Objectives. We sought to investigate whether alterations in cardiac high energy phosphates occur in postischemic “stunned” human myocardium.Background. Transient postischemic myocardial dysfunction is a common phenomenon that occurs in a variety of clinical settings in the absence of necrosis, and its pathogenesis is still unclear. Cardiac high energy phosphates are reduced during ischemia, and persistently altered myocardial high energy phosphate metabolism has been suggested as a mechanism contributing to stunning.Methods. We studied 29 patients with a first anterior myocardial infarction (MI) who underwent successful reperfusion within 6 h of the onset of chest pain. These patients underwent 31P magnetic resonance spectroscopy (MRS) a mean of 4 days after MI for measurement of left ventricular contractility and relative high energy phosphate metabolites. Twenty-one patients underwent a second 31P MRS study a mean of 39 days after MI. Eight volunteers served as control subjects.Results. Global and infarct area wall motion scores improved significantly between the early and late studies. No difference was found between early cardiac phosphocreatine (PCr)/beta-adenosine triphosphate (beta-ATP) ratios in patients and control subjects ([mean ± SD] 1.51 ± 0.17 vs. 1.61 ± 0.18, respectively, p = 0.17) or between early and late study results in patients (1.51 ± 0.17 vs. 1.53 ± 0.17, respectively, p = 0.6). For alpha of 0.05, the study had a 90% power to detect a 9% difference.Conclusions. The results of this study demonstrate normal myocardial PCr/ATP ratios in patients with myocardial stunning after reperfusion and suggest that relative cardiac high energy phosphates are not depleted in stunned human myocardium.