The role of the heart's complex shape in causing the fragmentation of activation wave fronts characteristic of ventricular fibrillation (VF) has not been well studied. We used a finite element model of cardiac propagation capable of simulating functional reentry on curved two-dimensional surfaces to test the hypothesis that uneven surface curvature can cause local propagation block leading to proliferation of reentrant wave fronts. We found that when reentry was induced on a flat sheet, it rotated in a repeatable meander pattern without breaking up. However, when a model of the rabbit ventricles was formed from the same medium, reentrant wave fronts followed complex, nonrepeating trajectories. Local propagation block often occurred when wave fronts propagated across regions where the Gaussian curvature of the surface changed rapidly. This type of block did not occur every time wave fronts crossed such a region; rather, it only occurred when the wave front was very close behind the previous wave in the cycle and was therefore propagating into relatively inexcitable tissue. Close wave front spacing resulted from nonstationary reentrant propagation. Thus, uneven surface curvature and nonstationary reentrant propagation worked in concert to produce wave front fragmentation and complex activation patterns. None of the factors previously thought to be necessary for local propagation block (e.g., heterogeneous refractory period, steep action potential duration restitution) were present. We conclude that the complex geometry of the heart may be an important determinant of VF activation patterns. © 2002 American Institute of Physics.