PubMedDate not supplied
Although the mechanisms involved in stunning remain incompletely defined, it appears that intracellular calcium overload, sarcoplasmic reticulum dysfunction, and the generation of OFR are important components of post-ischemic myocyte dysfunction. It is likely that a variety of mechanisms, some possibly remaining to be elucidated, are operative in the pathogenesis of stunning, and that the contribution of a particular process may be influenced by the model and the method of inducing ischemia. Myocardial stunning has been shown to be prevalent in patients with diverse cardiac diseases. Small clinical trials have suggested that electrocardiography, echocardiography, and radionuclide imaging techniques may be useful in identifying patients with stunned myocardium. In patients with depressed cardiac performance due to stunning, therapy with inotropic agents may recruit the viable but injured myocardium to contract and improve cardiac output in the short term. An important issue that will be addressed over the next decade is whether aggressive therapy aimed at reducing myocardial stunning in stable patients should be attempted. Some authorities have suggested that stunning may represent an adaptive response to limit reperfusion injury, and that interfering with this response may not be beneficial in the long term. Further investigation into the cellular and molecular basis of ischemic injury should provide insight into these and other important aspects of myocardial stunning. Methods of attenuating postischemic ventricular dysfunction that appear convincing in the research laboratory may not translate to clinical benefit when applied to humans.