急性梗死后六个月升至58.0 nmol/L(14.8,176.8)(P = 0.02)。亚组分析显示,STEMI组和NSTEMI组之间以及接受依洛尤单抗组和未接受依洛尤单抗组之间,基线、六个月时或基线与六个月Lp(a)值变化无差异。 结论:本研究表明,急性心肌梗死患者首次事件发生六个月后Lp(a)水平显著升高。因此,梗死周围期单次测量Lp(a)不足以预测梗死后期与Lp(a)相关的CAD风险。 注册信息:急性冠状动脉综合征中的依洛尤单抗试验[EVACS I] NCT03515304,急性心肌梗死患者中的依洛尤单抗试验[EVACS II],NCT04082442。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/357a/10122422/d9bb76ed5f43/oead035f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/357a/10122422/cb9df7e05cd8/oead035_ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/357a/10122422/d9bb76ed5f43/oead035f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/357a/10122422/cb9df7e05cd8/oead035_ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/357a/10122422/d9bb76ed5f43/oead035f1.jpg

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本文引用的文献

[1]
Small Interfering RNA to Reduce Lipoprotein(a) in Cardiovascular Disease.

N Engl J Med. 2022-11-17

[2]
Relationship of low-density lipoprotein-cholesterol and lipoprotein(a) to cardiovascular risk: The Multi-Ethnic Study of Atherosclerosis (MESA).

Atherosclerosis. 2022-12

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Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement.

Eur Heart J. 2022-10-14

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The Trajectory of Lipoprotein(a) During the Peri- and Early Postinfarction Period and the Impact of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibition.

Am J Cardiol. 2022-5-15

[5]
Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk.

J Am Coll Cardiol. 2022-2-22

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Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association.

Arterioscler Thromb Vasc Biol. 2022-1

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N Engl J Med. 2020-1-1

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Eur Heart J. 2020-1-1

[9]
Clinical Pharmacokinetics and Pharmacodynamics of Evolocumab, a PCSK9 Inhibitor.

Clin Pharmacokinet. 2018-7

[10]
Lp(a): an acute-phase reactant?

Chem Phys Lipids. 1994-1

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