Electroanatomical mapping is currently used to provide clinicians with information about the electrophysiological state of the heart and to guide interventions like ablation. These maps can be used to identify ectopic triggers of an arrhythmia such as atrial fibrillation (AF) or changes in the conduction velocity (CV) that have been associated with poor cell to cell coupling or fibrosis. Unfortunately, many factors are known to affect CV, including membrane excitability, pacing rate, wavefront curvature, and bath loading, making interpretation challenging. In this work, we show how endocardial conduction velocities are also affected by the geometrical factors of muscle thickness and wall curvature. Using an idealized three-dimensional strand, we show that transverse conductivities and boundary conditions can slow down or speed up signal propagation, depending on the curvature of the muscle tissue. In fact, a planar wavefront that is parallel to a straight line normal to the mid-surface does not remain normal to the mid-surface in a curved domain. We further demonstrate that the conclusions drawn from the idealized test case can be used to explain spatial changes in conduction velocities in a patient-specific reconstruction of the left atrial posterior wall. The simulations suggest that the widespread assumption of treating atrial muscle as a two-dimensional manifold for electrophysiological simulations will not accurately represent the endocardial conduction velocities in regions of the heart thicker than 0.5 mm with significant wall curvature.