It has been known since the mid 1980s that systolic performance (systolic shortening and wall thickening) is depressed in the non-ischemic borderzone (BZ) after antero-apical myocardial infarction (MI). It was initially thought that the reduced BZ function was due to mechanical tethering by the infarct. However, finite element based inverse calculations of regional contractility (i.e., active force/stress development), in which optimization routines attempt to match computed and experimentally measured LV volume and strain, suggest that BZ contractility is reduced by more than 50%. Moreover, BZ contractility appears to vary linearly across the BZ and the BZ may be as much as 3 cm in width after antero-apical MI. Finally, preliminary calculations in a single sheep suggest that borderzone contractility is depressed after postero-lateral MI.