This study utilized porcine models of postinfarction LV remodeling (MI: n=8) and concentric LVH secondary to aortic banding (AoB: n=8) to examine the relationships between regional myocardial contractile function (tagged MRI), wall stress (MRI and LV pressure), and bioenergetics (P-31 MR spectroscopy). Physiological assessments were conducted at a 4 week time point after myocardial infarction or aortic banding surgery. Comparisons were made with size matched normal animals (normal: n=8). Both myocardial infarction and aortic banding instigated significant LV hypertrophy. Ejection fraction was not significantly altered in the AoB group, but significantly decreased in the MI group (p<0.01 vs. normal and AoB). Systolic and diastolic wall stresses were approximately two times greater than normal in the infarct region and border zone. Wall stress in the AoB group was not significantly different from normal hearts. The infarct border zone demonstrated profound bioenergetic abnormalities, especially in the subendocardium, where the ratio of phosphocreatine to adenosine triphosphate (PCr/ATP) decreased from 1.98 ± 0.16 (normal) to 1.06 ± 0.30 (MI, p<0.01). The systolic radial thickening fraction and the circumferential shortening fraction in the anterior wall were severely reduced (MI, p<0.01 vs Normal). The radial thickening fraction and circumferential shortening fraction in the AoB group were not significantly different from normal. The severely elevated wall stress in the infarct border zone was associated with a significant increase in chemical energy demand and abnormal myocardial energy metabolism. Such severe metabolic perturbations cannot support normal cardiac function, which may explain the observed regional contractile abnormalities in the infarct border zone.