Comparative analysis of the ten Tusscher and Tomek human ventricular cell models at cellular, tissue, and organ levels: Implications for post‐infarct ventricular tachycardia simulation
Abstract Computational modeling is a tool for exploring both normal electrical propagation in healthy hearts and cardiac arrhythmias in patients. While numerous human ventricular cell models exist, the ten Tusscher (TT2) model is one of the most used for simulating ventricular arrhythmia. Recently,...
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| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2025-07-01
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| Series: | Physiological Reports |
| Subjects: | |
| Online Access: | https://doi.org/10.14814/phy2.70435 |
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| Summary: | Abstract Computational modeling is a tool for exploring both normal electrical propagation in healthy hearts and cardiac arrhythmias in patients. While numerous human ventricular cell models exist, the ten Tusscher (TT2) model is one of the most used for simulating ventricular arrhythmia. Recently, the Tomek model has been proposed, offering improved accuracy by better reproducing key depolarization, repolarization, and calcium dynamics in healthy ventricular cardiomyocytes. However, a quantitatively comprehensive comparison of these models at the single‐cell, tissue, and organ levels has not been conducted. This study systematically compared the TT2 and Tomek models by evaluating electrophysiological parameters and reentrant properties in 0‐dimensional(0D), 1‐dimensional(1D), 2‐dimensional (2D), and 3‐dimensional (3D) simulations. Additionally, the effects of ion currents modifications to simulate ischemic scar‐related tissue were analyzed. These results reveal that although the TT2 and Tomek models demonstrate distinct 0D, 1D, and 2D characteristics, their 3D reentrant properties—specifically in terms of reentry locations and critical conduction channels—are highly comparable. Therefore, both models are suitable for simulating post‐infarct ventricular tachycardia (VT), as their shared 3D features effectively capture the essential mechanisms underlying this arrhythmia. |
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| ISSN: | 2051-817X |