Infarct size is the decisive determinant of the extent and severity of remodeling (1) and of the prognosis of patients after myocardial infarction (2). Timely reperfusion is the only way to reduce ultimate infarct size. However, reperfusion comes at a price and induces injury per se. The immediate and full restoration of coronary blood flow results in arrhythmias, contractile dysfunction (stunning), and microvascular impairment. Although previously debated (3, 4), it is now clear that there also is irreversible reperfusion injury through apoptosis and necrosis (5, 6). The mechanisms of reperfusion injury relate to the excess formation of free radicals (7), to calcium overload, and finally to hypercontracture (6, 8).