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循环凝集素通路蛋白不能预测心肌梗死后的短期心脏结局。

Circulating lectin pathway proteins do not predict short-term cardiac outcomes after myocardial infarction.

机构信息

Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark.

Department of Biomedicine, Aarhus University, Aarhus, Denmark.

出版信息

Clin Exp Immunol. 2019 Oct;198(1):94-100. doi: 10.1111/cei.13315. Epub 2019 Jun 3.

DOI:10.1111/cei.13315
PMID:31104331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6718281/
Abstract

Despite improvements in treatment, coronary artery disease is still responsible for one-third of all deaths globally, due predominantly to myocardial infarction (MI) and stroke. There is an important potential in developing new strategies for treatment of patients with these conditions. Inflammation, and in particular the actions of the complement system, has emerged as part of the pathogenesis in reperfusion injury in patients with MI. To further qualify this, we examined the association between the plasma levels of lectin pathway proteins and myocardial end-points, left ventricular ejection fraction (LVEF) and infarct size in a cohort of patients with ST-elevation myocardial infarction (STEMI). A blood sample was drawn the day after percutaneous coronary intervention from 73 patients with STEMI. The primary end-points, LVEF and infarct size, were measured with magnetic resonance imaging 6-9 days after the infarct. Complement pattern-recognition molecules of the lectin pathway (mannan-binding lectin, H-ficolin, L-ficolin and M-ficolin) were analysed along with soluble membrane attack complex (sMAC) and C-reactive protein (CRP) in plasma with immunofluorometric assays <50%. CRP correlated negatively with LVEF, regression coefficient = -0·17 (P = 0·01). None of the lectin pathway proteins correlated to LVEF or infarct size, nor did soluble membrane attack complex (sMAC). There were no differences in plasma levels of these complement proteins when comparing patients with ejection fraction <50% to patients with ejection fraction <50%. Pattern-recognition molecules of the lectin pathway and sMAC do not predict short-term cardiac outcomes after MI.

摘要

尽管治疗有所改善,但冠状动脉疾病仍然是全球三分之一死亡的原因,主要是由于心肌梗死(MI)和中风。对于开发这些疾病患者的新治疗策略,存在着重要的潜在可能性。炎症,特别是补体系统的作用,已成为 MI 患者再灌注损伤发病机制的一部分。为了进一步证明这一点,我们研究了补体凝集素途径蛋白的血浆水平与心肌终点(左心室射血分数[LVEF]和梗死面积)之间的关系,在一组 ST 段抬高型心肌梗死(STEMI)患者中。从 73 例 STEMI 患者经皮冠状动脉介入治疗后一天抽取血液样本。在梗塞后 6-9 天用磁共振成像测量主要终点 LVEF 和梗死面积。通过免疫荧光测定法分析血浆中的补体凝集素途径模式识别分子(甘露聚糖结合凝集素、H 型纤维胶凝蛋白、L 型纤维胶凝蛋白和 M 型纤维胶凝蛋白)以及可溶性膜攻击复合物(sMAC)和 C 反应蛋白(CRP)<50%。CRP 与 LVEF 呈负相关,回归系数为-0·17(P = 0·01)。凝集素途径的任何蛋白与 LVEF 或梗死面积均无相关性,可溶性膜攻击复合物(sMAC)也是如此。比较射血分数<50%的患者与射血分数<50%的患者,这些补体蛋白的血浆水平没有差异。凝集素途径和 sMAC 的模式识别分子不能预测 MI 后短期心脏结局。

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本文引用的文献

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Pentraxin-3 in coronary artery disease: A meta-analysis.Pentraxin-3 在冠状动脉疾病中的作用:一项荟萃分析。
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Relation of inflammatory markers with myocardial and microvascular injury in patients with reperfused ST-elevation myocardial infarction.炎症标志物与再灌注治疗的 ST 段抬高型心肌梗死患者心肌和微血管损伤的关系。
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