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Aleksandar JeremiC and Arye Nehorai

EECS Department (M/C 154) The University of Illinois at Chicago 851 S.Morgan Street Chicago, Illinois 60607-7053
We-pFesent an algorithm for estimating active and passive mechanical properties of the heart using magnetic resonance imaging (MRI) tissue-tagging and blood pressure measurements. We combine physical modeling with a finite-element formulation and dynamic analysis, and apply non-linear optimization to estimate the unknown parameters. We assume that the myocardium's stiffness tensor is anisotropic and non-homogeneous. In this paper (see also [2]) we present a method for determining both active and passive regional mechanical properties (stiffness parameters) of the myocardium using 2D tagged MR images and pressure measurements. Tissue-tagging MR imaging technique permits characterization of the deformative behavior of intra-myocardial tissue using radio-frequency (RF) pulses to set up grid of t,ag lines whose motion (systolic contraction and diastolic expansion) is tracked throughout the cardiac cycle. We model the heart's motion using small strain dynamic analysis based on the the theory of continuum mechanics assuming that the myocardium is heterogeneous, anisotropic and nonlinear hyper-elastic material. To account for regional variations (heterogeneity) we model the mechanical parameters of the heart using a set of a priori known basis functions and a set of unknown coefficients. By applying time-dependent FE analysis to the resulting equation, we develop a 2D model to relate displacements of the tag points at various locations in the cross-sectional plane, during the heart cycle, t o the mechanical parameters and ventricular pressure. To compute the displacement field we develop an automated algorithm for detecting the tag points i.e. intersection of individual pairs of tag lines. We then estimate the mechanical parameters by minimizing a distance measure between the predicted pressure and pressure measurements using the displacements measured from the tagged MRI.

The development of i n vivo techniques for quantifying regional myocardial mechanical properties is important from both basic and clinical research standpoints. For basic research, such techniques enable testing of constitutive models for the intact, in vivo heart. Clinically, they may be useful for developing ventricular function measures with sufficient sensitivity to pre-date the onset of cardiac dysfunctions. Historically, mechanical properties of the heart i n vivo have been determined by pressure-volume studies employing simple mathematical models. This approach is useful for estimating global characteristics of the ventricles but is unsuitable for understanding the regional variations in the material properties or the anisotropy of the cardiac muscle. To fully characterize the complexities of the myocardial mechanical properties, an approach based on the theory of continuum mechanics is required. Recent advances in magnetic resonance imaging (MRI) and finite-element (FE) methods have enabled estimation of passive mechanical properties i n vivo [l].
This work was supported by the the Air Force Office of Scientific Research under Grants F49620-97-1-0481 and F4962099-1-0067, the National Science Foundation under Grant MIP9615590 and the Office of Naval Research under Grant N0001498-1-0542.


The heart is a complex mechanical system with respect to its geometry, structure, mechanical properties and processes that govern its motion. We model the myocardium as an anisotropic, nonlinear, non-homogeneous, hyper-elastic solid, [3]. A large number of existing ventricular models also assume incompressibility of the cardiac tissue, i.e., the volume does not change with stress. However, it has been

0-7803-6293-4/00/$10.00 02000 IEEE.


shown that the intra-coronary blood volume varies in time [4], which makes the incompressibility assumption questionable in most models. Furthermore, in the case of 2D cross-sectional models, the 2D incompressibility condition, i.e., constant cross-sectional area, is unrealistic since the cardiac through-plane motion is substantial, and hence incompressibility does not imply that the cross-sectional area remains constant. Therefore, we assume that cardiac tissue in the cross-sectional plane is compressible. We use two coordinate systems in the governing equations. As a reference system we use a Cartesian coordinate system whose z,y plane lies in the crosssectional plane of the ventricle. The deformation of the left ventricle is described by a motion in which a point (2, y) in the urideformed cross-sectional plane S (at time 0) moves t o (z(t),y(t))in the deformed plane S ( t ) (at time t). Following [5] we select the end of the diastole as reference time t = 0 a t which the ventricle is undeformed. The second coordinate system is defined with respect to the muscle fibers. These fibers are arranged in the continuum of helixal layers and run parallel in each of them [6]. Thus, the material coordinate system is chosen as follows: the fiber axis 2 lies in the layer and points in the fiber direction, the cross-fiber axis y is the in-plane axis perpendicular to xi,and the transmural axis z forms the right coordinate system i.e. z = 2 x 9. We split the ventricular stress vector r ( x , y, t ) into two parts: passive stress r p ( z , y , t ) ,resulting from the area change of the myocardial tissue, and active (contractile) stress r,(x, y, t ) resulting from the isometric contraction of the muscle fiber . The passive stress vector is related to the potential function zu(2,y) (strain energy per unit volume) through

where { 4fj (2, y)} is the set of basis functions, 12b is the number of functions, and ctj the coefficients. Note that in our model the non-homogeneity corresponds t o the myocardium stiffness whereas the myocardium density p is assumed to be uniform. However, non-homogeneous density can be modeled similarly t o the myocardium stiffness, with an appropriate set of basis functions. We adopt the active stress model is adopted from [7].Accordingly
Tf ( t ) = Tmax [ 1 - cosw ( t ) ] .


