Atrial fibrosis is known to be a factor in the perpetu ation of atrial arrhythmia. Despite the thinness of atrial tissue, the fibrosis distribution may not be homogeneous through the entire thickness of the atria. This study aims to elucidate the respective influences of a transmural and a non-transmural distribution of fibrosis, described as a slow conduction zone, on the perpetuation of an arrhythmic episode, compared to a control situation. We used a bilayer monodomain representation of the atria that included transmural heterogeneities of fibre organisation. This model allowed long simulations for a sustainable computational load. We observed that when the fibrosis was transmural, the centre of the rotor was anchored in the slow conduction zone and was stable during a 10 seconds simulation, whereas the other simulations showed meandering rotors that disappeared after a few seconds. This study provided insight into the influence of transmural fibrosis on atrial arrhythmia perpetuation. In our model framework, only a transmural fibrosis distribution had a stabilizing effect on reentrant circuits. The bilayer model proved to be a good trade-off between accuracy and speed for observing the influence of transmural heterogeneities on atrial arrhythmia over long periods.