Stunned myocardium?an unfinished puzzle

See article by Colantonio et al. [15] (pages 217–225) in this issue. Myocardial stunning describes the phenomenon of reversible contractile dysfunction of viable myocardium after restoration of normal or nearly normal epicardial coronary flow following myocardial ischemia. In man, myocardial stunning has been observed following cardiac surgery (global ischemia and reperfusion), in myocardial infarction after timely reperfusion therapy (regional prolonged severe ischemia and reperfusion with stunned myocardium around areas of necrosis), in unstable angina and coronary spasm (regional transient ischemia without or with minimal necrosis), and in exercise-induced angina (demand ischemia with almost normal blood flow). Recurrent episodes of stunning might result in hibernating myocardium [1,2]. The designs of experiments used to elucidate the cellular and molecular mechanisms involved in myocardial stunning were as heterogeneous as the clinical settings involved in this phenomenon. Oxygen-free radicals and intracellular calcium overload have been identified as two pathogenetic mechanisms inducing intracellular damage that results in contractile dysfunction [1–3]. These pathogenetic processes adversely affect several molecular targets that can potentially contribute to myocardial stunning (Table 1 and Refs. [1–3]), and will result in a change of the proteomics of the myocyte.