an artificial “capacitor” affecting the dynamics of the re-entry, and significantly prolongated life time of the re-entry initiated at particular locations/orientation respective to the “capacitor”.

Finally, the 3D anatomically realistic simulations of the foetal heart show that the realistic anisotropy of the heart causes the fast transient distortion of the vortex filament, and the typical fast drift towards the apex area of the inexcitable boundary of the heart, which ultimately results in the fast self-termination of the excitation vortex, see Figs. \[3D\_iso\]-\[3D\_X\_shaven\_aniso\] and the corresponding movies in the Supplementary Material section \[Suppl\].

\[Discussion\] DISCUSSION AND FUTURE DIRECTIONS
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![image](Table1.pdf)

![image](quant.pdf)

Although the role of heart anatomy and anisotropy in the origin and sustainability of cardiac arrhythmias has been appreciated for a long time, the experimental evidence capable to clarify the detail of the effects of the heart anatomy on the persistent cardiac arrhythmias and fibrillation are limited. [[ In particular, the theoretically plausible hypothesis that the anisotropic discontinuities in the heart might be a source of rise for cardiac re-entry due to the abrupt change in conduction velocity and wavefront curvature was in controversy with the observation that the transmural fiber arrangement, including the range of transmural change in fiber 