Strain-controlled electrophysiological wave propagation alters in silico scar-based substrate for ventricular tachycardia

Introduction: Assessing a patient’s risk of scar-based ventricular tachycardia (VT) after myocardial infarction is a challenging task. It can take months to years after infarction for VT to occur. Also, if selected for ablation therapy, success rates are low. Methods: Computational ventricular models have been presented previously to support VT risk assessment and to provide ablation guidance. In this study, an extension to such virtual-heart models is proposed to phenomenologically incorporate tissue remodeling driven by mechanical load. Strain amplitudes in the heart muscle are obtained from simulations of mechanics and are used to adjust the electrical conductivity. Results: The mechanics-driven adaptation of electrophysiology resulted in a more heterogeneous distribution of propagation velocities than that of standard models, which adapt electrophysiology in the structural substrate from medical images only. Moreover, conduction slowing was not only present in such a structural substrate, but extended in the adjacent functional border zone with impaired mechanics. This enlarged the volumes with high repolarization time gradients (≥ 10 ms/mm). However, maximum gradient values were not significantly affected. The enlarged volumes were localized along the structural substrate border, which lengthened the line of conduction block. The prolonged reentry pathways together with conduction slowing in functional regions increased VT cycle time, such that VT was easier to induce, and the number of recommended ablation sites increased from 3 to 5 locations. Discussion: Sensitivity testing showed an accurate model of strain-dependency to be critical for low ranges of conductivity. The model extension with mechanics-driven tissue remodeling is a potential approach to capture the evolution of the functional substrate and may offer insight into the progression of VT risk over time.<br/

Post-infarct evolution of ventricular and myocardial function

Adverse ventricular remodeling following acute myocardial infarction (MI) may induce ventricular dilation, fibrosis, and loss of global contractile function, possibly resulting in heart failure (HF). Understanding the relation between the time-dependent changes in material properties of the myocardium and the contractile function of the heart may further our understanding of the development of HF post-MI and guide the development of novel therapies. A finite element model of cardiac mechanics was used to model MI in a thick-walled truncated ellipsoidal geometry. Infarct core and border zone comprised 9.6 and 8.1% of the LV wall volume, respectively. Acute MI was modeled by inhibiting active stress generation. Chronic MI was modeled by the additional effect of infarct material stiffening, wall thinning and fiber reorientation. In acute MI, stroke work decreased by 25%. In the infarct core, fiber stress was reduced but fiber strain was increased, depending on the degree of infarct stiffening. Fiber work density was equal to zero. Healthy tissue adjacent to the infarct showed decreased work density depending on the degree of infarct stiffness and the orientation of the myofibers with respect to the infarct region. Thinning of the wall partially restored this loss in work density while the effects of fiber reorientation were minimal. We found that the relative loss in pump function in the infarcted heart exceeds the relative loss in healthy myocardial tissue due to impaired mechanical function in healthy tissue adjacent to the infarct. Infarct stiffening, wall thinning and fiber reorientation did not affect pump function but did affect the distribution of work density in tissue adjacent to the infarct

Isogeometric-mechanics-driven electrophysiology simulations of ventricular tachycardia

Computational cardiac models are progressively being used to understand, predict, and improve the treatment of cardiac diseases. These models commonly rely on the traditional finite element analysis (FEA), where the geometry description and consequent mesh generation are separate preprocessing steps that are required before conducting numerical analyses. The recent isogeometric analysis (IGA) paradigm eliminates the separate meshing step and integrates geometry construction and solution approximation using higher-order splines. In this study, we first investigate whether IGA can be efficiently used to model post-infarction left ventricular mechanics. Mechanics results from an established FEA model with a fine homogeneous mesh are used to investigate to what extent similar results could be obtained using hierarchical mesh refinement in IGA. The IGA-mechanics results show a good agreement while providing a mesh-independent geometry, but deviations are noticed close to the base, apex, and partially the endocardium. Second, both the FEA- and IGA-model results are used as input for an FEA-mechanics-driven electrophysiology model which is used for a ventricular tachycardia (VT)-inducibility study, as abnormal mechanics is believed to be a potential driving factor for the development of VT. The resulting VT propagation patterns agree visually for both mechanical inputs and differences in VT-exit points are within 1–7 mm for simulations where VT occurred. Furthermore, an agreement of 85% in the binary VT results is observed, where the 15% difference displays the electrophysiology-model sensitivity to deviations in mechanical input