After myocardial infarction (MI), patients with type 2 diabetes have an increased rate of adverse outcomes, compared to patients without. Diabetes confers a 1.5–2-fold increase in early mortality and, importantly, this discrepancy has been consistent over recent decades, despite advances in treatment and overall survival. Certain assumptions have emerged to explain this increased risk, such as differences in infarct size or coronary artery disease severity. Here, we re-evaluate that evidence and show how contemporary analyses using state-of-the-art characterization tools suggest that the received wisdom tells an incomplete story. Simultaneously, epidemiological and mechanistic biological data suggest additional factors relating to processes of diabetes-related inflammation might play a prominent role. Inflammatory processes after MI mediate injury and repair and are thus a potential therapeutic target. Recent studies have shown how diabetes affects immune cell numbers and drives changes in the bone marrow, leading to pro-inflammatory gene expression and functional suppression of healing and repair. Here, we review and re-evaluate the evidence around adverse prognosis in patients with diabetes after MI, with emphasis on how targeting processes of inflammation presents unexplored, yet valuable opportunities to improve cardiovascular outcomes in this vulnerable patient group.

中文翻译：

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针对炎症的新兴机会：心肌梗死和 2 型糖尿病


心肌梗死 （MI） 后，与非心肌梗死患者相比，2 型糖尿病患者的不良结局发生率增加。糖尿病使早期死亡率增加了 1.5-2 倍，重要的是，尽管治疗和总生存期取得了进步，但这种差异在近几十年来一直存在。已经出现了某些假设来解释这种增加的风险，例如梗死面积或冠状动脉疾病严重程度的差异。在这里，我们重新评估了这些证据，并展示了使用最先进的表征工具的当代分析如何表明公认的智慧讲述了一个不完整的故事。同时，流行病学和机制生物学数据表明，与糖尿病相关炎症过程相关的其他因素可能起着重要作用。MI 后的炎症过程介导损伤和修复，因此是潜在的治疗靶点。最近的研究表明，糖尿病如何影响免疫细胞数量并驱动骨髓的变化，从而导致促炎基因表达和对愈合和修复的功能抑制。在这里，我们回顾并重新评估了 MI 后糖尿病患者不良预后的证据，重点是炎症的靶向过程如何为改善这一脆弱患者群体的心血管结局提供未探索但有价值的机会。