where q ( t ) is the magnitude of the active stress in the fiber coordinate system, rmax the maximum isometric tension value, and w ( t ) is given in [7]. The active stress 7, in the cross-sectional plane consists of two longitudinal components, T ~and , T~,,, ~ as well as shear stress Ta,xy. The cross-sectional active stress is computed from q ( t ) by applying a transformation [8] from the fiber coordinate system to the reference coordinate system. This transformation is a function of the fiber elevation and azimuth angles. Because both angles change smoothly from epicardium t o endocardium, the cross-sectional active stress is nonhomogeneous and can be approximated, similarly t o the myocardium stiffness, using a different set of basis functions.


We continue t o consider the heart as an elastic body with varying surface S ( t ) . The cross-sectional plane is loaded by a boundary traction (pressure) per unit length of the boundary S ( t ) that is in equilibrium with the internal traction vector or equivalently with stress. To formulate the governing equations of the motion we use the principle of virtual work At any time t the equilibrium equations of the crosssectional plane are given by [8]

rp =

dw(x, Y)


4 5 , Y ) = eo (exp { ETD(z,! / ) E } - 1) ,

where eo is the initial normal stiffness, E is a vector of strains, and D(z,y) is the non-homogeneous myocardium stiffness matrix. For our 2D non-homogeneous, anisotropic heart model D(z,y) is a 3 x 3 symmetric matrix. To model the non-homogeneity we propose to use a linear combination of an a priori known set of basis functions with unknown coefficients. Then, the (i,j ) t h entry of D(s,y) is given by

Dij(GY) = cc:j4:j(2,Y),


where p is the density of myocardium. We will use the following notation for the boundaries of the crosssectional plane: lepi denotes the epicardium boundary, lien denotes endocardium boundary in the left ventricle, and similarly I,, denotes endocardium boundary in the right ventricle. The positive normal direction is the outward normal t o S ( t ) and the positive tangential direction is counterclockwise. The endocardium boundary conditions are given in terms of normal components of the traction vector.


Solution of this continuum mechanics problem requires the enforcement of const,raints on rigid body translation and rotation. Following the approach of [9] we use the spring constraints to model this effect. We assume that epicardial edges are constrained by tractions proportional t o the normal displacement

for all b, where


r, = Icu,




where 7 , is the normal traction, U , is the normal component of displacement and Ic is a linear spring constant. Assume that at time t the displacement of material points in the cross-sectional plane of the heart is given by U ( % ,y, t ) and let w(z,y) be the virtual displacement applied to the cross-sectional plane. The principle of virtual work requires that the work of internal stresses B(u,v,t) is equal to the work of the external forces

The matrix K is called the global stiffness matrix or assembled stiffnes matrix, and the vector r is called the global load vector or assembled load vector. With this notation the condition (9) is satisfied only when

K a = r.


F ( vI t).
Then we can express the principle of virtual work in the following form


The detailed expressions and procedures for computing the elements of the global stiffness matrix and load vector are given in [la].

(Dv)TE(u)Dudzdy =

We wish to estimate the unknown active and passive mechanical properties of the heart. The active mechanical properties (parameters), denoted by e,, are the coefficients of the basis functions used for modeling the active stress. The passive mechanical properties 8, are the coefficients of the basis functions from equation (2) used for modeling the myocardial stiffness. To obtain an adequate statistical model we make the following assumptions: the MR images are taken at time points { t , = mAt, 1 5 m 5 n } where At is the time interval between two consecutive images, the nodal displacement vectors d, = d(t,) are measured exactly from each image, and the ventricular pressures are measured during each image acquisition. Similarly, Km(8) = K ( 8 , t m ) and M , = M ( O , t , ) where 8 = [e,, @,IT. Before applying estimation techniques we need to discretize the model (9). Our goal is to minimize the distance measure between predicted and measured displacements. To obtain an objective function we need t o solve equation (9). Due t o the timedependence of matrices K and M the analytical solution cannot be obtained but we can obtain an approximate solution using finite-difference approach based on a discrete second derivative. We first lump the nodal displacement vectors into one vector d = [ d l T , . . ,d,IT T and similarly r = [rT, . . .,r n3 . Then our model becomes

