Aim: Mutations in the SCN5A gene encoding for the α-subunit of the cardiac sodium channel, I_Na, might result in dysfunction of cardiac excitation wave propagation. In this study we computationally evaluated the functional impacts on atrial excitation of a recently identified mutation SCN5A-W1191X in patients with Brugada syndrome and complication of atrial fibrillation (AF) [1]. By using biophysical simulations, we investigated (a) the effects of the mutation on atrial electrical action potentials (AP) at the cellular level; (b) the effects of the mutation on propagation of atrial excitation waves on spatially extended virtual human atrial tissues. Methods: The Courtemanche et al. [2] model of human atrial cell was modified to incorporate experimental data of Shin et al. [1] on the mutation-induced loss-of-function in I_Na, which resulted in a reduction in the maximal channel conductance. The modified model was implemented to simulate APs under control and mutation conditions. Characteristics of APs for both conditions were computed that include the resting potential, AP amplitude (APA), maximum upstroke velocity (dV/dt_max), AP duration at 50 % repolarisation (APD₅₀) and at 90 % repolarisation (APD₉₀) and over shoot (OS). Single cell model was then incorporated into an one-dimensional reaction diffusion partial differential equation model of human atrial strand, using which the conduction velocity (CV) was determined by pacing the 1D strand with standard S1-S2 stimulus protocols. Results: The SCN5A-W1191X mutation resulted in no significant change in either APD₅₀ or APD₉₀. However, it reduced substantially the dV/dt_max, which reduced from 217.081 mV/ms in Control to 109.5 mV/ms under mutant conditions. Consequentially the computed OS was also decreased from 24.75 mV in Control to 8.5 mV in mutation. In the 1D simulations, the measured CV for solitary excitation waves was reduce from 0.27 mm/ms in Control to 0.20 mm/ms in mutation conditions. Conclusions: SCN5A-W1191X does not alter the human atrial AP morphology significantly, but decrease its excitability resulting in a dramatic slowing of CV. Reduction of CV shortens the wavelength of atrial excitation waves, allowing 2D and 3D substrates to sustain re-entrant waves, which is pro-arrhythmic.