Moe et al11 hypothesized that the constant formation of new wavelets occurs through the process of wave splitting (wavebreak), resulting in multiple wavelet fibrillation. The wave splitting occurs because of nonuniform dispersion of refractoriness and anatomic heterogeneity. Nonuniform dispersion of refractoriness naturally occurs in the normal myocardium as a result of transmural and base-to-apex heterogeneity of action potential durations12 and is further exacerbated by disease. The anatomic heterogeneities, which are naturally present, also facilitate conduction blocks and wavebreaks through the source-sink mismatches. 13 For example, epicardial coronary arteries, 14 papillary muscles, 15 transmural sites with abrupt fiber orientation changes, 16 and increased fibrosis resulting from cardiomyopathy17 can all serve as sites of wavebreaks. With the more recent appreciation that dynamic factors related to electrical restitution also play a key role in facilitating wavebreak, an updated version of the Multiple Wavelet Hypothesis emphasizes that the synergy between dynamic factors and preexisting tissue heterogeneities are the fundamental cause of wavebreaks perpetuating VF. 18