Despite its importance, the mechanisms underlying ventricular fibrillation (VF) remain poorly understood. Experimental studies are mainly limited to the study of activity on the heart surface, yet the reentrant mechanisms believed to sustain VF are three-dimensional. In 3D, a reentrant wave rotates around a linear filament, and the properties of these filaments can contribute to the stability of reentry. In this paper we describe how filaments can be detected during reentry in cardiac virtual tissues, and how their length and twist can be extracted from numerical results. As an example, we present some results showing the behavior of reentry in 3D virtual tissues with both idealized slab geometry, and anatomically detailed right ventricular (RV) free wall geometry derived from the Auckland canine ventricles. In the slab geometry reentry was stable even with 120° rotational anisotropy, but with a transmural gradient of action potential duration (APD) to mimic the normal distribution of APD across the ventricular wall, reentry became unstable. In contrast, we found that reentry in the anisotropic RV free wall with uniform APD was unstable, possibly because the rotation of fibers is not uniform as in the slab geometry. With transmural differences in APD the instability was augmented, indicating that transmural differences can act synergistically with other mechanisms to increase instability of reentry. This study shows that numerical models can generate information about the behavior of filaments during reentry in 3D, and highlights the need for a theoretical foundation to explain this observed behavior.