Numerical aspects of anisotropic failure in soft biological tissues favor energy-based criteria: A rate-dependent anisotropic crack phase-field model.

A deeper understanding to predict fracture in soft biological tissues is of crucial importance to better guide and improve medical monitoring, planning of surgical interventions and risk assessment of diseases such as aortic dissection, aneurysms, atherosclerosis and tears in tendons and ligaments. In our previous contribution (Gültekin et al., 2016) we have addressed the rupture of aortic tissue by applying a holistic geometrical approach to fracture, namely the crack phase-field approach emanating from variational fracture mechanics and gradient damage theories. In the present study, the crack phase-field model is extended to capture anisotropic fracture using an anisotropic volume-specific crack surface function. In addition, the model is equipped with a rate-dependent formulation of the phase-field evolution. The continuum framework captures anisotropy, is thermodynamically consistent and based on finite strains. The resulting Euler-Lagrange equations are solved by an operator-splitting algorithm on the temporal side which is ensued by a Galerkin-type weak formulation on the spatial side. On the constitutive level, an invariant-based anisotropic material model accommodates the nonlinear elastic response of both the ground matrix and the collagenous components. Subsequently, the basis of extant anisotropic failure criteria are presented with an emphasis on energy-based, Tsai-Wu, Hill, and principal stress criteria. The predictions of the various failure criteria on the crack initiation, and the related crack propagation are studied using representative numerical examples, i.e. a homogeneous problem subjected to uniaxial and planar biaxial deformations is established to demonstrate the corresponding failure surfaces whereas uniaxial extension and peel tests of an anisotropic (hypothetical) tissue deal with the crack propagation with reference to the mentioned failure criteria. Results favor the energy-based criterion as a better candidate to reflect a stable and physically meaningful crack growth, particularly in complex three-dimensional geometries with a highly anisotropic texture at finite strains.

A phase-field approach to model fracture of arterial walls: Theory and finite element analysis.

This study uses a recently developed phase-field approach to model fracture of arterial walls with an emphasis on aortic tissues. We start by deriving the regularized crack surface to overcome complexities inherent in sharp crack discontinuities, thereby relaxing the acute crack surface topology into a diffusive one. In fact, the regularized crack surface possesses the property of Gamma-Convergence, i.e. the sharp crack topology is restored with a vanishing length-scale parameter. Next, we deal with the continuous formulation of the variational principle for the multi-field problem manifested through the deformation map and the crack phase-field at finite strains which leads to the Euler-Lagrange equations of the coupled problem. In particular, the coupled balance equations derived render the evolution of the crack phase-field and the balance of linear momentum. As an important aspect of the continuum formulation we consider an invariant-based anisotropic constitutive model which is additively decomposed into an isotropic part for the ground matrix and an exponential anisotropic part for the two families of collagen fibers embedded in the ground matrix. In addition we propose a novel energy-based anisotropic failure criterion which regulates the evolution of the crack phase-field. The coupled problem is solved using a one-pass operator-splitting algorithm composed of a mechanical predictor step (solved for the frozen crack phase-field parameter) and a crack evolution step (solved for the frozen deformation map); a history field governed by the failure criterion is successively updated. Subsequently, a conventional Galerkin procedure leads to the weak forms of the governing differential equations for the physical problem. Accordingly, we provide the discrete residual vectors and a corresponding linearization yields the element matrices for the two sub-problems. Finally, we demonstrate the numerical performance of the crack phase-field model by simulating uniaxial extension and simple shear fracture tests performed on specimens obtained from a human aneurysmatic thoracic aorta. Model parameters are obtained by fitting the set of novel experimental data to the predicted model response; the finite element results agree favorably with the experimental findings.

"What makes blood clots break off?" A Back-of-the-Envelope Computation Toward Explaining Clot Embolization.

PURPOSE: One in four deaths worldwide is due to thromboembolic disease; that is, one in four people die from blood clots first forming and then breaking off or embolizing. Once broken off, clots travel downstream, where they occlude vital blood vessels such as those of the brain, heart, or lungs, leading to strokes, heart attacks, or pulmonary embolisms, respectively. Despite clots' obvious importance, much remains to be understood about clotting and clot embolization. In our work, we take a first step toward untangling the mystery behind clot embolization and try to answer the simple question: "What makes blood clots break off?" METHODS: To this end, we conducted experimentally-informed, back-of-the-envelope computations combining fracture mechanics and phase-field modeling. We also focused on deep venous clots as our model problem. RESULTS: Here, we show that of the three general forces that act on venous blood clots-shear stress, blood pressure, and wall stretch-induced interfacial forces-the latter may be a critical embolization force in occlusive and non-occlusive clots, while blood pressure appears to play a determinant role only for occlusive clots. Contrary to intuition and prior reports, shear stress, even when severely elevated, appears unlikely to cause embolization. CONCLUSION: This first approach to understanding the source of blood clot bulk fracture may be a critical starting point for understanding blood clot embolization. We hope to inspire future work that will build on ours and overcome the limitations of these back-of-the-envelope computations.

