Current Management of the Wolff-Parkinson-White Syndrome

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.

Improvement in Dyssynchrony with Pharmacological Ablation of Right-Sided Accessory Pathway-Induced Cardiomyopathy in Infants

“…Consequently, cardiac dyssynchrony due to an accessory pathway seems responsible for such left ventricular dilation and functional impairment in accessory pathway-induced DCM. 2,6) Although flecainide, a group Ic Na channel blocker, inhibits the accessory pathway conduction in WPW syndrome, 11) to the best of our knowledge, there has been no report of the usefulness of flecainide for accessory pathway-induced DCM. Although flecainide use has been associated with an increase of proarrythmic events in adult patients with acute recurrent myocardial infarctions 12) , and with an increase in cardiovascular hospitalizations in adult patients with atrial fibrillation, 13) flecainide use has been reported effective and safe in the pediatric population 14) even in those with a reduced EF.…”

A Fetal Wolff-Parkinson-White Syndrome Diagnosed Prenatally by Magnetocardiography

“…Patients with WPW syndrome experience attacks of supraventricular tachycardia (SVT), which are triggered by changes in physical or mental conditions, and autonomic neurological states [8]. The key etiology of the SVT is the formation of a re-entry circuit of conduction waves in a heart.…”

Palpitations in a 43-year-old man

“…3 What treatment options are available in the acute phase? 4 What is the long-term strategy in treating this condition? Answers QUESTION 1 UNDERLYING RHYTHM Atrial fibrillation with pre-excited complexes.…”