In this review, we discuss the pathophysiology of the Wolff-Parkinson-
White (WPW) syndrome and describe medical, surgical, and catheter base
d principles. WPW syndrome results from the congenital presence of imp
ulse-conducting fascicles, known as accessory pathways (APs) or bypass
tracts, which connect atria and ventricles across the annulus fibrosi
s and are capable of preexciting portions of the ventricular myocardiu
m. Once triggered, atrioventricular reciprocating tachycardias (AVRTs)
generally result from depolarization wavefronts moving anterograde th
rough the AV node to the ventricles and returning retrograde to the at
ria along the AP. Rapid AVRT decreases ventricular filling time and ca
rdiac output, resulting in symptoms. Medications that prolong AP refra
ctory periods (flecainide, propafenone, and amiodarone) prevent rapid
AP anterograde conduction (from atria to ventricles) in atrial tachyca
rdias such as atrial fibrillation or flutter. In emergencies, adenosin
e can be used to terminate the AVRT of WPW syndrome. Otherwise, Class
IA or IC antiarrhythmic agents are used to slow AP conduction either w
ith 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 divid
ing APs were refined and an alternative epicardial approach has been d
eveloped. Reported mortality rates in experienced hands were 0% to 1.5
% in large series for patients without additional cardiac abnormalitie
s. Catheter delivered radiofrequency (RF) energy is now applied intrav
ascularly to ablate APs. Since the first large series of patients unde
rgoing RF ablation was reported in 1989, the procedure had proved safe
, cost effective, and well tolerated. RF ablation has become the initi
al nonpharmacological treatment of choice for WPW syndrome; surgical a
blation has become relegated to those cases where symptoms are intoler
able and RF ablation is not feasible.