This study demonstrates the functionality of a novel simulation environment, Beatbox [1], in a study of the effects of altered inward rectifier potassium current (IK1). Beatbox provides model repositories of cardiac cells as well as tissue and anatomies. The human atrial cell model by Courtemanche et al. [2] (CRN) was used in this study. The conductance of the IK1 current (gK1) was altered in a graded manner to simulate atrial fibrillation (AF) or drug effects. The effects on action potential (AP), [Ca2+]i, and AP duration (APD90) restitution were quantified using established pacing protocols [3]. Beatbox offers a user friendly computational mechanism for constructing spatially extended tissue models. It was used to construct 1D strands and 2D sheets of atrial tissue. The tissue level simulations were conducted using Beatbox’s parallel domain decomposition algorithms. Inter-cellular coupling was chosen to give a conduction velocity (CV) of 0.33 mm/ms in solitary planar waves [3]. Using the 1D strands, CV restitution and vulnerability window (VW) were quantified at various values of gK1. The 2D atrial sheets were taken to be 37.5 mm x 37.5 mm. Re-entrant waves were efficiently initiated by the phase distribution method [4] and optimised using the on screen run-time graphical functions. Re-entrant waves were allowed to evolve for 10 s. The stability of re-entrant waves was quantified by means of tip meander. Scroll waves in a 3D anatomical model were also simulated in the basal case. In all simulations, the time step for the forward Euler time solutions was taken to be 5 μs [1] and a space step of 0.1 mm [2]. The basal AP duration (APD90) in the CRN model is 312.1 ms. Upon increasing gK1 by 35% (simulation of paroxysmal AF), APD90 reduced to 260.3 ms, while reducing it by the same amount increased APD90 to 344.3 ms (effects of β-blockers). Chronic AF (CAF), simulated as a 200% increase of gK1, gave an APD90 of 200.3 ms. APD90 in the physiological range of conductance values is shown in Fig 1A. In 1D strand models, CV restitution shows that an increase of gK1 increases the propensity of atrial tissue to sustain electrical propagation at high pacing rates. In the 2D simulations, re-entrant waves became stable with an increase of gK1, and became hyper-meandering when gK1 was at or below the basal value of 0.09 nS/pF. The re-entrant wave tip trajectories under Control and CAF conditions are shown in Fig 1B. Scaling of these 2D simulations was quantified by running in serial and parallel mode. The scaling of Beatbox is shown in Fig 1C. The capability of Beatbox to simulate 3D phenomena is illustrated in Fig. 1D. These simulations confirm our previous findings [3] obtained using alternative simulation environments. Beatbox was seen to be more flexible, and gave better performance on local and national HPC facilities.