The spatial localization of Ryanodine receptor (RyR) clusters, and the number of RyRs per cluster affects the initiation and propagation of intracellular calcium waves [1]. Previous simulation studies have been based on simplified approximations of the distribution of RyR clusters. We embedded a three dimensional rat ventricular myocyte dataset (x,y: 0.05 µm; z:0.15 µm voxels) obtained by confocal microscopy [2] of part of an individual Z disk within a 300 by 450 by 40 cuboid of 0.05 µm voxels that extends into the adjacent sarcomeres, into a rat ventricular 3Dv E-Cell [3]. This represents part of a transverse slab, 2 µm thick, centered on the centre of the Z disk. To simulate spontaneous resting intracellular calcium dynamics we neglect voltage dependent sarcolemmal currents, and intracellular calcium dynamics were modelled by a set of reaction-diffusion equations based on Izu et al [1], with stochastic rules for triggering [Ca]²⁺ release and parameters given in [3]. The rate of change of [Ca]²⁺ depends on fluxes via RyR, pumps, leaks and buffers, where the firing probability of a RyR cluster is governed by probability function. In our simulations with diffusion coefficients of 7.9 µm²/s (transverse) and 17.1 µm²/s (longitudinal), sparse, localised regions/islands with high density of RyR clusters can act as foci for the initiation of propagating calcium events, and the peripheral region of the Z-disk produced more calcium release than the centre due to boundary effects.