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Atrial fibrillation is the most common arrhythmia in humans. The mechanisms underlying its induction and maintenance are not fully understood. However, it seems likely that, similar to sustained ventricular tachyarrhythmias, atrial fibrillation induction and maintenance are related to the presence of an anatomical and/or electrophysiological substrate, activated by specific triggers (ectopic beats), in the presence of a modulating factor (autonomic system status). It has been suggested, by Moe in the 1960s and subsequently confirmed by atrial mapping in animals and humans, that the substrate comprises multiple wavelets. This hypothesis states that the induction of sustained atrial fibrillation depends on the average number of reentrant circuits present in the atria. If the number of the wavelets is high, the statistical probability that they will die at the same time will be small and atrial fibrillation will persist; on the other hand, when the number of reentrant wavelets is small, the chance that they will die out simultaneously is higher, and the termination of the arrhythmia more likely. The number of wavelets that can coexist is determined both by the atrial tissue mass and the wavelength (wavelength= conduction velocity refractory period) of the atrial impulse. The smaller the wavelength of circulating wavelets the more easily atrial fibrillation is induced and maintained. Consequently, a slower conduction velocity, a shorter refractory period or both reduce the wavelength, thus increasing the number of possible circuits in the atria and leading to a more stable atrial fibrillation.

Update on atrial remodelling owing to rate. Does atrial fibrillation always 'beget' atrial fibrillation?