Translating cardioprotective strategies into clinical settings

Abstract

The major objective of the treatment of ST elevation myocardial infarction (STEMI) patients is to reduce infarct size, which is the major prognostic factor in this population. Most of the progress has consisted in improving reperfusion therapy, both by opening as quickly as possible and by preventing reocclusion of the culprit coronary artery. Basic science research used in well-described animal models allowed to clearly establish the major determinants of infarct size, i.e., area at risk, collateral flow, duration of ischemia, and timing of the protective intervention with respect to reflow. Recent reports have proven that lethal reperfusion injury exists, that it is of significant importance, and that it can be prevented by protective interventions applied immediately before reflow. Therefore, after taking care of the vessel, it is now time to better protect the muscle against lethal reperfusion injury. In spite of several past negative infarct size reduction studies, recent proof-of-concept studies have shown that infarct size reduction is possible in STEMI patients, at least in part because the major determinants of infarct size have been taken into account. Increased understanding of underlying mechanisms from animal models together with encouraging results from phase II infarct size reduction clinical trials should help us improve the design of future studies aimed at reducing infarct size in STEMI patients.