Triggers propagating into atrial myocardium may initiate reentering wavelets if the wavelength is sufficiently short. Wavelength shortening can occur even in normal atria if the effective refractory period (ERP) or conduction velocity is decreased. Initiation and maintenance of AF may depend on uninterrupted periodic activity of a few discrete reentrant sources localized to the left atrium, emanating from such sources to propagate through both atria and interact with anatomical and/or functional obstacles, leading to fragmentation and wavelet formation. 18, 19 Factors such as wavefront curvature, 20 sink-source relationships, 21 and spatial and temporal organization22, 23 all are relevant to our understanding of the initiation of AF by the interaction of the propagating wave fronts with such anatomic or functional obstacles. Indeed, all these factors, which differ from triggers, may be considered initiators of AF.

Having been initiated, AF may be brief. A variety of factors may act as perpetuators, ensuring the persistence of AF for longer periods. One is persistence of the triggers and initiators that induce AF, 24 but at some point, AF persists even in their absence. 25–27 Persistence here may result from electrical and structural remodeling, characterized by atrial dilatation and shortening of the atrial ERP. This combination, along with other remodeling changes, likely facilitates the appearance of multiple reentrant wavelets (a final common pathway for AF).