Profiling the Evolution of Inflammatory Response and Exploring Its Prognostic Significance in Acute Myocardial Infarction: The First Step to Establishing Anti-Inflammatory Strategy.

Acute myocardial infarction (AMI) is defined as myocardial tissue necrosis owing to abrupt decrease incoronary arterial blood supply, of which the most common cause is atheroma-mediated thromboembolism. From the onset of acute tissue necrosis to the later healing process, a myriad of inflammatory reactions are involved in the pathophysiology of AMI. 1 Through upregulation of pro-inflammatory cytokines [such as tumor necrosis factor (TNF), interleukin (IL)-6, and IL-1 ] and activation of toll-like receptor/p38 mitogen-activated protein kinase (MAPK) signaling pathway, 2 necrotic tissue triggers innate immune responses and leukocyte infiltration to remove tissue debris for the following tissue repair. While timely reperfusion to viable, but ischemic myocardial tissue has been demonstrated to be effective in confining the extent of myocardial necrosis in acute phase, 3 experimental evidence has shown that, prolonged and over-reactive necrotizing inflammation could worsen myocardial damage and cause detrimental left ventricular (LV) remodeling. 1 For restraining necrotizing inflammatory reactions in a timely manner, anti-inflammatory subsets of leukocytes are then recruited and transformed to avoid excessive myocardial damage and to facilitate healing process, including CD14+CD16+ monocyte, 4 reparative M2 macrophages, and regulatory T lymphocytes. Of note, transforming growth factor has been recognized as the key mediator to activate anti-inflammatory process and profibrotic reparative pathways. 1 Epidemiological evidence has indicated that in AMI patients, elevated serum levels of TNF and IL-6 raised the risk of mortality, and increased IL-1 was associated with developing heart failure. 5