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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

Models of human atrial electrophysiology. (A) Schematic of the cell membrane including the different modeled ionic currents and intracellular ion concentrations. (B) Schematic of the calcium handling with different compartments and currents of the models. (C,D) Resulting APs and the corresponding intracellular calcium concentrations after pacing for 50 s with a BCL of 1 s. Curves of N and M model calcium transient overlap. Detailed description of the figures and current abbreviations is given in section 2.1.
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Figure 1: Models of human atrial electrophysiology. (A) Schematic of the cell membrane including the different modeled ionic currents and intracellular ion concentrations. (B) Schematic of the calcium handling with different compartments and currents of the models. (C,D) Resulting APs and the corresponding intracellular calcium concentrations after pacing for 50 s with a BCL of 1 s. Curves of N and M model calcium transient overlap. Detailed description of the figures and current abbreviations is given in section 2.1.

Mentions: In this work, five different models of atrial electrophysiology were benchmarked. We will refer to the human atrial models specified in the following with the initial of the last name of the first author: C (Courtemanche et al., 1998), N (Nygren et al., 1998), M (Maleckar et al., 2008), K (Koivumäki et al., 2011), and G (Grandi et al., 2011). In all figures, the traces of the C model are red, those of the N model are orange, the M model dark blue, the K model light blue, and the G model green. An overview of the structure of the models, the differences in intracellular calcium handling, the resulting APs and the intracellular calcium concentrations are given in Figures 1A–D. Specific detail regarding the origin of experimental data used in model creation and validation and the resulting kinetic parameters of the current formulations is beyond the scope of this article and can be referenced in entirety in the original model publications.


Benchmarking electrophysiological models of human atrial myocytes.

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

Models of human atrial electrophysiology. (A) Schematic of the cell membrane including the different modeled ionic currents and intracellular ion concentrations. (B) Schematic of the calcium handling with different compartments and currents of the models. (C,D) Resulting APs and the corresponding intracellular calcium concentrations after pacing for 50 s with a BCL of 1 s. Curves of N and M model calcium transient overlap. Detailed description of the figures and current abbreviations is given in section 2.1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Models of human atrial electrophysiology. (A) Schematic of the cell membrane including the different modeled ionic currents and intracellular ion concentrations. (B) Schematic of the calcium handling with different compartments and currents of the models. (C,D) Resulting APs and the corresponding intracellular calcium concentrations after pacing for 50 s with a BCL of 1 s. Curves of N and M model calcium transient overlap. Detailed description of the figures and current abbreviations is given in section 2.1.
Mentions: In this work, five different models of atrial electrophysiology were benchmarked. We will refer to the human atrial models specified in the following with the initial of the last name of the first author: C (Courtemanche et al., 1998), N (Nygren et al., 1998), M (Maleckar et al., 2008), K (Koivumäki et al., 2011), and G (Grandi et al., 2011). In all figures, the traces of the C model are red, those of the N model are orange, the M model dark blue, the K model light blue, and the G model green. An overview of the structure of the models, the differences in intracellular calcium handling, the resulting APs and the intracellular calcium concentrations are given in Figures 1A–D. Specific detail regarding the origin of experimental data used in model creation and validation and the resulting kinetic parameters of the current formulations is beyond the scope of this article and can be referenced in entirety in the original model publications.

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