Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, Singapore; National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.
Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russian Federation; German Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany.
Pharmacol Ther. 2018 Jun;186:73-87. doi: 10.1016/j.pharmthera.2018.01.001. Epub 2018 Jan 9.
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.
急性心肌梗死（AMI）和随之而来的心力衰竭是全球范围内主要的死亡和残疾原因。因此，需要新的治疗方法来限制心肌梗死（MI）的范围，防止左心室（LV）不良重构，并减少 AMI 后心力衰竭的发生。AMI 后的炎症反应在确定 MI 范围方面起着关键作用，持续的促炎反应可导致 AMI 后 LV 重构不良，使炎症成为改善 AMI 预后的重要治疗靶点。在本文中，我们概述了参与 AMI 后复杂炎症反应和随后的 LV 重构的多个参与者（及其动态作用），并强调了将炎症作为一种治疗策略来限制 MI 范围、防止 LV 重构不良和减少 AMI 患者心力衰竭的未来机会。
