title: Infarct size reduction in patients with STEMI: why we can do it!
abstract: Major progress has been made over the last three decades for the treatment of patients with ST elevation myocardial infarction (STEMI). The major objective of this treatment is to reduce infarct size, which is the major prognostic factor in this population. Most of the efforts have been focused on improving reperfusion therapy in order to open as quickly as possible, and to prevent reocclusion, of the culprit coronary artery. During the past years, preclinical research has allowed researchers to well-characterize animal models of acute MI and precisely describe the major determinants of infarct size, that is area at risk, collateral flow, duration of ischemia, and timing of the protective intervention with respect to reflow. Recent reports have clearly demonstrated that lethal reperfusion injury exists, that it is of significant importance, and that it can be prevented by protective interventions applied immediately before reflow. Time has come to, on top of reperfusion therapy, better protect the muscle against lethal reperfusion injury. Although many past infarct size reduction studies have been negative, recent proof-of-concept studies have shown that infarct size reduction is possible in patients with STEMI, at least in part because the major determinants of infarct size have been taken into account. Accumulated knowledge from animal models together with encouraging results obtained in phase II infarct size reduction clinical trials should help us improve the design of future studies aimed at reducing infarct size in patients with STEMI.
authors.affiliation: Inserm U 1060, CARMEN, Lyon, France.
authors.forename: Nathan
authors.initials: N
authors.lastname: Mewton
authors.forename: Meier
authors.initials: M
authors.lastname: Elbaz
authors.forename: Christophe
authors.initials: C
authors.lastname: Piot
authors.forename: Michel
authors.initials: M
authors.lastname: Ovize
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D006801:Humans; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control* / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control* / Q000628:therapy