循环 CD14++CD16+ 单核细胞与纤维蛋白原在预测心肌梗死后心血管事件中的协同作用。
Synergistic role of circulating CD14++CD16+ monocytes and fibrinogen in predicting the cardiovascular events after myocardial infarction.
机构信息
Department of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Heart Center, Pingjin Hospital, Tianjin, China.
出版信息
Clin Cardiol. 2023 May;46(5):521-528. doi: 10.1002/clc.24005. Epub 2023 Mar 22.
BACKGROUND
Monocytes and fibrinogen (FIB) play important roles in driving acute and reparative inflammatory pathways after myocardial infarction (MI). In humans, there are three subsets of monocytes, namely, CD14++CD16- (Mon1), CD14++CD16+ (Mon2), and CD14+CD16++ (Mon3). During the inflammatory response, monocyte subsets express high levels of integrin α β and protease-activated receptors 1 and 3 to interact with FIB.
HYPOTHESIS
However, whether there is a synergistic role of FIB combined with Mon2 counts in prioritizing patients at high risk of future major adverse cardiovascular events (MACEs) after MI remains unknown.
METHODS
The MI patients who treated with primary percutaneous coronary intervention were enrolled. MI patients were categorized into four groups, that is, low FIB/low Mon2, low FIB/high Mon2, high FIB/low Mon2, and high FIB/high Mon2, according to cutoff values of 3.28 g/L for FIB and 32.20 cells/μL for Mon2. Kaplan-Meier survival analysis and Cox proportional hazards models were used to estimate the risk of MACEs of MI patients during a median follow-up of 2.7 years. Mediating effects of high FIB levels and MACEs associated with high monocyte subsets were calculated by mediation analysis.
RESULTS
High FIB/high Mon2 group had the highest risk of MACEs during a median follow-up of 2.7 years. Moreover, mediation analysis showed that a high FIB level could explain 24.9% (p < .05) of the increased risk of MACEs associated with Mon2.
CONCLUSION
This work provides evidence indicating the translational potential of a synergistic role of FIB combined with Mon2 in prioritizing patients at high risk of future MACEs after MI.
背景
单核细胞和纤维蛋白原（FIB）在驱动心肌梗死后急性和修复性炎症途径中发挥重要作用。在人类中，单核细胞有三个亚群，即 CD14++CD16-（Mon1）、CD14++CD16+（Mon2）和 CD14+CD16++（Mon3）。在炎症反应中，单核细胞亚群表达高水平的整合素 α β 和蛋白酶激活受体 1 和 3 与 FIB 相互作用。
假说
然而，在 MI 后，FIB 与 Mon2 计数联合是否具有协同作用，从而优先考虑未来发生主要不良心血管事件（MACEs）的高危患者，目前尚不清楚。
方法
纳入接受直接经皮冠状动脉介入治疗的 MI 患者。根据 FIB 的截断值 3.28 g/L 和 Mon2 的截断值 32.20 个/μL，将 MI 患者分为四组，即低 FIB/低 Mon2、低 FIB/高 Mon2、高 FIB/低 Mon2 和高 FIB/高 Mon2。采用 Kaplan-Meier 生存分析和 Cox 比例风险模型估计 MI 患者在中位 2.7 年随访期间发生 MACEs 的风险。通过中介分析计算高 FIB 水平和与高单核细胞亚群相关的 MACEs 的中介效应。
结果
在中位 2.7 年的随访中，高 FIB/高 Mon2 组发生 MACEs 的风险最高。此外，中介分析表明，高 FIB 水平可解释 Mon2 与 MACEs 相关的风险增加的 24.9%（p<0.05）。
结论
这项工作提供了证据，表明 FIB 与 Mon2 联合具有协同作用，可优先考虑 MI 后未来发生 MACEs 的高危患者，具有转化潜力。
Zotero 插件