The recent advances in cardiovascular pathophysiology have changed our interpretation of the interplay between myocardial metabolism and contractile function which takes place during acute ischemia. For instance, the use of nuclear magnetic resonance (NMR) spectroscopy has allowed to document that the rapid impairment in contractility seen during acute myocardial ischemia is not directly related to depletion of high energy phosphate levels, nor to decreased availability of intracellular calcium. Rather, acidosis and inorganic phosphate accumulation cooperate to decrease myofilament sensitivity to calcium. Marked alterations of cardiac function and metabolism may also accompany the postischemic period. Positron emission tomography studies have shown that myocardial uptake of glucose remains disproportionately elevated in areas of myocardium which have been rendered transiently ischemic by an episode of stress-induced angina in patients with coronary artery disease. This phenomenon may have important practical applications, as it may be used as a metabolic marker to detect areas of myocardium which is viable, but potentially at risk for ischemic episodes. Reduced ATP levels are another biochemical alteration which can be typically found in postischemic hearts. Again, NMR spectroscopy has allowed to establish that these hearts often display near-normal mitochondrial function, and that the delayed resynthesis of ATP is due to lack of purine nucleotide precursors. A most interesting functional peculiarity of postischemic hearts is represented by the prolonged impairment of contractility, which largely outlasts the duration of the period of flow deprivation. This phenomenon, which eventually subsides over the course of hours or days, has been termed myocardial stunning, to underline its occurrence despite the absence of ultrastructural signs of irreversible damage.(ABSTRACT TRUNCATED AT 250 WORDS)