title: Pathophysiological role of neutrophils in acute myocardial infarction.
abstract: The pathogenesis of acute myocardial infarction is known to be mediated by systemic, intraplaque and myocardial inflammatory processes. Among different immune cell subsets, compelling evidence now indicates a pivotal role for neutrophils in acute coronary syndromes. Neutrophils infiltrate coronary plaques and the infarcted myocardium and mediate tissue damage by releasing matrix-degrading enzymes and reactive oxygen species. In addition, neutrophils are also involved in post-infarction adverse cardiac remodelling and neointima formation after angioplasty. The promising results obtained in preclinical modelswith pharmacological approaches interfering with neutrophil recruitment or function have confirmed the pathophysiological relevance of these immune cells in acute coronary syndromes and prompted further studies of these therapeutic interventions. This narrative review will provide an update on the role of neutrophils in acute myocardial infarction and on the pharmacological means that were devised to prevent neutrophil-mediated tissue damage and to reduce post-ischaemic outcomes.
authors.affiliation: Fabrizio Montecucco, Cardiology Division, Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, 64 Avenue Roseraie, 1211 Geneva, Switzerland, Tel.: +41 223827238, Fax: +41 223827245, E-mail: Fabrizio.montecucco@unige.ch.
authors.forename: F
authors.initials: F
authors.lastname: Carbone
authors.forename: A
authors.initials: A
authors.lastname: Nencioni
authors.forename: F
authors.initials: F
authors.lastname: Mach
authors.forename: N
authors.initials: N
authors.lastname: Vuilleumier
authors.forename: F
authors.initials: F
authors.lastname: Montecucco
mesh_terms: D054058:Acute Coronary Syndrome / Q000378:metabolism; D017130:Angioplasty; D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000473:pathology; D007511:Ischemia / Q000473:pathology; D008075:Lipoproteins, HDL / Q000737:chemistry; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood*; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000166:cytology* / Q000378:metabolism; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D018925:Chemokines; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008075:Lipoproteins, HDL; D017382:Reactive Oxygen Species