• ABSTRACT
    • In this review, we discuss the pathophysiology of the Wolff-Parkinson-White (WPW) syndrome and describe medical, surgical, and catheter based principles. WPW syndrome results from the congenital presence of impulse-conducting fascicles, known as accessory pathways (APs) or bypass tracts, which connect atria and ventricles across the annulus fibrosis and are capable of preexciting portions of the ventricular myocardium. Once triggered, atrioventricular reciprocating tachycardias (AVRTs) generally result from depolarization wavefronts moving anterograde through the AV node to the ventricles and returning retrograde to the atria along the AP. Rapid AVRT decreases ventricular filling time and cardiac output, resulting in symptoms. Medications that prolong AP refractory periods (flecainide, propafenone, and amiodarone) prevent rapid AP anterograde conduction (from atria to ventricles) in atrial tachycardias such as atrial fibrillation or flutter. In emergencies, adenosine can be used to terminate the AVRT of WPW syndrome. Otherwise, Class IA or IC antiarrhythmic agents are used to slow AP conduction either with or without AV nodal blocking agents. Open chest surgical ablation of a bypass tract in a symptomatic patient was first reported in 1968. The original endocardial surgical techniques for localizing and dividing APs were refined and an alternative epicardial approach has been developed. Reported mortality rates in experienced hands were 0% to 1.5% in large series for patients without additional cardiac abnormalities. Catheter delivered radiofrequency (RF) energy is now applied intravascularly to ablate APs. Since the first large series of patients undergoing RF ablation was reported in 1989, the procedure had proved safe, cost effective, and well tolerated. RF ablation has become the initial nonpharmacological treatment of choice for WPW syndrome; surgical ablation has become relegated to those cases where symptoms are intolerable and RF ablation is not feasible.