斑块表型的免疫差异介导心肌梗死后心脏重构及精准诊疗

Immune differences in plaque phenotypes mediate post-myocardial infarction cardiac remodeling and precision medicine

摘要:

急性心肌梗死以及心肌梗死后诱发的心力衰竭仍是目前全球范围内导致死亡的主要原因之一。斑块的组成特征决定了其更易发生破裂或侵蚀,这两种斑块表型的差异可通过炎症信号通路调控斑块局部的特异性免疫微环境,最终影响心肌修复的质量。该文从免疫炎症反应的角度出发,系统梳理了从差异化斑块表型,到差异化动脉血栓形成,再到差异化心肌梗死发生与心脏修复的完整心血管事件链条。在总结心肌梗死及后续心脏修复相关机制的基础上,该文最终提出了针对斑块表型分层的诊疗新方向,即通过探索靶向生物标志物与差异化干预策略,实现对梗死后心脏重构更精准的个体化管理。

Abstract:

Acute myocardial infarction and post-myocardial infarction heart failure are still one of the main causes of death worldwide. The compositional characteristics of plaques determine that they are more prone to rupture or erosion, and the phenotypic differences between these two plaque subtypes can regulate the specific immune microenvironment of the plaque through inflammatory signaling pathways, ultimately affecting the quality of myocardial repair. From the perspective of immune-inflammatory responses, this article systematically reviews the entire chain of cardiovascular events from distinct plaque phenotypes, distinct arterial thrombosis, to divergent myocardial infarction episodes and cardiac repair.On the basis of summarizing the mechanisms related to myocardial infarction and subsequent cardiac repair, this article ultimately proposes a new direction for stratified diagnosis and treatment based on plaque phenotypes, which is to explore targeted biomarkers and differentiated intervention strategies to achieve more precise individualized management of post-infarction cardiac remodeling.