Wall thickening (WT) is impaired in non-infarcted regions adjacent to Myocardial Infarction (MI) and is thought to be caused by mechanical overload and geometric chamber distortion. The contribution of abnormalities intrinsic to the myocyte to impaired WT during remodeling has not been examined. To correlate local WT in vivo with myocyte morphology and function during LV remodeling, magnetic resonance imaging (MRI) was performed 2 weeks after MI (left coronary artery ligation) by obtaining EKG-gated spin-echo shortaxis images (1.5 Tesla, 3 inch coil). Myocytes were isolated from 14 rats with MI and 4 shams. Local WT in regions adjacent (A) and remote (R) to the infarct scar visible by MRI was correlated with cell morphology and function, studied in myocytes isolated from A and R. MI size measured by planimetry ranged from 5% to 30% (mean 18.7%) of the outer LV area. Regional differences in local WT were present in MI hearts: average %WT in A was lower than in R (27.8 ± 6.14 (sem) vs 54.0 ± 10.17: p < 0.01). In rats with large MI (MI > 20%, n = 7). cells were longer than in sham (p < 0.05: n = 175) both in R(143.1 ± 1.76 vs 120.9 ± 2.40 μm) and in A (150.3 ± 1.89 vs 122.6 ± 2.02 μm) while no changes were evidenced in cell width. Cells from A were longer than those from R(p < 0.05). A positive correlation between MI size and cell length was found (for A: r = 0.8, slope 0.07). Electrically-stimulated cell contraction (see figure, %ES: cell shortening / diastolic length: values aTe mean ± sem), was impaired in A with respect to sham (**: p < 0.05) and to R (*: p = 0.06). Thus, during post-MI remodeling, dysfunction in A non-infarcted regions is associated with greater myocyte elongation and dysfunction than in R. In conclusion, local myocyte dysfunction contributes to WT impairment in adjacent regions after MI.