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

Figures

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  FIGURE 1. The figure compares the membrane potential, APD restitution curves, and CV restitution curves for the TT2 and Tomek models (ENDO tissue) across time steps (5–30 μs). (a) The membrane potential with different timesteps; (b) APD restitution curves in the S1‐S2 protocol with different timesteps; (c) APD restitution curves in the dynamic protocol with different timesteps; (d) CV restitution curves with different timesteps. (e) The membrane potential with different timesteps; (f) APD restitution curves in the S1‐S2 protocol with different timesteps; (g) APD restitution curves with the dynamic protocol with different timesteps; (h) CV restitution curves with different timesteps; APD represents APD90; CI, coupling interval; CV, conduction velocity; DI, diastolic interval.

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  FIGURE 2. The morphologies of the action potential and major ion currents in the Tomek and the TT2 models (ENDO) with 10 μs timestep. (a) The membrane potentials, (b–j) major ion currents, including INa, Ito, IKr, IKs, IK1, INaK, ICaL, INaCa,i, and [Ca2+]i. ENDO, endocardial.

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  FIGURE 3. The APD restitution curves of S1‐S2 and dynamic protocol in the Tomek and the TT2 models (ENDO) with 10 μs timestep. (a) APD restitution curves with S1‐S2 protocol in the TT2 and the Tomek models, (b) APD restitution curves with dynamic protocol in the TT2 and the Tomek models, (c) the slope of APD restitution curves with S1‐S2 protocol in the TT2 and the Tomek models, (d) the slope of APD restitution curves with dynamic protocol in the TT2 and the Tomek models. APD represents APD90; DI, diastolic interval; dyn, dynamic protocol; ENDO, endocardial; S1S2, S1‐S2 protocol.

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  FIGURE 4. Properties of gray zone in the Tomek and the TT2 models (ENDO) with 10 μs timestep. (a) membrane potentials, (b‐f) major ion currents modified in the model of gray zone, including INa, IKr, IKs, IK1, ICaL, and [Ca2+]i, (G) APD restitution curves in S1‐S2 protocol, (H) the slope of APD restitution curves in S1‐S2 protocol, (i) APD restitution curves in dynamic protocol, (j) the slope of APD restitution curves in dynamic protocol. APD represents APD90; DI, diastolic interval; dyn, dynamic protocol; ENDO, endocardial; S1S2, S1‐S2 protocol.

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  FIGURE 5. CV restitution curves and its slope of normal and infarct tissue in the Tomek and the TT2 models (ENDO) measured in a 1D cable model with 10 μs timestep. (a) CV restitution curve of normal tissue; (b) the slope of CV restitution curve in normal tissue; (c) CV restitution curve of infarct tissue; (d) the slope of CV restitution curves in infarct tissue. CI, coupling interval; CV, conduction velocity; ENDO, endocardial.

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  FIGURE 6. The electrical propagation at simulation time of 250, 2000, 5300, 8200, 8700, and 9990 ms with 5, 10, 15, 20, 25, and 30 μs timesteps, respectively, with the Tomek model (endocardium).

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  FIGURE 7. The electrical propagation at simulation times of 300, 2000, 3000, 5000, and 9990 ms with 5, 10, 15, 20, 25, and 30 μs timesteps respectively with the TT2 model (endocardium).

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  FIGURE 8. Reentry simulation in 2D tissue with the TT2 and the Tomek model with 10 μs timestep. The first row showed the reentry induced with the TT2 model at different simulation times. The second row was the reentry induced with the Tomek model at different simulation times.

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  FIGURE 9. [Ca2+]i in 2D tissue with the TT2 and the Tomek model with a 10 μs timestep. The first row shows [Ca2+]i with the TT2 model at different simulation times. The second row was [Ca2+]i with the Tomek model at different simulation times.

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  FIGURE 10. Reentry simulation in 2D tissue using the TT2 and Tomek gray zone models with a 10 μs time step. The first row shows reentry patterns induced by the TT2 gray zone model at various simulation times. The second row displays reentry patterns induced by the Tomek gray zone model at corresponding simulation times.

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  FIGURE 11. The three types of reentries induced in patient‐specific simulation with the TT2 and the Tomek models. (a–c) showed the activation maps of the TT2 model, and (d) and (e) showed the activation maps of the Tomek model. (f) showed an image of the membrane potential change of the Tomek model, whose reentry pattern began in a chaotic state but finally stabilized. (a) The reentry induced at the posterior wall with the TT2 model; (b) the reentry induced at the anterior lateral wall with the TT2 model; (c) the reentry only induced in the TT2 model, which was not found in the Tomek, was in the upper front wall; (d) the reentry induced at the posterior wall with the Tomek model; (e) the reentry induced at the anterior lateral wall with the Tomek model; (f) the unique reentry only induced in the Tomek model, which was not found in TT2, was in the lower part of the anterior wall.

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  FIGURE 12. The reentries' location induced in patient‐specific simulation with the TT2 and the Tomek models. (a) The reentry induced at the posterior wall with the TT2 model; (b) the reentry induced at the anterior lateral wall with the TT2 model; (c) the reentry only induced in the TT2 model, which was not found in the Tomek, was in the upper front wall; (d) the reentry induced at the posterior wall with the Tomek model; (e) the reentry induced at the anterior lateral wall with the Tomek model; (f) the unique reentry only induced in the Tomek model, which was not found in TT2, was in the lower part of the anterior wall.