Proceedings of the 2011 SCATh Joint Workshop on New Technologies for Computer/Robot Assisted Surgery July 11-13, 2011,

Graz, Austria

Modeling of damage-induced softening for arterial tissues

Hannah Weisbecker
Institute of Biomechanics Graz University of Technology Graz, Austria

David M. Pierce
Institute of Biomechanics Graz University of Technology Graz, Austria

Gerhard A. Holzapfel
Institute of Biomechanics Graz University of Technology Graz, Austria and Department of Solid Mechanics Royal Institute of Technology Stockholm, Sweden

AbstractCardiovascular diseases are among the leading causes of death in the EU. Several treatments such as angioplasty and endovascular aneurysm repair require the insertion of stents which induce high tissue stresses which may cause damage in the arterial wall. A better understanding of tissue damage mechanisms and accurate modeling of the material behavior at supra-physiological load ranges may help to improve nite element modeling of surgical procedures and the design of stent geometries. To these ends several damage models for soft biological tissues have been proposed which are able to describe the Mullins effect. These models are capable of accounting for damage accumulation in both matrix and bers of the arterial wall. This communication gives an overview of the existing damage models for arterial tissue and highlights their limitations. Keywords - artery; constitutive modeling continuum damage model; pseudo-elastic damage model

I. I NTRODUCTION The arterial wall consists of three layers intima, media and adventitia. In young arteries the intima consists of a layer of endothelial cells and only the media and the adventitia are load bearing, and hence of solid mechanical relevance. In aged arteries, however, the intima thickens and all three layers are load bearing so that all three layers are all relevant from the mechanical point of view. The individual layers can be modeled as a ber-reinforced composite with an isotropic matrix, mainly comprised of elastin, and two symmetrically arranged families of collagen bers [1], see also the recent experimental study in [2]. In most applications arteries are modeled elastically, and this approximation is justied after the material has been preconditioned [3]. However, the consideration of the Mullins effect describing discontinuous softening, as illustrated in Fig. 1, allows a more accurate model of the behavior of the tissue, especially if supra-physiological load ranges are considered. The communication is structured as follows. The next section describes a very short selection of common hyperelastic models for arterial tissue. Then two different approaches for damage modeling, the continuum damage and the pseudoelastic approach, are introduced, and examples for specic strain-energy functions including the softening behavior of the

Fig. 1. Schematic of the Mullins effect showing stress vs. stretch . Primary loading from point A to point B occurs on path a, whereas unloading and reloading to point B occurs on path b. For loads higher than B the primary loading curve is reached again and path c describes the unloading and reloading path to point C.

tissue are presented. In the last section the models and their limitations are discussed. II. M ATERIAL MODELING A. Kinematics The deformation of the material is described by the deformation gradient F and the related right Cauchy-Green tensor C = FT F. A multiplicative decomposition F = J 1/3 F is introduced that splits the deformation into a volumetric J 1/3 I and an isochoric F part, where J = det F. This multiplicative decomposition yields C = J 2/3 C, where C = FT F. It is usually assumed that damage is solely associated with the deviatoric part of the deformation, therefore, only the deviatoric parts of the strain-energy function and the stresses are introduced here, and the bars are omitted for the sake of simplicity. B. Constitutive equation Commonly, the passive behavior of arterial tissue is modeled as an incompressible ber-reinforced tissue. Assuming that the

(elastin) matrix behaves isotropically, it is modeled with an isotropic strain-energy function m (subsequently, subscript m refers to matrix). The symmetrically aligned collagen bers stiffen exponentially and are modeled with an anisotropic strain-energy function f (subsequently, subscript f refers to ber). A simple form of the deviatoric part of such a strainenergy function is introduced in [1] as = m + f k1 [exp[k2 (Ii 1)2 ] 1], = (I1 1) + 2 2k2 i=4,6

of the material. Two different approaches originally developed to describe the mechanical behavior of rubber are introduced. A. Continuum damage models The continuum damage model has the form [8] (C, D) = (1 D)0 (C), (2) where 0 is the effective strain-energy function and 0 < D 1 is an internal variable describing the softening of the material. Assuming that softening occurs in the isotropic term (i.e. the elastin matrix) as well as in the anisotropic term (i.e. the collagen ber fabric) of the tissue response we may write the constitutive equation as = (1 Dm )0 + (1 Df )0 m f = (1 Dm ) (I1 1) 2 k1 + (1 Df,i ) [exp[k2 (Ii 1)2 ] 1]. 2k2 i=4,6

