Stunned and hibernating myocardium: possibility of intervention.
There are several potential outcomes of myocardial ischemia. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When myocardial ischemia 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 ischemia, 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 ischemia, which results in further damage on reperfusion, is, most likely, related to residual coronary flow. In the hibernating myocardium, which is always 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 pH changes that, in turn, are responsible for the downregulation of myocardial contractility. The level of underperfusion is sufficient to maintain aerobic metabolism of the quiescient myocardium as demonstrated by the absence of lactate and creatine phosphokinase release. There are no doubts that revascularization is essential for hibernated myocardium, and the clinical goal to achieve is the possibility of accurately distinguishing viable from infarcted tissue. A third possible outcome of myocardial ischemia is a postischemic ventricular dysfunction or myocardial stunning. This term describes a transient mechanical dysfunction that persists on reperfusion after a short period of ischemia, despite the absence of irreversible damage. There are numerous clinical conditions in which stunning might manifest.(ABSTRACT TRUNCATED AT 250 WORDS)