excitable medium support a rigidly rotating vortex with positive filament tension [@ft]. The simplified FHN model was intentionally chosen for this study in order to fully eliminate the possible effects of a realistic cell excitation kinetics, such as *e.g.* meander [@Winfree-1991], alternans[@Karma_Chaos1994], negative filament tension[@ft], etc., and in order to enhance and highlight the pure effects of the heart anatomy and anisotropy on the cardiac re-entry outcome. $\hat{{\mathbf{D}}}={{\mathbf{Q}}}\hat P$, where ${{\mathbf{Q}}}=\mathrm{diag}(1,0)=\begin{bmatrix}1&0\\0&0\end{bmatrix}$ is the matrix of the relative diffusion coefficients for $u$ and $v$ components, and $\hat
P=[P_{\j\k}]\in{\mathbb{R}}^{3\times 3}$ is the $u$ component diffusion tensor, which has only two different eigenvalues: the bigger, simple eigenvalue $\Ppar$ corresponding to the direction along the tissue fibers, and the smaller, double eigenvalue $\Port$, corresponding to the directions across the fibres, so that $$P_{\j\k} = \Port{\delta}_{\j\k} +
  \left(\Ppar-\Port\right)\fib_\j\fib_\k,
                                        \label{sigma}$$ where $\fibvec=\left(\fib_\k\right)$ is the unit vector of the fiber direction; $\normv$ is the vector normal to the tissue boundary $G$. In the isotropic simulation, $\Ppar$ and $\Port$ values were fixed at $\Ppar=\Port=1$ (corresponding 1D conduction velocity [1.89]{}). In the anisotropic simulations, $\Ppar$ and $\Port$ values were fixed at $\Ppar=2$, $\Port=0.5$ (corresponding conduction velocities [2.68]{} and [1.34]{} respectively). All the conduction velocities have been computed for the 