(1)

where > 0 and k1 > 0 are stress like parameters and k2 > 0 is a dimensionless parameter. The invariant I1 is the trace of C and the pseudo-invariants I4 = C : M M and I6 = C : M M represent the square of the stretch of the (collagen) bers and account for the anisotropy of the tissue response. The vectors M and M denote the directions of the alignment of the two families of bers. It is assumed that the bers can only bear load under tension, therefore, the anisotropic term f only contributes to when I4 and/or I6 are greater than 1. C. Fiber dispersion In arterial tissue the bers usually are not perfectly aligned along the two directions M and M . It is possible to account for the dispersion of the load bearing bers by replacing the exponential term in equation (1) with exp{k2 [(1 )(I1 3)2 + (Ii 1)2 ]}, where 0 1 is a dimensionless parameters [4]. The greater the parameter , the greater the anisotropic contribution in the exponential response of the bers. A more structurally motivated derivation to introduce ber dispersion inserts the parameter in equation (1) where the pseudo-invariants Ii are replaced by Ii = I1 +(13)Ii , [5]. Again, the value of determines the proportion of the isotropic contribution in the mechanical response of the bers. Both models can be traced back to equation (1) for = 1 and = 0, respectively. D. Fiber crimping The collagen bers show a wavy arrangement in the unloaded conguration and are only load bearing after they are straightened. One approach to account for this is the introduction of the additional parameters I04 > 1 and I06 > 1 that account for the crimping of the bers in the unloaded state by altering the exponential expression in equation (1) to exp[k2 (Ii I0i )2 ] 1] with i = 4, 6, [6]. In this case the anisotropic term only contributes if Ii > I0i , i.e. when the square of the stretch of the bers is greater than I0i . A different approach was used by Li and Robertson [7], who introduced an activation criterion for the recruitment of the collagen bers using a metric for the deformation following a scalar measure of strain. III. DAMAGE MODELS For both the continuum damage model and the pseudoelastic model, a hyperelastic strain-energy function is multiplied by a reduction factor that governs the softening behavior

(3)

Hence, the deviatoric part of the second Piola-Kirchhoff stress tensor S is obtained by the differentiation of the strain-energy function with respect to C, and it has the form S = 2(1 Dm ) 0 0 f,i m + 2(1 Df,i ) . C C i=4,6 (4)

The Cauchy stress tensor can be obtained by the pushforward operation = J 1 FSFT . A possible evolution for the damage variable is given by Miehe [9] as D() = Dmax [1 exp(/)], (5)

where Dmax and are dimensionless model parameters. Dmax constrains the maximal softening and determines how fast this softening occurs during the loading process. The evolution of the damage is governed by the variable which depends on the maximum thermodynamic force that occurred over the history of the loading. Examples of other evolution equations are given in [10]. The continuum damage approach allows the inclusion of continuous softening as shown in [9]. Here damage does not only accumulate during primary loading and, hence, the unloading and reloading path do not coincide any more. B. Pseudo-elastic damage models In a general formulation, the deviatoric part of a pseudoelastic strain-energy function has the form [11] (C, ) = 0 (C) + (), where 0 < strain-energy is referred to strain-energy (6) 1 is a damage variable, 0 (C) is the function of the undamaged material and () as a damage function. A possible pseudo-elastic function for soft tissue is

= m 0 + f 0 + m + f m f = m (I1 1) 2 k1 + f,i [exp[k2 (Ii 1)2 ] 1] + m + f .(7) 2k2 i=4,6

