Background Infarcted segments of myocardium demonstrate functional impairment ranging in severity from hypokinesis to dyskinesis. We sought to better define the contributions of passive material properties (stiffness) and active properties (contracting myocytes) to infarct thickening. Using a finite element (FE) model, we tested the hypothesis that infarcted myocardium must contain contracting myocytes to be akinetic and not dyskinetic. Methods and Results: A three-dimensional FE mesh of the left ventricle was developed using echocardiographs from a reperfused ovine anteroapical infarct. The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction and an elastance model for active fiber stress was incorporated. The diastolic stiffness, C, and systolic material property, T_max, of the uninfarcted remote myocardium were assumed to be normal (C=0.876 kPa, T_max=135.7 kPa). Diastolic and systolic properties of the infarct necessary to produce akinesis, defined as an average radial strain between ±0.01, were determined by assigning a range of diastolic stiffnesses and scaling infarct T_max to represent the percentage of contracting myocytes between 0% and 100%. As C was increased to eleven times normal (C=10 kPa) the percentage of T_max necessary for akinesis increased from 20 to 50%. Without contracting myocytes, C=250 kPa was necessary to achieve akinesis. Conclusions If infarct stiffness is less than 285 times normal, contracting myocytes are required to prevent dyskinetic infarct wall motion.