Wolff-Parkinson-White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles (bundle of Kent), which leads to an atrioventricular re-entry tachycardia (AVRT).
It can degenerate rapidly into ventricular fibrillation since the accessory pathway does not slow conduction.
It is more common in younger patients.
Types of WPW
| Type | Characteristic |
|---|---|
| Type A (left-sided pathway) | Dominant R wave in V1 |
| Type B (right-sided pathway) | No dominant R wave in V1 |
| Type C (rare) | Delta waves are upright in V1 – V4 but negative in V5 – V6 |
- Associated conditions
- Hypertrophic obstructive cardiomyopathy
- Mitral valve prolapse
- Ebstein’s anomaly
- Thyrotoxicosis
- Secundum ASD
- Signs and symptoms
- Often asymptomatic and found incidentally
- Palpitations
- Lightheadedness
- Syncopal episodes
- EKG findings
- Short PR interval
- Wide QRS complexes with a slurred upstroke (delta wave)
- Left axis deviation (for right-sided accessory pathway)
- Right axis deviation (for left-sided accessory pathway)
- Treatment
- Unstable patient
- Cardioversion
- Medical treatment: sotalol, amiodarone, or flecainide
- Amiodarone instead of Adenosine (lack of response to adenosine suggests sinus tachycardia or atrial tachycardia)
- Sotalol is avoided if there is coexisting atrial fibrillation since prolonging the refractory period at the AV node increases the rate of transmission through the accessory pathway, thus increasing the ventricular rate and deteriorating into ventricular fibrillation
- Definitive treatment
- Radiofrequency ablation of the accessory pathway
- Unstable patient