Abstract
Since the advent of catheter ablation for atrial fibrillation (AF) aiming the pulmonary veins a few years ago, there has been an overwhelming interest and a dramatic increase in AF investigation. AF has a different dimension in the context of the Wolff-Parkinson-White (WPW) syndrome. Indeed, AF may be a nightmare in a young person that has an accessory pathway (AP) with fast anterograde conduction. It may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation. Therefore, it is very important to know the mechanisms involved in the development of AF in the WPW syndrome. There are several possible mechanisms that may be involved in the development of AF in the WPW syndrome, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into AF, the electrophysiological properties of the AP, the effects of AP on atrial architecture, and intrinsic atrial muscle vulnerability. Focal activity, multiple reentrant wavelets, and macroreentry have all been implicated in AF, perhaps under the further influence of the autonomic nervous system. AF can also be initiated by ectopic beats originating from the pulmonary veins, and elsewhere. Several studies demonstrated a decrease incidence of AF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of AF. However, since AF still occurs in some patients with the WPW syndrome even after successful ablation of the AP, there should be other mechanisms responsible for the development of AF in the WPW syndrome. There is a clear evidence of an underlying atrial muscle disease in patients with the WPW syndrome. Atrial myocardial vulnerability has been studied performing an atrial endocardial catheter mapping during sinus rhythm, and analizing the recorded abnormal atrial electrograms. This review analizes the available data on this singular setting since AF has a reserved prognostic significance in patients with the WPW syndrome, and has an unusually high incidence in the absence of any clinical evidence of organic heart disease.