Detail regarding electrophysiological modeling in the swine hearts can be found in our recent paper29 (link). Detail on all aspects of human ventricular electrophysiological modeling in myocardial infraction is presented in our recent publication11 (link). Briefly, for all heart models, both animal and human, once the 3D finite-element ventricular mesh was generated, regionally-uniform cell and tissue electrophysiological properties were assigned to the three regions outlined in the virtual heart from the LGE-MRI scans: scar, GZ, and non-infarcted tissue. All finite elements that belonged to the scar region were considered electrically non-conductive. In the patient-specific heart models, finite elements that belonged to non-infarcted tissue and GZ were assigned human ventricular cell action potential dynamics31 (link); a different action potential model was used in the animal study29 (link). Modifications to the ionic model based on experimental recordings were implemented to represent electrophysiological remodeling in the GZ11 (link),29 (link). Overall, the GZ action potentials were characterized by a longer duration, decreased upstroke velocity, and decreased peak amplitude compared to those in the non-infarcted myocardium, similar to what has been previously reported32 (link),33 (link). Specifically, as described in the animal model study23 (link), action potential remodeling in the GZ was implemented by decreasing, the original action potential parameters as follows: peak sodium current to 38%, peak L-type calcium current to 31%, and peak potassium currents IKr and IKs to 30 and 20%, respectively. The human action potential model in the patient studies was similarly modified to represent electrophysiological remodeling in the GZ, based on experimental data, as described in our previous patient study11 (link): 62% reduction in peak sodium current, 69% reduction in L-type calcium current and a reduction of 70 and 80% in potassium currents IKr and IKs, respectively.
Tissue properties representing animal or human ventricular cell-to-cell electrical communication were also assigned to the non-infarcted and GZ regions, as described previously11 (link); the GZ region was characterized with a decrease in transverse conductivity to reflect connexin-43 remodeling in the infarct border zone. Similar to the latter study, the values of the non-infarcted tissue conductivities used here were 0.255 and 0.0775 S/m in the longitudinal and transverse directions, respectively.
Tissue properties representing animal or human ventricular cell-to-cell electrical communication were also assigned to the non-infarcted and GZ regions, as described previously11 (link); the GZ region was characterized with a decrease in transverse conductivity to reflect connexin-43 remodeling in the infarct border zone. Similar to the latter study, the values of the non-infarcted tissue conductivities used here were 0.255 and 0.0775 S/m in the longitudinal and transverse directions, respectively.
