Building a Unified Mechanistic Insight Into the Bimodal Pattern of Edema in Reperfused Acute Myocardial Infarctions: Observations, Interpretations, and Outlook.

O ver the past 50 years, the understanding of the pathophysiology of myocardial edema in the setting of acute myocardial infarction (MI) has evolved significantly. Controlled animal studies have demonstrated that ischemia or transient ischemia followed by reperfusion lead to myocardial edema. In particular, ischemia promotes intracellular edema and the extent of edema is directly related to ischemia duration. Several studies have also shown that reperfusion after transient ischemia can lead to extensive interstitial edema. The evidence supporting these findings has been based on invasive standards: histologic observations of changes in tissue ultrastructure; and desiccation studies, which report on tissue water content based on relative differences between wet and dry weight of myocardial samples of interest. Although these invasive measurements can provide direct evidence, assessment of edema on the basis of these standards is limited to a single time point. Thus, to determine temporal changes of edema in the same subject pertaining to given pathology (e.g., ischemia or ischemia followed by reperfusion), serial assessments on the basis of noninvasive methods are necessary.