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The corresponding second Piola-Kirchhoff stress tensor S has the form 0 0 f,i m S = 2m + 2f,i . (8) C C i=4,6 A possible evolution equation for the damage variable is proposed in [11] as 1 1 = 1 erf[ (max 0 )], r m (9)

than modeling mechanical damage due to supra-physiological stresses. Pe a et al. [10] considered continuous and discontinuous n damage in their damage model following an approach introduced in [9]. In [19] and [20] the authors considered viscoelasticity in the damage models. To the authors knowledge, the pseudo-elastic approach has not yet been applied to arterial tissue. IV. D ISCUSSION Two approaches for modeling the softening behavior of arterial tissues were briey described, and an overview of damage models for soft biological tissues was presented. The two main approaches for damage modeling include a reduction factor in front of an elastic strain-energy function, that also reduces the contribution to the stresses. Only the continuum mechanics approach allows the inclusion of continuous softening in addition to the discontinuous softening. On the other hand, the calibration of the pseudo-elastic model to experimental data is easier because this approach allows the tting of the material parameters independently of the tting of the damage parameters. Several damage models for soft biological tissues are proposed in the literature either accounting for softening in both matrix and bers or accounting for softening in the bers only. To the authors knowledge there are no experimental data available that support either of these hypotheses, showing the need to study the damage mechanisms more closely with appropriate experiments. Furthermore, the damage models are not calibrated to experimental data from human tissue which is important in order to model surgical procedures. To the authors knowledge there are currently no layer-specic experimental data available that describe the damage behavior of human arterial tissue. The data on the intact wall published in [21] are a rst step towards the modeling of damage in human tissue, however, the authors do not perform an evaluation and comparison of the softening in the different arterial layers. Hence, experimental data are a prerequisite for validation, calibration and further advancement of existing damage models. R EFERENCES
[1] G. A. Holzapfel, T. C. Gasser, and R. W. Ogden, A new constitutive framework for arterial wall mechanics and a comparative study of material models, Journal of Elasticity, vol. 61, pp. 148, 2000. [2] A. J. Schrie, G. Zeindlinger, D. M. Pierce, P. Regitnig, and G. A. Holzapfel, Determination of the layer-specic distributed collagen ber orientations in human thoracic and abdominal aortas and common iliac arteries, submitted. [3] J. D. Humphrey, Cardiovascular Solid Mechanics, Cells, Tissues, and Organs. Springer, 2002. [4] G. A. Holzapfel, G. Sommer, C. T. Gasser, and P. Regitnig, Determination of layer-specic mechanical properties of human coronary arteries with nonatherosclerotic intimal thickening and related constitutive modeling, American Journal of Physiology Heart and Circulatory Physiology, vol. 289, pp. H2048H2058, 2005. [5] T. C. Gasser, R. W. Ogden, and G. A. Holzapfel, Hyperelastic modelling of arterial layers with distributed collagen bre orientations, Journal of the Royal Society Interface, vol. 3, pp. 1535, 2006.

where max is the maximum of the strain energy reached over the history of the deformation. The parameter r > 1 denes the maximum of the damage that can be accumulated as the error function erf(x) for x 0 spans values only between 0 and 1. The parameter m > 0 determines how fast damage is accumulated. The damage variable equals 1 on the primary loading path so that it is possible to t the material parameters independently of the damage parameters. The pseudo-elastic model can be extended to model the residual deformation after unloading which is also observed for arterial tissue [12]. C. Application of damage models to arterial tissue Hokanson and Yazdani [13] proposed a damage model for arteries by using a fourth-order weighting tensor to account for the anisotropy of the damage. The model can represent the Mullins effect, however, the approach is more complicated than utilizing a scalar damage variable as in equations (7) and (3). Balzani et al. [14] introduced a continuum damage model by using the approach from equation (3). They assumed that damage is only accumulated in the anisotropic part of the strain-energy function, i.e. in the collagen bers of the arterial tissue. The model describes the softening behavior qualitatively well, nonetheless, it is not calibrated to experimental data and the assumption of softening occurring just in the bers of the tissue has not yet been proven experimentally. Rodrguez et al. [6] introduced a stochastic model where the bers of different lengths are modeled with a worm-like chain model, and a damage mechanism is naturally introduced as bundles of collagen bers with different lengths fail successively. The nite element implementation and numerical examples are presented in [15]. Again, the calibration of this structurally-motivated model is the biggest challenge due to the lack of experimental data. Calvo et al. [16] presented a continuum damage model for brous biological tissue that describes discontinuous softening in both the matrix and the bers. Compared to the model presented in [6] it does not need to be calibrated at two different length scales. A comparison of the two models shows that the performance is similar with a larger localization of damage in the stochastic model [17]. In [18] Li and Robertson considered two damage mechanisms, mechanical damage and enzymatic damage for the matrix whereas for the collagen bers only a recruitment (but no softening) is considered. The motivation for the enzymatic damage is, however, to model the growth of aneurysms rather