A quasi-incompressible and quasi-inextensible finite element analysis of fibrous soft biological tissues.

The contribution presents an extension and application of a recently proposed finite element formulation for quasi-inextensible and quasi-incompressible finite hyperelasticity to fibrous soft biological tissues and touches in particular upon computational aspects thereof. In line with theoretical framework presented by Dal (Int J Numer Methods Eng 117:118-140, 2019), the mixed variational formulation is extended to two families of fibers as often encountered while dealing with fibrous tissues. Apart from that, the purely Eulerian setting features the additive decomposition of the free energy function into volumetric, isotropic and anisotropic parts. The multiplicative split of the deformation gradient and all the outcomes thereof, e.g., unimodular invariants, are simply dispensed with in the three element formulations investigated, namely Q1, Q1P0 and the proposed Q1P0F0. For the quasi-incompressible response, the Q1P0 element formulation is briefly outlined where the pressure-type Lagrange multiplier and its conjugate enter the variational formulation as an extended set of variables. Using the similar argumentation, an extended Hu-Washizu-type mixed variational potential is introduced where the volume averaged squares of fiber stretches and associated fiber stresses are additional field variables. The resulting finite element formulation called Q1P0F0 is very attractive as it is based on mean values of the additional field variables at element level through integration over the element domain in a preprocessing step, earning the model vast utilization areas. The proposed approach is examined through representative boundary value problems pertaining to fibrous biological tissues. For all the cases studied, the proposed Q1P0F0 formulation elicits the most compliant mechanical response, thereby outperforming the standard Q1 and Q1P0 element formulations through mesh-refinement analyses. Results prompt further experimental investigations as to true deformation fields under biologically relevant loading conditions which would make the assessment of Q1P0 and Q1P0F0 more based on physical grounds.

Computational modeling of progressive damage and rupture in fibrous biological tissues: application to aortic dissection.

This study analyzes the lethal clinical condition of aortic dissections from a numerical point of view. On the basis of previous contributions by Gültekin et al. (Comput Methods Appl Mech Eng 312:542-566, 2016 and 331:23-52, 2018), we apply a holistic geometrical approach to fracture, namely the crack phase-field, which inherits the intrinsic features of gradient damage and variational fracture mechanics. The continuum framework captures anisotropy, is thermodynamically consistent and is based on finite strains. The balance of linear momentum and the crack evolution equation govern the coupled mechanical and phase-field problem. The solution scheme features the robust one-pass operator-splitting algorithm upon temporal and spatial discretizations. Based on experimental data of diseased human thoracic aortic samples, the elastic material parameters are identified followed by a sensitivity analysis of the anisotropic phase-field model. Finally, we simulate an incipient propagation of an aortic dissection within a multi-layered segment of a thoracic aorta that involves a prescribed initial tear. The finite element results demonstrate a severe damage zone around the initial tear and exhibit a rather helical crack pattern, which aligns with the fiber orientation. It is hoped that the current contribution can provide some directions for further investigations of this disease.

An orthotropic viscoelastic model for the passive myocardium: continuum basis and numerical treatment.

This study deals with the viscoelastic constitutive modeling and the respective computational analysis of the human passive myocardium. We start by recapitulating the locally orthotropic inner structure of the human myocardial tissue and model the mechanical response through invariants and structure tensors associated with three orthonormal basis vectors. In accordance with recent experimental findings the ventricular myocardial tissue is assumed to be incompressible, thick-walled, orthotropic and viscoelastic. In particular, one spring element coupled with Maxwell elements in parallel endows the model with viscoelastic features such that four dashpots describe the viscous response due to matrix, fiber, sheet and fiber-sheet fragments. In order to alleviate the numerical obstacles, the strictly incompressible model is altered by decomposing the free-energy function into volumetric-isochoric elastic and isochoric-viscoelastic parts along with the multiplicative split of the deformation gradient which enables the three-field mixed finite element method. The crucial aspect of the viscoelastic formulation is linked to the rate equations of the viscous overstresses resulting from a 3-D analogy of a generalized 1-D Maxwell model. We provide algorithmic updates for second Piola-Kirchhoff stress and elasticity tensors. In the sequel, we address some numerical aspects of the constitutive model by applying it to elastic, cyclic and relaxation test data obtained from biaxial extension and triaxial shear tests whereby we assess the fitting capacity of the model. With the tissue parameters identified, we conduct (elastic and viscoelastic) finite element simulations for an ellipsoidal geometry retrieved from a human specimen.