Acute myocardial infarction (AMI) and the heart failure that often follows, are major causes of death and disability worldwide. As such, new therapies are required to limit myocardial infarct (MI) size, prevent adverse left ventricular (LV) remodeling, and reduce the onset of heart failure following AMI. The inflammatory response to AMI, plays a critical role in determining MI size, and a persistent pro-inflammatory reaction can contribute to adverse post-MI LV remodeling, making inflammation an important therapeutic target for improving outcomes following AMI. In this article, we provide an overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse LV remodeling, and reducing heart failure in AMI patients.

急性心肌梗塞 (AMI) 和经常发生的心力衰竭是全世界死亡和残疾的主要原因。因此，需要新的疗法来限制心肌梗塞 (MI) 的大小，防止不利的左心室 (LV) 重构，并减少 AMI 后心力衰竭的发生。对 AMI 的炎症反应在确定 MI 大小方面起着关键作用，而持续的促炎反应可导致 MI 后 LV 的不良重塑，使炎症成为改善 AMI 后预后的重要治疗靶点。在本文中，我们概述了参与对 AMI 和随后的 LV 重构的复杂炎症反应的多个参与者（及其动态作用），并强调了将炎症作为限制 MI 大小的治疗策略的未来机会，