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Learning While Burning:

Until recently, the most widely accepted mechanism of atrial fibrillation (AF) was the multiple wavelet hypothesis described by Moe and Abildskov1 in 1959. According to this hypothesis, AF is a self-sustaining process consisting of multiple wavelets that move randomly throughout the atria, independent of the initiating event. Experimental support for this hypothesis was provided in 1985 by Allessie et al.,2 who estimated that four to six wavelets were critical for maintenance of AF in the canine heart. This hypothesis was further strengthened by the clinical observation that AF could be cured by the placement of surgical or cryolesions (MAZE) to compartmentalize the atria into regions presumably unable to sustain the multiple wavelets.3 The discovery by Haissaguerre et al.4 in 1998 that focal ablation could eliminate AF represented a major therapeutic advance. A more important consequence of that finding was to revive the concept of AF as the result of a rapidly firing focus. This theory was described in 1925 by Sir Thomas Lewis,5 who observed that “. . . fibrillation, like flutter, may also on occasion be terminated in the auricle by cold or pressure very locally applied.” Additional support for this alternative view came later from Scherf et al.,6,7 who used local application of aconitine to induce AF and then demonstrated that obliteration of the site of aconitine application resulted in AF termination. However, this concept was not initially accepted by electrophysiologists, perhaps due to the limited investigative methodologies available at that time, which prevented exhaustive characterization of electrical waves propagation. With the development of high-resolution mapping techniques such as optical mapping, this task became achievable. A series of studies from the laboratory of Jalife et al.8-12 described vortex-like reentry (rotors) around minuscule cores, with high-frequency periodic activity in the posterior left atrium and the pulmonary veins ostia. Rapid and successive electrical impulses emanating from these rotors propagate throughout the atria and interact with functional and/or anatomic obstacles leading to fragmentation and wavelets formation. This “fibrillatory conduction” results in the seemingly random electrical activity that characterizes AF. The article by Scharf et al.13 in this issue of the Journal describes the acute outcome of left atrial ablation for AF. Although it was not the aim of this investigation to study the mechanisms of AF, some of its findings have important