where V is the differential operator matrix given by

Because we cannot work with infinitely many linearly independent functions we cannot in general find a displacement field U that satisfies the governing equations. Therefore we find approximation to U via a finite-element formulation for (6) following [lo]. We construct the FE mesh using the tag points as nodes. We approximate the epicardium and LV using a Fourier series representation of tag points located on these boundaries. As a result, the curved boundary segments and element shape functions can be represented by the linear blending method presented in [lo, pp. 107-1121. Our goal is to determine the function uo(z,y,t) such that q u o , v ,t ) = F(v1t ) (8) for all admissible v. By definition [lo] any displacement function can be written as uo = @a where a is the vector of the corresponding (unknown) amplitudes. Similarly v = a b , where b is a vector of arbitrary amplitudes. Thus, the FE model becomes bT(Ka-r) = O (9)


where the subscripts s and d refer to the corresponding variables in systole and diastole, respectively, and T is a Toeplitz matrix with ( i , j ) t h entry -2/(At)2 for = j, l/(At)2 for li - j l = 1, and 0 elsewhere. We seek a vector of material parameters 6 that minimizes the objective function


- 2

= Ild



where d are the measured displacements and d are the model displacements corresponding to the material parameters 8. Because the material parameters are nonlinear variables contained implicitly in the FE stiffness matrix, the minimization of (14) requires a nonlinear optimization algorithm. We approximate the objective function c(8) in the neighborhood of any particular estimate of the parameter solution 80, by a second order Taylor series expansion:
c ( e ) = C(e,,)

than the others. In addition, the matrix H ( 8 ) may not be positive definite for non-optimal 8;even if H ( 6 ) is, : may be a poor search direction. A subin which case 8 stantial variation of this idea, which avoids inversion, is to replace H-' (Oi)by another positive-definite matrix the structure of which evolves during the course of iteration. There are different methods which are used for implementation of this idea such as Davidon-FletcherPowell approach or Broyden-Fletcher-Goldfarb-Shanno. To simplify the computational complexity we simply substitute eigenvalues Xf with llXf11 and obtain

+ XqT8: - + X 2 q T H q ,


where H is the Hessian matrix of second partial derivatives and q = &/de of c both evaluated a t 80. The iterative Newton-Raphson procedure is given by

where q: is the eigenvector associated with the eigenvalue Xf. We compute the best step length using the well-known step-doubling method, i.e., if an initial value of X leads to an actual increase in c we double the step and try again. When we finally get a decrease in c from its previous value, we perform an interpolation for the value of X which will yield the maximum c based on a parabolic fit to the computed values.
[l] Moulton M. J. et. al., Znt. J . Cardiac Imaging, vol. 12,

where X i is a scalar chosen by the line search to maximize c(8i - Xi8;) for fixed 8 i and 8;. The necessary condition for a maximum along the direction 8 : is obtained by differentiating with respect to X resulting in

pp. 153-167, 1996.

[2] Nehorai A. et. al., Proc. IEEE Conference on Computers in Cardiology, pp.257-260, 1998.
[3] Fung Y . C., Biomechanics, Springer-Verlag, New York,

The change in c ( 8 ) is given by

Following the approach of [13] we choose the search direction to maximize the first order part of c(O), keeping the length of 8; fixed. This length is defined in terms of a positive definite metric matrix G , i.e. we require t?fTGi3; = h2. The solution of this problem is

8; = hG-'q/(qTG-' 9)'.
Without loss of generality we may take h2 = qTG-'q which gives 8: = G-'q and consequently
X = qTG-'q/(qTG-lHG-'q),


It can be easily shown that the choice G = H will give the maximum gain Ac. This algorithm tends t o converge slowly if some eigenvalues of H are much smaller

1987. [4] Spaan J. A. E., Circ. Res., vol. 56, pp. 293-309, 1985. [5] Redaelli A. et. al., Meccanica, vol. 32, pp. 53-70, 1997. [6] Streeter Jr. D. D. et al, in J. Baan, A. Noordergraaf, and J. Raines (eds), Cardiovascular System Dynamics, pp. 73-84, 1978. [7] Guiccione J. M. et al, ASME J. Biomech. Engng., vol. 115, pp. 82-90, 1993. [8] Biot M. A., Mechanics of Incremental Deformations, John Wiley & Sons, New York, 1948. [9] Moulton M. J. et al, Am. J. Physiol., vol. 270, pp. H:281-297, 1996. [lo] Szabo B., and Babuska I., Finite Element Analysis, John Wiley & Sons New York, 1991. [ll] Gordon W. J. , SIAM J . Numer. Anal., vol. 8, pp. 158177, 1971. [12] Nehorai A. et al, full version of this paper in preparation. [13] Crocket J. B. et al, Pacific Journal of Mathematics, vol. 5, pp. 33-50, 1993.