Experimental and clinical evidence suggests the role of fibrosis in the formation of a pro-arrhythmic substrate for atrial fibrillation (AF). This work presents a simulation model to investigate the interactions between excitation wavefronts and fibrosis. The Courtemanche-Ramirez-Nattel model of the human atrial potential was implemented on a sphere monolayer, and fibrosis was included replacing mesh nodes with non-excitable elements with no-flux boundary conditions. A stochastic algorithm was used to generate spatial patterns of fibrosis with specific density, patch dimension and orientation. Simulations run at different model parameters showed that the presence and spatial pattern of fibrosis could significantly alter the dynamics of propagating wavefronts, favoring the occurrence of reentrant activity and self-sustained propagation. Combined with more realistic atrial geometry, this simulation model may help to clarify the determinants of AF multifactorial substrate.