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Synergistic role of circulating CD14++CD16+ monocytes and fibrinogen in predicting the cardiovascular events after myocardial infarction

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 res...

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Detalles Bibliográficos
Autores principales: Zhang, Chong, Zeng, Shan, Ji, Wenjie, Li, Zhi, Sun, Haonan, Teng, Tianming, Yu, Ying, Zhou, Xin, Yang, Qing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10189084/
https://www.ncbi.nlm.nih.gov/pubmed/36946389
http://dx.doi.org/10.1002/clc.24005
Descripción
Sumario: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(M)β(2) 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.