Time-Varying Edema Requires Cautious Interpretation of Myocardium at Risk and Infarct Size by All Imaging Methods
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Article, see p 1288
Although it has been known for ≈50 years that the size of a myocardial infarction (MI) can be modulated by medications and other interventions, reperfusion by fibrinolysis or percutaneous coronary intervention remains the only treatment known to reduce infarct size in patients.1 Although many pharmacological treatments reduce infarct size in animal models, the overwhelming majority have failed in human clinical trials. The concept that cardiac magnetic resonance (CMR) could retrospectively image myocardium at risk (MaR), measure infarct size, and determine myocardial salvage in an examination conveniently 2 days after reperfusion2 was intriguing and garnered much attention over the past decade. However, with scrutiny, the simple explanation of why myocardial T2 could detect the area at risk in acute MI as edematous tissue has turned out to be more complicated and controversial. However, it seems clear that these magnetic resonance imaging (MRI) methods are providing insight into the pathophysiology of acute MI. Beyond methodological issues, which are fundamental to the field, it is important for clinicians and scientists to recognize that edema modulates the relationship between area at risk and infarct size, and thus one needs to interpret these measurements carefully regardless of the method used.
In this issue of Circulation, Fernández-Jiménez et al3 describe that a bimodal temporal course of myocardial T2 occurs in patients after reperfused acute MI—an important extension beyond their previous preclinical experiments. Their group was the first to notice that myocardial edema after ischemia/reperfusion goes through a bimodal pattern with a wave of substantial edema on the day of the infarct, a decline in edema 24 hours after reperfusion, and a rebound in edema 4 to 7 days after …