Models of cardiac mechanics are increasingly used to investigate cardiac physiology. These models are characterized by a high level of complexity, including the particular anisotropic material properties of biological tissue and the actively contracting material. A large number of independent simulation codes have been developed, but a consistent way of verifying the accuracy and replicability of simulations is lacking. To aid in the verification of current and future cardiac mechanics solvers, this study provides three benchmark problems for cardiac mechanics. These benchmark problems test the ability to accurately simulate pressure-type forces that depend on the deformed objects geometry, anisotropic and spatially varying material properties similar to those seen in the left ventricle and active contractile forces. The benchmark was solved by 11 different groups to generate consensus solutions, with typical differences in higher-resolution solutions at approximately 0.5%, and consistent results between linear, quadratic and cubic finite elements as well as different approaches to simulating incompressible materials. Online tools and solutions are made available to allow these tests to be effectively used in verification of future cardiac mechanics software.
Many biological tissues exhibit a non-standard continuum mechanics behavior: they are able to modify their placement in absence of external loads. The activity of the muscles is usually represented in solid mechanics in terms of an active stress, to be added to the standard one. A less popular approach is to introduce a multiplicative decomposition of the tensor gradient of deformation in two factors: the passive and the active one. Both approaches should satisfy due mathematical properties, namely frame indifference and ellipticity of the total stress. At the same time, the constitutive laws should reproduce the observed physiological behavior of the specific living tissue. In this paper we focus on cardiac contractility. We review some constitutive examples of active stress and active strain taken from the literature and we discuss them in terms of precise mathematical and physiological properties. These arguments naturally suggest new possible models.
The experimental evidence that a feedback exists between growth and stress in tumors poses challenging questions. First, the rheological properties (the "constitutive equations") of aggregates of malignant cells are still a matter of debate. Secondly, the feedback law (the "growth law") that relates stress and mitotic-apoptotic rate is far to be identified. We address these questions on the basis of a theoretical analysis of and experiments that involve the growth of tumor spheroids. We show that solid tumors exhibit several mechanical features of a poroelastic material, where the cellular component behaves like an elastic solid. When the solid component of the spheroid is loaded at the boundary, the cellular aggregate grows up to an asymptotic volume that depends on the exerted compression. Residual stress shows up when solid tumors are radially cut, highlighting a peculiar tensional pattern. By a novel numerical approach we correlate the measured opening angle and the underlying residual stress in a sphere. The features of the mechanobiological system can be explained in terms of a feedback of mechanics on the cell proliferation rate as modulated by the availability of nutrient, that is radially damped by the balance between diffusion and consumption. The volumetric growth profiles and the pattern of residual stress can be theoretically reproduced assuming a dependence of the target stress on the concentration of nutrient which is specific of the malignant tissue.
State-of-the-art cardiac electrophysiology models that are able to deliver physiologically motivated activation maps and electrocardiograms (ECGs) can only be solved on high-performance computing architectures. This makes it nearly impossible to adopt such models in clinical practice. ECG imaging tools typically rely on simplified models, but these neglect the anisotropic electric conductivity of the tissue in the forward problem. Moreover, their results are often confined to the heart-torso interface. We propose a forward model that fully accounts for the anisotropic tissue conductivity and produces the standard 12-lead ECG in a few seconds. The activation sequence is approximated with an eikonal model in the 3d myocardium, while the ECG is computed with the lead-field approach. Both solvers were implemented on graphics processing units and massively parallelized. We studied the numerical convergence and scalability of the approach. We also compared the method to the bidomain model in terms of ECGs and activation maps, using a simplified but physiologically motivated geometry and 6 patient-specific anatomies. The proposed methods provided a good approximation of activation maps and ECGs computed with a bidomain model, in only a few seconds. Both solvers scaled very well to high-end hardware. These methods are suitable for use in ECG imaging methods, and may soon become fast enough for use in interactive simulation tools.
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