Model Of Ventricular Mechanics Research Articles

Computational Modeling of Ventricular Mechanics and Energetics

The system of equations, material constitutive laws, and boundary conditions required to construct an anatomically and biophysically based model of ventricular mechanics is reviewed. The models use high-order field descriptions to represent the geometry and embedded microstructural information relevant to whole organ function. Constitutive laws are presented which characterize the nonlinear passive elasticity of cardiac tissue and model the active development of tension produced by myocyte contraction. Finally, the integration of metabolic energetics with organ-scale mechanical simulations is discussed and future research directions are proposed.

Ventricular mechanics in diastole: material parameter sensitivity

Models of ventricular mechanics have been developed over the last 20 years to include finite deformation theory, anisotropic and inhomogeneous material properties and an accurate representation of ventricular geometry. As computer performance and the computational efficiency of the models improve, clinical application of these heart mechanics models is becoming feasible. One such application is to estimate myocardial material properties by adjusting the constitutive parameters to match wall deformation from MRI or ultrasound measurements, together with a measurement (or estimate) of ventricular pressure. Pigs are now the principal large animal model for these studies and in this paper we present the development of a new three-dimensional finite element model of the heart based on measurements of the geometry and the fibre and sheet orientations of pig hearts. The end-diastolic deformation of the model is computed using the “pole-zero” constitutive law which we have previously used to model the mechanics of passive myocardial tissue specimens. The sensitivities of end-diastolic fibre-sheet material strains and heart shape to changes in the material parameters are computed for the parameters of the pole-zero law in order to assess the utility of the models for inverse material property determination.

The effects of cross-fiber deformation on axial fiber stress in myocardium.

We incorporated a three-dimensional generalization of the Huxley cross-bridge theory in a finite element model of ventricular mechanics to examine the effect of nonaxial deformations on active stress in myocardium. According to this new theory, which assumes that macroscopic tissue deformations are transmitted to the myofilament lattice, lateral myofilament spacing affects the axial fiber stress. We calculated stresses and deformations at end-systole under the assumption of strictly isometric conditions. Our results suggest that at the end of ejection, nonaxial deformations may significantly reduce active axial fiber stress in the inner half of the wall of the normal left ventricle (18-35 percent at endocardium, depending on location with respect to apex and base). Moreover, this effect is greater in the case of a compliant ischemic region produced by occlusion of the left anterior descending or circumflex coronary artery (26-54 percent at endocardium). On the other hand, stiffening of the remote and ischemic regions (in the case of a two-week-old infarct) lessens the effect of nonaxial deformation on active stress at all locations (9-32 percent endocardial reductions). These calculated effects are sufficiently large to suggest that the influence of nonaxial deformation on active fiber stress may be important, and should be considered in future studies of cardiac mechanics.

On modelling the function of sympathetic ventricular augumentor fibres.

A mathematical model of the function of sympathetic neural terminations in ventricular tissue is developed by analogy with various interneural and neuromuscular juctions. The model characterises the ventricular neuromuscular junction in terms of two subsystems—a neurotransmitter release mechanism and a ventricular contraction mechanism. The output of the transmitter release mechanism is the noradrenaline concentrationNE(t) in a lumped steady-state behaviour that mimics the data of Rosenbleuth (1932) and a realistic dynamic response to multiple stimuli of frequencyfs. The ventricular contraction mechanism in this study is based on an extension of an existing functional model of ventricular mechanics for the denervated heart (Greeneet al., 1973) to a consideration of various states of positive inotropic intervention. Overall, this study results in a model of ventricular mechanics that reflects changes in inotropic state, end-diastolic volume (preload) and time.