First evidence postischemic dysfunction of viable myocardium

Stunned myocardium is viable previously ischemic tissue, which exhibits prolonged but transient postischemic contractile dysfunction. This phenomenon occurs both following brief episodes of ischemia (as might occur in experimental models that mimic angina) and following more prolonged episodes of ischemia as would occur following reperfusion of an acute myocardial infarction. Stunning has been reported to last for hours to days following reflow, but the duration of dysfunction is dependent upon the experimental model being used. Determinants of stunning include the severity and duration of ischemia, the degree of paradoxical systolic bulging of the ischemic segment, the region of the heart under study, and the mode by which reperfusion is induced. Stunned myocardium is also characterized by a decrease in myocardial ATP and purine content, subtle ultrastructural abnormalities (i.e., vacuoles adjacent to mitochondria), electrophysiological abnormalities, 'low reflow,' and reduced coronary vasodilator reserve. It should be noted that total coronary artery occlusion is not a prerequisite for stunning: postischemic dysfunction has been documented following exercise-induced ischemia, in models of partial coronary artery stenosis, and in hypertrophied ventricles without coronary stenosis.