Cardiovascular diseases account for one third of all deaths worldwide, more than 33% of which are related to ischemic heart disease, involving a myocardial infarction (MI). Following myocardial infarction, the injured region and ventricle undergo structural changes which are thought to be caused by elevated stresses and reduction of strains in the infarcted wall. The fibrotic phase is defined as the period when the amount of new collagen and number of fibroblasts rapidly increase in the infarcted tissue. We studied through finite element analysis the mechanics of the infarcted and remodeling rat heart during diastolic filling. Biventricular geometries of healthy and infarcted rat hearts reconstructed from magnetic resonance images were imported in Abaqus©. The passive myocardium was modelled as a nearly incompressible, hyperelastic, transversely isotropic material represented by the strain energy function W = ½C(eQ − 1) with Q = bfE112 + bt(E222 + E332 + E322) + bfs(E122 + E212 + E132 + E312). Material parameters were obtained from literature [1]. As boundary conditions, the circumferential and longitudinal displacements at the base were set to zero. The radial displacements at the base were left free. A linearly increasing pressure from 0 to 3.80 kPa and 0.86 kPa, respectively, was applied to the endocardial surfaces of left and right ventricle. Average radial, circumferential and longitudinal strains during passive filling were −0.331, 0.135, 0.042 and −0.250, −0.078 and 0.046 for the healthy heart and the infarcted heart, respectively. The average radial, circumferential and longitudinal stresses were −1.196 kPa, 3.87 kPa in the healthy heart and 0.424 kPa and −1.90 kPa, 8.74 kPa and 1.69 kPa in the infarcted heart. The strains were considerable lower in the infarcted heart compared to the health heart whereas stresses were higher in the presence of an infarct compared to the healthy case. The results of this study indicate the feasibility of the models developed for a more comprehensive assessment of mechanics of the infarcted ventricle including extension to account for cardiac contraction.

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