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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

Long term stability of the models. (A–C) APD50, APD90, and AP amplitude over 20 min pacing with a BCL of 1 s. (D) RMP over 20 min without pacing followed by 10 min pacing with a BCL of 1 s. The resulting curves of the different models are compared in detail in the section 3.1.
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Figure 2: Long term stability of the models. (A–C) APD50, APD90, and AP amplitude over 20 min pacing with a BCL of 1 s. (D) RMP over 20 min without pacing followed by 10 min pacing with a BCL of 1 s. The resulting curves of the different models are compared in detail in the section 3.1.

Mentions: Further simulations examined models' long term stability (Figure 2). The M, K, and G models show slight adaptation of APD50 during the first minutes of simulation at a BCL of 1 s, until a steady state close to the initial value is reached. In contrast, the C and N models reach steady state after a much longer simulation time. The APD50 in C has decreased by 42% over this period, whereas that of the N model by roughly 2.7%.


Benchmarking electrophysiological models of human atrial myocytes.

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

Long term stability of the models. (A–C) APD50, APD90, and AP amplitude over 20 min pacing with a BCL of 1 s. (D) RMP over 20 min without pacing followed by 10 min pacing with a BCL of 1 s. The resulting curves of the different models are compared in detail in the section 3.1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Long term stability of the models. (A–C) APD50, APD90, and AP amplitude over 20 min pacing with a BCL of 1 s. (D) RMP over 20 min without pacing followed by 10 min pacing with a BCL of 1 s. The resulting curves of the different models are compared in detail in the section 3.1.
Mentions: Further simulations examined models' long term stability (Figure 2). The M, K, and G models show slight adaptation of APD50 during the first minutes of simulation at a BCL of 1 s, until a steady state close to the initial value is reached. In contrast, the C and N models reach steady state after a much longer simulation time. The APD50 in C has decreased by 42% over this period, whereas that of the N model by roughly 2.7%.

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