Echocardiographic determination of myocardial viability

Myocardial “stunning” (dysfunction despite normalization of coronary perfusion) is a state of contraction-perfusion mismatch that may be seen in the context of successful reperfusion therapy of myocardial infarction. Animal models of this condition exist and its etiology at a cellular level is being elucidated (1). Typically, this process occurs early after acute ischemic events and resolves spontaneously (2,3). Later after the event, dysfunction in viable tissue has been ascribed to chronic reduction of flow, which is often termed “hibernation” (4), because resumption of normal function is contingent upon myocardial revascularization. The existence of this phenomenon has been shown experimentally (5) and in humans (6). However, in contrast to the original “contraction-perfusion match” concept of hibernating myocardium, many of these dysfunctional segments have normal resting myocardial perfusion and intact cellular architecture (7), suggesting that they are recurrently stunned. With recurrent ischemia, the tissue develops progressive ultrastructural damage and behaves more like hibernating myocardium (8). Viable myocardium is therefore composed of stunned and hibernating tissue, the combination of which vary both in time and space.