Myocardial infarction (MI) induces cardiomyocyte death and scar formation, triggering functional adaptations of the left ventricle (LV). The quantification of cardiac contractile function via regional indices such as cardiac strains and torsion has shown the potential to provide a mechanistic link between LV structure and function. Indeed, torsion is an integral component of contractility resulting from the complex helical arrangement of myofibers within the LV microstructure. We hypothesize that MI-associated impaired contractility may be quantified through region-specific LV torsion, thus providing added prognostic value to functional indices such as ejection fraction (LVEF). A longitudinal study evaluated LV torsion in a rodent model of MI at 2 weeks (2-WK) and 4 weeks (4-WK) post-MI. Speckle-tracking echocardiography was used to calculate regional cardiac rotations at basal, mid, and apical slices. Torsion was subsequently evaluated as the two-dimensional shear angle at all slices relative to basal and mid slices. Whereas the reduction in LVEF was insignificant at 2-WK post-MI, a significant drop in torsion was evident in 2-WK and statistically maintained in 4-WK post-MI. While reduced LVEF is a crucial indicator of LV systolic dysfunction, assessing regional adaptations through cardiac torsion may provide the pathophysiological link between LV myocardial remodeling and organ-level functional indices such as LVEF in MI.