are applied to the CMP model to simplify simulations and analysis.

All tissue instances are generated at a fixed transverse coupling fraction of $\nu = 0.2$ which is approximately the degree of fibrosis at which we observe paroxysmal AF. We also work in the low noise limit where $\delta = 0$. As a result, temporary critical circuits cannot spontaneously form in the tissue as shown in part (d) of Fig. \[fig:rotorform\]. The limitations of this decision are discussed in section \[sec:lims\]. The low noise limit inhibits the formation of new, stable re-entrant circuits. Instead, a single circuit is artificially constructed by picking a random point in the CMP tissue and removing the coupling to the muscle fibre above and below of the 28 cells to the right of the randomly chosen cell. This gives a rectangular circuit of path length $60$ – this is an arbitrary choice which is slightly larger than the refractory period of $\tau = 50$. The circuit is then artificially forced to start driving AF by the introduction of a single ectopic beat in the circuit.

The procedure to be tested is split into two sections. First, the CMP tissue must be initialised to generate fibrillatory 