Paroxysmal atrial fibrillation (PAF) develops in up to one-third of patients with the Wolff Parkinson−White syndrome (WPW). The reason for this high incidence of PAF in the WPW syndrome is not yet clearly understood. When PAF appears in patients with WPW syndrome who have anterograde conduction via the accessory pathway (AP), it may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation.

Several mechanisms responsible for the genesis of PAF in WPW patients were hypothesized, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into atrial fibrillation (AF), electrical properties of the APs, effects of APs 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 PAF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of PAF. However, PAF still occurs in some patients with the WPW syndrome even after successful elimination of the AP. There is an important evidence of an underlying atrial disease in patients with the WPW syndrome.

Atrial vulnerability has been studied performing an atrial endocardial catheter mapping and analysing abnormal atrial electrograms. Other studies evaluated atrial refractoriness and intraatrial conduction times, suggesting an intrinsic atrial vulnerability as the mechanism of PAF and considering the AP as an innocent bystander. It is our intention to analyse the available data on this particular and interesting topic since AF has a singular prognostic significance in patients with the WPW syndrome, and its incidence is unusually high in the absence of any clinical evidence of cardiac organic disease.