\[3D\_aniso\]. ]{}

Fig. \[3D\_X\_iso\] shows the *isotropic dynamics* of the excitation vortex, that is with the fiber orientation data “turned OFF”, so that only the geometry of the otherwise isotropic homogeneous foetal heart affects the dynamics of the vortex. Here, contrary to the expectation for the positive filament tension vortex to always contract, the organising filament first transiently extends intramurally along the tissue walls, before finally breaking up to the two ring-like pieces, each of which quickly contracts and terminates at the opposite base and apex regions of the heart.

Fig. \[3D\_X\_aniso\] shows the *anisotropic dynamics* of the excitation vortex, that is with the fiber orientation data “turned ON”, so that both the anatomically realistic geometry and the anisotropy of the otherwise homogeneous foetal heart affect the dynamics of the initial vortex leading to its really fast termination at the apex of the heart.

[[In the raw DT-MRI model simulations shown in Fig. \[3D\_iso\], Fig. \[3D\_aniso\], Fig. \[3D\_X\_iso\], and Fig. \[3D\_X\_aniso\], it can be seen that although the organising filament of the vortex could not get through into the accidental “leftover” piece of tissue adjacent to the apical region, the piece got activated and might have served as an artificial 