Atrial fibrillation: towards an understanding of initiation, perpetuation, and specific treatment

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Abstract
Recently, clinical and experimental studies have indicated that rapid repetitive activation of the atrial myocardium may play a role in the genesis of atrial fibrillation.3 It has long been recognised that patients with a variety of regular tachycardias involving the atria, such as accessory pathway mediated junctional reentrant tachycardia, can have an associated tendency to atrial fibrillation, which may be abolished by successfully ablating the underlying arrhythmia. Although this observation has remained largely unexplained, it raises the question of whether the tendency to atrial fibrillation may be causally related to the frequency of atrial myocardial activation during tachycardia. This concept is reinforced by a recent report of an unusual cohort of patients with recurrent atrial fibrillation who can be cured by radiofrequency ablation of a rapidly discharging focal atrial tachycardia that is underlying and apparently “driving” the fibrillation.4 This small subset of patients so far identified as having atrial fibrillation that can be cured by focal ablation to a single atrial site have a characteristic phenotype: young, of either sex, with no structural heart disease, frequent episodes of intermittent atrial fibrillation interspersed with a distinct rapid atrial tachycardia, and isolated atrial extrasystoles from the same focus typically found to be near the ostia of the pulmonary veins or venae cavae.4