Sinus node dysfunction (SND) is a known cause of bradycardia, sinus arrest, and sinus pause, and leads to subnormal atrial pacing. Experimental evidence shows that SND is correlated to the pacemaker sinoatrial node (SAN) cell apoptosis [1]. The effect of such a dysfunctional SAN on electrical propagation into neighboring atrial tissue remains under explored. A novel computational cardiology simulation environment, BeatBox [2], which provides a versatile computational tool to develop and construct simulation models and was used in this study. The computationally efficient Fenton-Karma (FK) model [3] was extended to simulate mouse SAN and atrial cell action potentials (APs). To simulate atrial AP, the basal model parameters [3] were altered. Further, a hyperpolarisation activated current was incorporated into the basal model, and then the parameters altered to simulate the SAN pacemaking AP. The cell models were incorporated into a 2D model consisting of a central SAN region surrounded by atrial tissue. In each 2D simulation, 10 s of electrical activity were simulated. First, the basal size of mouse SAN pacemaking region was estimated using the 2D model. Then in multiple simulations, SAN cell apoptosis was simulated by randomly eliminating a proportion of SAN cells from the pacemaking region. The effects of an increasing proportion of apoptotic pacemaker cells on atrial tissue pacing were simulated and quantified. The modified FK model that reproduces SAN and atrial APs as well as validation with experimental observations is shown in Fig. 1. The SAN size that gave a basal mouse atrial cycle length (ACL) of 295 ms was found to be 0.6 mm in radius. In the simulations where pacemaker cell apoptosis was considered (Fig. 2), a more dramatic effect was seen. At low pacemaker cell apoptosis proportion, there was a drastic increase of ACL. At modest increase in the number of apoptotic cells, bradycardia was observed. The incidence of sinus arrest was also found to be high. When the numbers of apoptotic cells were 10% of the total number of pacemaking cells, all pacemaking was arrested. Our computational findings agree with recent experimental results [1]. Novel phenomenological models have been developed to facilitate the study of mouse atrial electrophysiology as well as tissue behaviour. The results show the significance of cell apoptosis as a major mechanism of SND. Novel computational modules in the simulation environment were developed to enable this study. BeatBox is an ideal computational environment to conduct such large scale studies.