Among the pathogenetic mechanisms proposed for myocardial stunning, three have emerged as more likely: generation of oxygen radicals, calcium overload, and decreased responsiveness of contractile filaments to calcium. These are not mutually exclusive and may represent different steps of the same pathophysiological cascade. Thus, generation of oxyradicals may cause calcium overload, both processes resulting in damage and dysfunction of myofilaments. Unravelling the molecular mechanisms whereby a brief episode of ischemia can cause such a prolonged period of contractile dysfunction will be a major challenge. Stunning appears to develop in various settings in which transient ischemia occurs, eg, unstable angina, acute myocardial infarction with early reperfusion, exercise-induced ischemia, cardiac surgery, and cardiac transplantation. A potentially important consideration is that frequent episodes of ischemia, particularly in the ambulatory setting, may have a cumulative effect and cause protracted or chronic postischemic LV dysfunction, mistakenly diagnosed as hibernation when in fact it is a result of repetitive stunning. Recognition of myocardial stunning may impact upon patient management, as imaging techniques now allow prospective diagnosis. While no current diagnostic technique is ideal, thallium-201 scintigraphy or dobutamine echocardiography are available and should be applied in the appropriate clinical setting...