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Infarct size is the major determinant of post myocardial infarction remodeling and heart failure1 and ultimately of patients' prognosis.2,3 Infarct size itself is determined by the area at risk, that is, the perfusion territory of the occluded coronary artery, the duration of ischemia, the magnitude of collateral blood flow, and only to a small extent by the hemodynamic situation, notably heart rate.4 The only way to salvage ischemic myocardium from impending infarction is by timely reperfusion; however, reperfusion also inflicts injury on the previously ischemic myocardium and contributes to final infarct size.5 Such reperfusion injury can be attenuated by ischemic conditioning strategies and certain drugs, which recruit part of the signal transduction of ischemic conditioning strategies,6,7 both in experimental animal models and in patients with reperfused acute myocardial infarction.8Article, see p 254 The magnitude of salvage by reperfusion and cardioprotective strategies can only be quantified by comparing the actual infarct size to the hypothetical infarct size if no reperfusion had occurred, that is, the area at risk of infarction. In experimental animals, such quantitative comparison is performed by delineation of the area at risk, that is, by measurement of regional myocardial blood flow with microspheres during coronary occlusion or by infusion of a dye into the aorta during postmortem coronary reocclusion, and of infarct size by postmortem triphenyl tetrazolium …

Is MRI Really the Gold Standard for the Quantification of Salvage From Myocardial Infarction?