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There are several potential outcomes of myocardial ischaemia. When ischaemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When myocardial ischaemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischaemia, leading to a reversible, chronic left ventricular dysfunction, has been termed hibernating myocardium. The difference between this condition and that described before, i.e. prolonged ischaemia, which results in further damage on reperfusion, is, most likely, related to residual coronary flow. In the hibernating myocardium, which is supplied by a narrow coronary artery, blood flow is not low enough to cause progression toward tissue necrosis, but it is low enough to cause intracellular changes and adaptative mechanisms which, in turn, are responsible for the down-regulation of myocardial contractility and for the preservation of viability. The level of underperfusion is sufficient to maintain aerobic metabolism of the quiescent myocardium as demonstrated by the absence of lactate and creatine phosphokinase releases. There are no doubts that revascularization is essential for hibernating myocardium, and the clinical goal to achieve is the possibility of accurately distinguishing viable from infarcted tissue. A third possible outcome of myocardial ischaemia is a post-ischaemic ventricular dysfunction or myocardial stunning. This term describes a transient mechanical dysfunction that persists on reperfusion after a short period of ischaemia, despite the absence of irreversible damage.