Wolff-Parkinson-White syndrome !

In WPW an extra electrical bridge links the upper and lower heart chambers. It can cause bursts of fast heartbeat and, rarely, sudden death.

Updated 2026-11-01

Structures involved

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In embryology

Why it happens

What it is

A congenital accessory pathway (bundle of Kent) connects atrium and ventricle outside the atrioventricular node. The ECG shows ventricular pre-excitation, and the syndrome is defined by pre-excitation together with episodes of tachycardia.

Who gets it

Pre-excitation is found in roughly 1 to 3 per 1,000 people; many never have symptoms. It is a common cause of tachycardia in children and young adults. It is often detected on ECGs done for sports screening, school medical exams or before surgery.

Causes

Persistence of muscular connections between atria and ventricles that normally disappear during fetal development
Mostly sporadic; a minority are familial
Association with congenital heart disease, especially Ebstein anomaly, and with some cardiomyopathies

Risk factors

Ebstein anomaly and other congenital heart disease
Family history of pre-excitation
Multiple accessory pathways or a pathway with a short refractory period (higher risk of sudden death)

Pathophysiology

The accessory pathway conducts faster than the atrioventricular node, so part of the ventricle is activated early: short PR interval and a slurred QRS upstroke (delta wave). The pathway and the node form a circuit for re-entry. In orthodromic atrioventricular re-entrant tachycardia (the most common), the impulse goes down the node and back up the pathway, giving a narrow QRS. If atrial fibrillation develops, a pathway with fast conduction can transmit very high rates to the ventricles and degenerate into ventricular fibrillation.

Classification

WPW pattern: pre-excitation on the ECG without symptoms
WPW syndrome: pre-excitation plus tachycardia episodes
Orthodromic atrioventricular re-entrant tachycardia (narrow QRS) and antidromic (wide QRS)
Pre-excited atrial fibrillation (irregular, wide and varying QRS)
By pathway location: left free wall (most common), posteroseptal, right free wall, anteroseptal

Symptoms and signs

Sudden-onset and sudden-offset palpitations
Dizziness, chest discomfort or dyspnoea during episodes
Syncope
Sudden cardiac arrest as the first event, rarely
Often asymptomatic, found on a routine ECG

Diagnosis

Clinical: Suspect it in a young person with recurrent episodes of paroxysmal palpitations, or when the ECG shows pre-excitation.
Tests: Resting 12-lead ECG: short PR interval, delta wave and wide QRS with secondary ST-T changes. ECG during an episode, Holter or event monitor, and exercise testing (abrupt loss of pre-excitation suggests a lower-risk pathway). An electrophysiological study maps the pathway, assesses risk and allows ablation in the same session.
Imaging: Echocardiography to look for structural heart disease such as Ebstein anomaly or hypertrophic cardiomyopathy.

Differential diagnosis

Atrioventricular nodal re-entrant tachycardia
Atrial fibrillation with bundle branch block
Ventricular tachycardia
Lown-Ganong-Levine pattern or other short-PR variants
Hypertrophic cardiomyopathy with ECG abnormalities

Goal of treatment

Terminate acute episodes safely, avoid drugs that block the atrioventricular node in pre-excited atrial fibrillation, and eliminate the accessory pathway with ablation in symptomatic or high-risk patients.

Treatment

Acute: Unstable patient (any tachycardia): synchronised electrical cardioversion.
Acute: Stable orthodromic narrow-complex tachycardia: vagal manoeuvres, then adenosine or other atrioventricular nodal blockers, with a defibrillator available.
Acute: Pre-excited atrial fibrillation: cardioversion or procainamide (or ibutilide); avoid adenosine, beta-blockers, non-dihydropyridine calcium channel blockers, digoxin and intravenous amiodarone, which can speed conduction over the pathway and cause ventricular fibrillation.
Procedure: Catheter ablation of the accessory pathway: first-line definitive treatment for symptomatic patients and high-risk asymptomatic ones, with a high cure rate.
Follow-up: Nursing priorities: continuous ECG monitoring during episodes, defibrillator at the bedside when giving drugs, blood pressure checks and education to recognise and report episodes.

Complications

Pre-excited atrial fibrillation degenerating into ventricular fibrillation
Sudden cardiac death
Tachycardia-induced cardiomyopathy with frequent long episodes
Rare complications of ablation (atrioventricular block, vascular injury, tamponade)

Prognosis

Excellent after successful ablation, which cures most patients. The risk of sudden death is low overall but real, especially with a fast-conducting pathway, which is why risk assessment is recommended even in asymptomatic people with high-risk occupations or sports.

Prevention

Pre-participation ECG screening where available and evaluation of young people with palpitations or syncope
Electrophysiological risk assessment of asymptomatic pre-excitation in selected patients

Test yourself

Think of the answer, then tap the question to see it.

Which three ECG findings define pre-excitation in WPW?

Short PR interval, delta wave (slurred QRS upstroke) and wide QRS.

What is the most common tachycardia in WPW syndrome?

Orthodromic atrioventricular re-entrant tachycardia, with a narrow QRS (down the node, up the pathway).

Which drugs must be avoided in pre-excited atrial fibrillation, and why?

Atrioventricular nodal blockers such as adenosine, beta-blockers, verapamil or diltiazem, and digoxin, because they favour conduction down the accessory pathway and can cause ventricular fibrillation.

Which drug or intervention is preferred for stable pre-excited atrial fibrillation?

Procainamide (or ibutilide); synchronised cardioversion if unstable.

Which congenital heart defect is classically associated with WPW?

Ebstein anomaly of the tricuspid valve.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Wolff-Parkinson-White syndrome (WPW): MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

Atrioventricular (AV) node highlighted on the Durgical 3D model