Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals on reperfusion and by a loss of sensitivity of contractile filaments to calcium. These hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, a burst of free radical generation after reperfusion could alter contractile filaments in a manner that renders them less responsive to calcium. Increased free radical formation could also cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. There is now considerable evidence that myocardial stunning occurs clinically in various situations in which the heart is exposed to transient ischemia, such as unstable angina, acute myocardial infarction with early reperfusion, exercise-induced ischemia, cardiac surgery, and cardiac transplantation. Recognition of myocardial stunning is clinically important and may impact patient treatment. Although no ideal diagnostic technique for myocardial stunning has yet been developed, thallium-201 scintigraphy or dobutamine echocardiography are available and can be useful to identify viable myocardium with reversible wall motion abnormalities. An intriguing possibility is that so-called chronic hibernation may in fact be the result of repetitive episodes of stunning, which have a cumulative effect and cause protracted postischemic left ventricular dysfunction. A better understanding of myocardial stunning will expand our knowledge of the pathophysiology of myocardial ischemia and provide a rationale for developing new therapeutic strategies designed to prevent postischemic dysfunction.