title: Systemic inflammatory response following acute myocardial infarction.
abstract: Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.
authors.affiliation: Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia.
authors.forename: Lu
authors.initials: L
authors.lastname: Fang
authors.affiliation: Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia.
authors.forename: Xiao-Lei
authors.initials: XL
authors.lastname: Moore
authors.affiliation: Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia ; Department of Cardiovascular Medicine, the Alfred Hospital, Commercial Road, Melbourne, Vic, Australia.
authors.forename: Anthony M
authors.initials: AM
authors.lastname: Dart
authors.affiliation: Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
authors.forename: Le-Min
authors.initials: LM
authors.lastname: Wang
keywords: Acute myocardial infarction; Inflammatory markers; Leukocytes; Systemic inflammatory response