A transmurally heterogeneous orthotropic activation model for ventricular contraction and its numerical validation

\u3cp\u3eModels for cardiac mechanics require an activation mechanism properly representing the stress-strain relations in the contracting myocardium. In this paper, we propose a new activation model that accounts for the transmural heterogeneities observed in myocardial strain measurements. In order to take the anisotropy of the active mechanics into account, our model is based on an active strain formulation. Thanks to multiplicative decomposition of the deformation gradient tensor, in this formulation, the active strains orthogonal to the fibers can be naturally described. We compare the results of our novel formulation against different anisotropic models of the active contraction of the cardiac muscle, as well as against experimental data available in the literature. We show that with the currently available models, the strain distributions are not in agreement with the reported experimental measurements. Conversely, we show that our new transmurally heterogeneous orthotropic activation model improves the accuracy of shear strains related to in-plane rotations and torsion.\u3c/p\u3

Post-infarct evolution of ventricular and myocardial function

Adverse ventricular remodeling following acute myocardial infarction (MI) may induce ventricular dilation, fibrosis, and loss of global contractile function, possibly resulting in heart failure (HF). Understanding the relation between the time-dependent changes in material properties of the myocardium and the contractile function of the heart may further our understanding of the development of HF post-MI and guide the development of novel therapies. A finite element model of cardiac mechanics was used to model MI in a thick-walled truncated ellipsoidal geometry. Infarct core and border zone comprised 9.6 and 8.1% of the LV wall volume, respectively. Acute MI was modeled by inhibiting active stress generation. Chronic MI was modeled by the additional effect of infarct material stiffening, wall thinning and fiber reorientation. In acute MI, stroke work decreased by 25%. In the infarct core, fiber stress was reduced but fiber strain was increased, depending on the degree of infarct stiffening. Fiber work density was equal to zero. Healthy tissue adjacent to the infarct showed decreased work density depending on the degree of infarct stiffness and the orientation of the myofibers with respect to the infarct region. Thinning of the wall partially restored this loss in work density while the effects of fiber reorientation were minimal. We found that the relative loss in pump function in the infarcted heart exceeds the relative loss in healthy myocardial tissue due to impaired mechanical function in healthy tissue adjacent to the infarct. Infarct stiffening, wall thinning and fiber reorientation did not affect pump function but did affect the distribution of work density in tissue adjacent to the infarct

A computational approach on sensitivity of left ventricular wall strains to geometry

In this work we use a Finite Element model of the left ventricular (LV) mechanics to assess the sensitivity of strains to geometry. Six principal shape modes extracted from an atlas of LV geometries using principal component analysis, have been used to model the variability of the geometry of a population of 1991 asymptomatic volunteers. We observed that shear strains are more sensitive than normal strains to geometry. For all the strains, shape mode 1, related with variation in size within the population, plays an major role, but none of the six principal modes can be considered non influential