Assessment of reperfusion-induced myocardial injury by echocardiography.

In the early phase of acute myocardial infarction, timely reperfusion is a prerequisite to contain the extent of cellular and vascular injury. In the absence of reperfusion, severe ischaemia inevitably leads to myocardial necrosis involving all of the area at risk. Early reperfusion may prevent the death of ischaemic cardiomyocytes and is the therapeutic strategy of choice in patients with acute myocardial infarction. However, even after early and adequate reopening of the infarct-related artery, the full benefits of reperfusion may be attenuated by a decrease in microvascular reflow and lethal injury to potentially viable endothelial and myocardial cells during the restoration of flow. In this issue of European Heart Journal, Turshner and colleagues1 revisit the sequential changes in regional myocardial thickness and function after reperfusion of transmural infarct in an experimental closed-chest pig model by analysing M-mode radio-frequency (RF) data. The most striking results of this study are: (1) the ability of cardiac ultrasound to identify reperfusion-induced oedema as an acute and immediate increase in regional wall thickness in the reperfused infarct area and (2) the description of post-systolic thickening occurring in both transmural infarct and reperfused myocardium, indicating that this parameter is not a consistent marker of myocardial viability. Reperfusion induces prolonged, but ultimately reversible, myocardial contractile dysfunction (“stunned myocardium”). However, there is controversy over whether reperfusion results in further necrosis of is-