Using a three-dimensional propagation model of the human ventricular myocardium, we studied the role of fibrous structure in generating epicardial potential maps. This model represents the myocardium as an anisotropic bidomain with an equal anisotropy ratio, and it incorporates a realistic representation of anatomical features, including epi-endocardial fiber rotation in the compact portion of the wall (compacta) and a distinct fiber arrangement of the trabeculated portion (trabeculata). Activation sequences were elicited at various intramural depths, and maps were calculated throughout a 60 ms sequence. The simulated maps closely resembled those measured by others in the canine heart. During the early stages of activation, a typical map featuring a central minimum flanked by two maxima emerged, with the axis joining these extrema approximately parallel to the fibers near the pacing site, and the axis joining the maxima rotated in the same direction as the fibers for different pacing depths; for endocardial and subendocardial pacing this map changed into one with an oblong positive area. During the later stages of activation, the positive areas of the maps expanded and rotated with the transmural fiber rotation. In concurrence with experiments, we saw a fragmentation and asymmetry of expanding and rotating positive areas. The latter features—apparently caused by the interface between the compacta and trabeculata, variable local thickness of the wall, or local undulations of the vetricular surface—could not be reproduced by more idealized, slab models.