Effects of Heart Rate and Ventricular Wall Thickness on Non-invasive Mapping: An in silico Study

Figures

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  Figure 1. Computational models of the human ventricles and torso. (A) An open view of geometries representing (i) normal/control, (ii) thick-walled, and (iii) dilated human ventricles with the epicardial (blue), mid-myocardial (green), and endocardial (red) segmented regions shown. (B) Single cell ventricular action potentials representing (i) transmural (TM) heterogeneity in cells from the endocardium (ENDO), mid-myocardium (MCELL), and epicardium (EPI), (ii) apico-basal (AB) heterogeneity (shown for EPI cells), and (iii) short single cell action potentials used in this study. All models are uncoupled single cells paced at a cycle length of 1,000 ms. (C) (i) Fiber orientation (normalized z component of primary fiber; red and blue indicate parallel to the long axis of the heart from apex to base, green indicates perpendicular to the long axis of the heart); (ii) Heart-torso model used to compute the (iii) body surface potential.

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  Figure 2. Comparison of simulated BSP obtained from the three different geometries during ventricular activation. (A) BSP obtained for control case, the thick-walled and dilated geometry during simulated ectopic activation initiated in the right ventricular lateral wall (RV-LAT) at different instants of time: (i) 25 ms, (ii) 75 ms, (iii) 125 ms, and (iv) 175 ms. (B) (i) RMS for each case and (ii) rRMSe and (iii) PCC calculated vs. the control case.

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  Figure 3. Effects of heart geometry on the reconstructed epicardial potentials. (A) Original simulated ectopic activation initiated in the right ventricular lateral wall (RV-LAT) on all three geometries. (B) Reconstructed activation maps using Zero, First and Second order Tikhonov regularization using different geometries for the forward problem but the control/normal geometry for the inverse problem. Activation patterns were computed as the time of maximum negative first derivative dV/dt at each location. (C) RMS, rRMSe, and PCC calculated to quantify the differences between the reconstructed activation patterns using Zero (black), First (blue) and Second (red) order Tikhonov regularization.

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  Figure 4. Euclidean distance vs. (A) geometry and (B) BCL. Euclidean distances were calculated for each geometry case and BCL for Zero (black), First (Blue), and Second (red) order Tikhonov regularization. For (B), only control geometry was used. Data are the mean for all ectopic sites.

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  Figure 5. Effects of the heart rate on the reconstructed activation maps. (A) 3D activation maps at different basic cycle lengths (BCLs): 150, 300, 500, 750, and 1,000 ms; activation time is given as the maximum negative slope of each local membrane potential. (B) RMS, rMSe and PCC measure calculated using Zero (black), First (blue), and Second (red) order Tikhonov regularization of an ectopic activation starting on the middle of the left ventricle (LV-LAT).

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  Figure 6. RMS, rRMSe, and PCC of the reconstructed activation maps using (A) short and (B) normal AP durations at fast (BCL = 300 ms; upper panel) and slow (BCL = 1,000 ms; lower panel) pacing rates, for the Zero (black), First (blue), and Second (red) order Tikhonov regularization methods. (C) Corresponding snapshots of propagation at time t = 30 ms after stimulus of the LV-LAT ectopic site. The control geometry was used in all cases.