The mechanism of atrial fibrillation (AF) remains poorly understood. In this article, we present a new unifying hypothesis for the electrophysiologic basis of AF. We surmise that sustained AF depends on the uninterrupted periodic activity of discrete reentrant sites. The shorter reentrant circuits act as dominant frequency sources that maintain the overall activity. The rapidly succeeding wavefronts emanating from these sources propagate through both atria and interact with anatomic and/or functional obstacles, leading to the phenomenon of "vortex shedding" and to wavelet formation. As suggested by recent numerical and experimental results from our laboratory, some of such wavelets may shrink and undergo decremental conduction, others may be annihilated by collision with another wavelet or a boundary, and still others may curl to create new vortices. The end result would be the fragmentation of the periodic wavefronts into multiple independent daughter wavelets, giving rise to new wavelets, and so on in the ceaseless, globally aperiodic motion that characterizes fibrillatory conduction.