Wolff-Parkinson-White Syndrome

WPW pattern (asymptomatic) prevalence: 0.15–0.25% in the general population and 0.55% in pts with a primary relative with WPW; autosomal dominant trait.

WPW syndrome (ECG pattern and arrhythmia) prevalence is 0.005% to 0.07% in the general population and approximately 2% out of pts with WPW. It is often first presented in ages 20–40 y.

Definition: WPW syndrome is a preexcitation syndrome. Ventricular depolarization occurs in part via an AP from the atrium (bundle of Kent) bypassing the AV-His Purkinje conduction system.

The AP allows for antegrade or retrograde conduction which is faster than the AV node resulting in a shortened PR interval (<0.12 sec). The impulse then spreads through the muscle fibers until it joins the regular conduction system resulting in a slurred upstroke and widening of the QRS complex on the ECG.

PSVT results from a reentrant circuit involving the AV node and AP. The QRS complex during PSVT matches the usual QRS morphology when conduction is antegrade through the AV system and retrograde through the AP (i.e., orthodromic). 5–10% of the time, conduction through the AP is antegrade (i.e., antidromic in the reentrant circuit), producing a wide QRS complex. This rhythm may be confused with VTach.

AFIB and/or AFLT is more common in pts with WPW. Usually, AFIB is precipitated by an episode of PSVT. Rapid (≥300 bpm) ventricular rates may occur in pts with APs with short refractory periods. These pts are at risk for developing Vfib and hemodynamic collapse.

Other heart abnormalities (e.g., Ebstein’s anomaly) are often commonly (7–20%) associated with WPW.

AVRT (80% of pts WPW syndrome): Rapid HR impairs LV filling, leading to hemodynamic instability and/or myocardial ischemia.

AFIB (15–35%); increasing incidence with age. A major concern is rapid ventricular response due to antegrade conduction over AP.

Atrial flutter (5%).

VFIB/sudden death (0–0.4%): Out of rapid ventricular response due to antegrade conduction over AP in AFIB/AVRT.