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在接受直接经皮冠状动脉介入治疗的首次 ST 段抬高型心肌梗死患者中,入院时血清单核细胞趋化蛋白-1 与心肌功能早期变化之间存在显著相关性。

Significant association between admission serum monocyte chemoattractant protein-1 and early changes in myocardial function in patients with first ST-segment elevation myocardial infarction after primary percutaneous coronary intervention.

机构信息

Department of cardiology, Beijing Anzhen Hospital, Capital Medical University, #2, Anzhenlu, Chaoyang District, Beijing, 100029, China.

出版信息

BMC Cardiovasc Disord. 2019 May 10;19(1):107. doi: 10.1186/s12872-019-1098-z.

DOI:10.1186/s12872-019-1098-z
PMID:31077149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6511179/
Abstract

BACKGROUND

Recent studies have indicated that monocyte chemoattractant protein-1 (MCP-1) plays an important role in the initiation and progression of ischaemic heart disease. However, no previous research has investigated the correlation between serum MCP-1 levels and early changes in myocardial function in patients with ST-segmental elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI).

METHODS

A total of 87 STEMI patients who had undergone a successful primary PCI were consecutively recruited. All the patients included in this study were grouped into two subgroups according to the median value of MCP-1 upon admission. An early change in left ventricular ejection fraction (LVEF) was defined as (LVEF at 3 months post-STEMI)-(LVEF at 2 days post-STEMI).

RESULTS

Serum MCP-1 levels increased gradually over time during the first 72 h after the onset of STEMI. The concentration of hypersensitive cardiac troponin I (hs-cTnI) upon admission as well as at 24 h and 72 h after primary PCI, especially the peak hs-cTnI concentration, declined significantly in the low admission MCP-1 group. As continuous variable, admission MCP-1 also correlated positively with admission hs-cTnI, hs-cTnI at 24 h after primary PCI, and peak hs-cTnI. Additionally, the absolute early change in LVEF improved markedly in the low admission MCP-1 group (3.77% ± 6.05% vs - 0.18% ± 7.69%, p = 0.009) compared to that in the high admission MCP-1 group. Most importantly, the global LVEF in the low admission MCP-1 group also improved significantly at 3 months compared to baseline LVEF (55.79% ± 7.05% vs 59.60% ± 6.51%, p = 0.011), while an improvement in global LVEF was not observed in the high admission MCP-1 group. Furthermore, as a continuous variable, the MCP-1 level up admission also correlated negatively with early changes in LVEF (r = - 0.391, p = 0.001). After assessment by multiple linear regression analysis, the MCP-1 level upon admission remained correlated with early changes in LVEF [beta = - 0.089, 95% CI (- 0.163 to - 0.015), p = 0.020].

CONCLUSION

MCP-1 upon admission not only correlated positively with hs-cTnI at different time points and peak hs-cTnI, but also associated inversely with early improvements in myocardial function in patients with first STEMI. So we speculated that suppression the expression of MCP-1 via various ways may be a promising therapeutic target in myocardial I/R injury in the future.

摘要

背景

最近的研究表明,单核细胞趋化蛋白-1(MCP-1)在缺血性心脏病的发生和发展中起重要作用。然而,之前的研究并未探讨血清 MCP-1 水平与 ST 段抬高型心肌梗死(STEMI)患者经皮冠状动脉介入治疗(PCI)后早期心肌功能变化之间的相关性。

方法

连续纳入 87 例成功接受直接 PCI 的 STEMI 患者。根据入院时 MCP-1 的中位数,将所有纳入的患者分为两组。左心室射血分数(LVEF)的早期变化定义为(STEMI 后 3 个月的 LVEF)-(STEMI 后 2 天的 LVEF)。

结果

STEMI 发病后 72 小时内,血清 MCP-1 水平逐渐升高。入院时及 24 小时和 72 小时后超敏肌钙蛋白 I(hs-cTnI)浓度显著下降,特别是 hs-cTnI 峰值浓度在低入院 MCP-1 组显著下降。作为连续变量,入院 MCP-1 与入院时 hs-cTnI、直接 PCI 后 24 小时 hs-cTnI 和峰值 hs-cTnI 呈正相关。此外,低入院 MCP-1 组的 LVEF 绝对早期变化明显改善(3.77%±6.05% vs -0.18%±7.69%,p=0.009),而高入院 MCP-1 组无明显改善。最重要的是,与基线 LVEF 相比,低入院 MCP-1 组的整体 LVEF 在 3 个月时也明显改善(55.79%±7.05% vs 59.60%±6.51%,p=0.011),而高入院 MCP-1 组则没有改善。此外,作为连续变量,入院时的 MCP-1 水平与 LVEF 的早期变化呈负相关(r=-0.391,p=0.001)。经多元线性回归分析评估,入院时的 MCP-1 水平与 LVEF 的早期变化仍呈负相关[β=-0.089,95%CI(-0.163 至-0.015),p=0.020]。

结论

入院时的 MCP-1 不仅与不同时间点的 hs-cTnI 和峰值 hs-cTnI 呈正相关,而且与首次 STEMI 患者的早期心肌功能改善呈负相关。因此,我们推测通过多种途径抑制 MCP-1 的表达可能是未来心肌缺血再灌注损伤的一个有前途的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/cc0fb95eb405/12872_2019_1098_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/9f448d582f2a/12872_2019_1098_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/87311d001f79/12872_2019_1098_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/14e147a28fe9/12872_2019_1098_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/cc0fb95eb405/12872_2019_1098_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/9f448d582f2a/12872_2019_1098_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/87311d001f79/12872_2019_1098_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/14e147a28fe9/12872_2019_1098_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5046/6511179/cc0fb95eb405/12872_2019_1098_Fig4_HTML.jpg

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