[The atrial fibrillation substrate: pulmonary veins, posterior wall or both].

Atrial fibrillation (AF) is the most common arrhythmia seen in clinical practice and is associated with a notable increase in morbidity and mortality. Although there have been considerable advances in the treatment of AF, the results of drug treatment and ablation remain suboptimal.1 This is largely due to the fact that there is still little understanding of the mechanisms responsible for the initiation and maintenance of the arrhythmia. During the past 50 years, the multiple wavelet theory was the sominant concept proposed to explainet AF. According to that hypothesis, AF would be a consequence of functional reentry of multiple wavefronts that would spread throughout the excitable tissue of the atrium, tissue that can become depolarized at the moment it is reached by an activation front (Figure 1A). This hypothesis was questioned by Haissaguerre et al3 who found that extrasystoles and rapid atrial rhythm arising from within the pulmonary veins could initiate and, in some cases, maintain episodes of AF.4,5 According to this focal hypothesis, AF would not only be initiated but also maintained by a very high frequency source arising in or around the pulmonary veins with activation fronts that fractionate and become disorganized in the surrounding tissue, giving rise to what is known as fibrillatory conduction (Figure 1B). Finally, according to the last hypothesis, the beats arising in the pulmonary veins would only act as a trigger for the formation of a functional reentrant circuit generated by abnormal propagation of the electrical impulse in a more extensive area of the atrium (Figure 1C). Using sophisticated optical The Atrial Fibrillation Substrate: Pulmonary Veins, Posterior Wall, or Both