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Benchmarking electrophysiological models of human atrial myocytes.

Wilhelms M, Hettmann H, Maleckar MM, Koivumäki JT, Dössel O, Seemann G - Front Physiol (2013)

Bottom Line: The aim of this work is to give an overview of strengths and weaknesses of these models depending on the purpose and the general requirements of simulations.Therefore, these models were systematically benchmarked with respect to general mathematical properties and their ability to reproduce certain electrophysiological phenomena, such as action potential (AP) alternans.The healthy and remodeled model variants were compared with experimental results in single-cell, 1D and 2D tissue simulations to investigate AP and restitution properties, as well as the initiation of reentrant circuits.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Engineering, Karlsruhe Institute of Technology Karlsruhe, Germany.

ABSTRACT
Mathematical modeling of cardiac electrophysiology is an insightful method to investigate the underlying mechanisms responsible for arrhythmias such as atrial fibrillation (AF). In past years, five models of human atrial electrophysiology with different formulations of ionic currents, and consequently diverging properties, have been published. The aim of this work is to give an overview of strengths and weaknesses of these models depending on the purpose and the general requirements of simulations. Therefore, these models were systematically benchmarked with respect to general mathematical properties and their ability to reproduce certain electrophysiological phenomena, such as action potential (AP) alternans. To assess the models' ability to replicate modified properties of human myocytes and tissue in cardiac disease, electrical remodeling in chronic atrial fibrillation (cAF) was chosen as test case. The healthy and remodeled model variants were compared with experimental results in single-cell, 1D and 2D tissue simulations to investigate AP and restitution properties, as well as the initiation of reentrant circuits.

No MeSH data available.


Related in: MedlinePlus

Initiation of rotors in 2D tissue patch. (A) Overview of rotor initiation success and corresponding dominant frequency. Control C and G model failed to initiate a rotor in the 2D patch (100 × 100 × 0.1 mm). Higher dominant frequencies could be observed in case of cAF. (B) Screen shots of failed rotor initiation in the control C model, where the WL was too long related to the patch size. (C) Successful rotor initiation in the cAF C model. Dashed lines indicate stimulus sites and area, respectively.
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Figure 6: Initiation of rotors in 2D tissue patch. (A) Overview of rotor initiation success and corresponding dominant frequency. Control C and G model failed to initiate a rotor in the 2D patch (100 × 100 × 0.1 mm). Higher dominant frequencies could be observed in case of cAF. (B) Screen shots of failed rotor initiation in the control C model, where the WL was too long related to the patch size. (C) Successful rotor initiation in the cAF C model. Dashed lines indicate stimulus sites and area, respectively.

Mentions: As for 1D simulations, for 2D simulations 50 beats were first calculated in a single-cell environment in order to adapt all models to a BCL of 0.4 s. Four beats were then computed in an isotropic 2D tissue patch (100 × 100 × 0.1 mm) stimulated at the left side of the patch (see Figure 6). Following the fourth paced beat, a premature stimulus was simulated via stimulation applied to excited tissue at the patch's lower half. This cross-field (S1–S2) protocol with model-specific stimulation time S2 was used to initiate a rotor in the center of the patch. In case of rotor initiation success, the trajectories of the spiral cores were tracked using an algorithm based on that of Bray et al. (2001) which identifies phase singularities. The dominant frequency was also calculated via fast Fourier transform. For this purpose, a pseudo-ECG signal as described in Seemann et al. (2010a), was computed based on the intercellular current density distribution using two electrodes at 5 mm distance from the patch and 10 mm distance between each other in the center of the patch.


Benchmarking electrophysiological models of human atrial myocytes.

Wilhelms M, Hettmann H, Maleckar MM, Koivumäki JT, Dössel O, Seemann G - Front Physiol (2013)

Initiation of rotors in 2D tissue patch. (A) Overview of rotor initiation success and corresponding dominant frequency. Control C and G model failed to initiate a rotor in the 2D patch (100 × 100 × 0.1 mm). Higher dominant frequencies could be observed in case of cAF. (B) Screen shots of failed rotor initiation in the control C model, where the WL was too long related to the patch size. (C) Successful rotor initiation in the cAF C model. Dashed lines indicate stimulus sites and area, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3539682&req=5

Figure 6: Initiation of rotors in 2D tissue patch. (A) Overview of rotor initiation success and corresponding dominant frequency. Control C and G model failed to initiate a rotor in the 2D patch (100 × 100 × 0.1 mm). Higher dominant frequencies could be observed in case of cAF. (B) Screen shots of failed rotor initiation in the control C model, where the WL was too long related to the patch size. (C) Successful rotor initiation in the cAF C model. Dashed lines indicate stimulus sites and area, respectively.
Mentions: As for 1D simulations, for 2D simulations 50 beats were first calculated in a single-cell environment in order to adapt all models to a BCL of 0.4 s. Four beats were then computed in an isotropic 2D tissue patch (100 × 100 × 0.1 mm) stimulated at the left side of the patch (see Figure 6). Following the fourth paced beat, a premature stimulus was simulated via stimulation applied to excited tissue at the patch's lower half. This cross-field (S1–S2) protocol with model-specific stimulation time S2 was used to initiate a rotor in the center of the patch. In case of rotor initiation success, the trajectories of the spiral cores were tracked using an algorithm based on that of Bray et al. (2001) which identifies phase singularities. The dominant frequency was also calculated via fast Fourier transform. For this purpose, a pseudo-ECG signal as described in Seemann et al. (2010a), was computed based on the intercellular current density distribution using two electrodes at 5 mm distance from the patch and 10 mm distance between each other in the center of the patch.

Bottom Line: The aim of this work is to give an overview of strengths and weaknesses of these models depending on the purpose and the general requirements of simulations.Therefore, these models were systematically benchmarked with respect to general mathematical properties and their ability to reproduce certain electrophysiological phenomena, such as action potential (AP) alternans.The healthy and remodeled model variants were compared with experimental results in single-cell, 1D and 2D tissue simulations to investigate AP and restitution properties, as well as the initiation of reentrant circuits.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Engineering, Karlsruhe Institute of Technology Karlsruhe, Germany.

ABSTRACT
Mathematical modeling of cardiac electrophysiology is an insightful method to investigate the underlying mechanisms responsible for arrhythmias such as atrial fibrillation (AF). In past years, five models of human atrial electrophysiology with different formulations of ionic currents, and consequently diverging properties, have been published. The aim of this work is to give an overview of strengths and weaknesses of these models depending on the purpose and the general requirements of simulations. Therefore, these models were systematically benchmarked with respect to general mathematical properties and their ability to reproduce certain electrophysiological phenomena, such as action potential (AP) alternans. To assess the models' ability to replicate modified properties of human myocytes and tissue in cardiac disease, electrical remodeling in chronic atrial fibrillation (cAF) was chosen as test case. The healthy and remodeled model variants were compared with experimental results in single-cell, 1D and 2D tissue simulations to investigate AP and restitution properties, as well as the initiation of reentrant circuits.

No MeSH data available.


Related in: MedlinePlus