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[6] J. F. Rodrguez, F. Cacho, J. A. Bea, and M. Doblar , A stochastic e structurally based three dimensional nite-strain damage model for brous soft tissue, Journal of the Mechanics and Physics of Solids, vol. 54, pp. 864 886, 2006. [7] D. Li and A. M. Robertson, A structural multi-mechanism constitutive equation for celebral arterial tissue, International Journal of Solids and Structures, vol. 46, pp. 29202928, 2009. [8] J. C. Simo, On a fully three-dimensional nite-strain viscoelastic damage model: formulation and computational aspects, Compututer Methods in Applied Mechanics and Engineering, vol. 60, pp. 153173, 1987. [9] C. Miehe, Discontinuous and continuous damage evolution in ogdentype large-strain elastic materials, European Journal of Mechanics A/Solids, vol. 14, pp. 697720, 1995. [10] E. Pe a, J. A. Pe a, and M. Doblar , On the Mullins effect and hysn n e teresis of bered biological materials: A comparison between continuous and discontinuous damage models, International Journal of Solids and Structures, vol. 46, pp. 17271735, 2009. [11] R. W. Ogden and D. G. Roxburgh, A pseudo-elastic model for the mullins effect in lled rubber, Proceedings of the Royal Society A, vol. 455, pp. 28612877, 1999. [12] A. Dorfmann and R. W. Ogden, A constitutive model for the mullins effect with permanent set in particle-reinforced rubber, International Journal of Solids and Structures, vol. 41, pp. 18551878, 2004. [13] J. Hokanson and S. Yazdani, A constitutive model of the artery with damage, Mechanics Research Communications, vol. 24(2), pp. 151 159, 1997. [14] D. Balzani, Polyconvex anisotropic energies and modeling of damage applied to arterial walls, Ph.D. dissertation, Universit t Duisburg-Essen, a 2006. [15] J. F. Rodrguez, V. Alastru , and M. Doblar , Finite element imple e e mentation of a stochastic three dimensional nite-strain damage model for brous soft tissue, Computer Methods in Applied Mechanics and Engineering, vol. 197, pp. 946 958, 2008. [16] B. Calvo, M. Pe a, M. A. Martinez, and M. Doblar , An uncoupled n e directional damage model for bred biological soft tissues. formulation and computational aspects, International Journal for Numerical Methods in Engineering, vol. 69, pp. 20362057, 2007. [17] V. Alastru , J. F. Rodrguez, B. Calvo, and M. Doblar , Structural e e damage models for brous biological soft tissues, International Journal of Solids and Structures, vol. 44, pp. 58945911, 2007. [18] D. Li and A. M. Robertson, A structural multi-mechanism damage model for celebral arterial tissue, Journal of Biomechanical Engineering, vol. 131, pp. 101 0131, 2009. [19] E. Pe a, B. Calvo, M. A. Martnez, and M. Doblar , On nite-strain n e damage of viscoelastic-bred materials. application to soft biological tissues, International Journal for Numerical Methods in Engineering, vol. 74, pp. 11981218, 2008. [20] E. Pe a, V. Alastru , A. Laborda, M. A. Matrnez, and M. Doblar , n e e A constitutive formulation of vascular tissue mechanics including viscoelasticity and softening behaviour, Journal of Biomechanics, vol. 43, pp. 984989, 2010. [21] L. Horn , H. Gultov , H. Chlup, Sedl cek, J. Kronek, J. Vesel , and y a a y y R. Zitn , Mullins effect in aorta and limiting extensibility evolution, Bulletin of Applied Mechanics, vol. 6, pp. 15, 2010.

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