The Wolff-Parkinson-White (WPW) pattern is the ECG of an accessory pathway: a strand of muscle across the ring between the atria and the ventricles that conducts faster than the AV node. Each sinus impulse reaches the ventricle beside the pathway early, and that patch depolarises slowly, cell to cell, before the node's impulse arrives and activates the rest normally. So the PR is short, the QRS starts with a slurred delta wave and is wide, and the ST and T turn away from the delta. The pathway here is left lateral, the commonest site, which makes V1 positive (type A). The pattern alone is usually harmless; it becomes WPW syndrome with palpitations or a tachycardia, and atrial fibrillation conducted down the pathway can turn into ventricular fibrillation.
Remember
- A short PR: under 120 ms.
- A delta wave: the QRS slurs up slowly before its fast part, so it is wide.
- The ST and T turn away from the delta: a secondary change, not ischaemia.
How to recognise it
The short PR, the delta wave and the wide QRS are the criteria of the 2015 ACC/AHA/HRS guideline on supraventricular tachycardia. The direction of the delta, read with an algorithm such as Arruda's, places the pathway.
Mechanism
The AV node is the only normal connection between the atria and the ventricles, and it holds every impulse back for about a tenth of a second. An accessory pathway is a second connection, made of ordinary muscle, that conducts without that delay. So the sinus impulse reaches the ventricle beside the pathway early.
There it meets working muscle, not the fast His-Purkinje network, and spreads slowly, cell to cell. That slow start is the delta wave. Meanwhile the impulse that took the normal route clears the AV node, enters the bundles and activates the rest of the ventricles quickly. The two fronts fuse: the QRS starts early and slowly, then finishes at normal speed. The short PR and the wide QRS are the same event measured twice, because the delta pulls the start of the QRS back into the PR. How much of the QRS the delta takes depends on how far ahead the pathway gets: a slower AV node gives it more, a faster one less.
The delta points away from where the pathway inserts. This pathway is on the left lateral wall, at the mitral ring, the commonest site. Its early front runs to the right and forwards, so V1 to V3 show a positive delta and a tall R, and aVL a negative delta.
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Where the pathway is: type A and type B
A positive delta and a dominant R in V1 point to a left-sided pathway, the old "type A". A negative delta in V1, with the precordial transition after V2, points to a right-sided one, "type B". Algorithms built on the delta's polarity in each lead, such as Arruda's, go further and name the site; the ablation map then confirms it. The left lateral mitral annulus is the commonest site, 30 to 58% of pathways; posteroseptal is next, about a quarter.
The pseudo-infarct
A negative delta can look like a pathological Q wave. Here aVL shows one, which can be misread as an old lateral infarct. A positive delta and tall R in V1 can be misread as a posterior infarct or as right ventricular hypertrophy. The short PR and the slur are what give it away.
Why the ST and T turn
The ventricle near the pathway depolarises first, so it also starts to repolarise first, and the ST and T turn away from the delta: inverted in V1 and III on this tracing. That is a secondary change and says nothing about ischaemia. When the pathway is ablated, the T can stay inverted for weeks as "T-wave memory".
Pattern, syndrome and hidden pathways
The pattern is the ECG alone. The syndrome is the pattern with symptoms from an arrhythmia the pathway carries. A pathway that conducts only backwards leaves the resting ECG normal and can still carry a tachycardia: a normal ECG does not rule one out. That is the pattern's value: it shows that a pathway exists and can conduct forwards, before the day that matters. Pre-excitation can also come and go from beat to beat. Delta waves that disappear at ordinary heart rates, or suddenly on exercise, suggest a pathway that cannot conduct fast.
The tachycardias
The commonest is orthodromic atrioventricular re-entry: down the AV node, back up the pathway. During it the delta disappears and the QRS is narrow. Atrial fibrillation, in about 6% of people with WPW, is the dangerous one: the pathway does not slow down as the node does, so it can pass impulses at rates the node would block. A shortest pre-excited R-R of 250 ms or less in atrial fibrillation, or a pathway refractory period under 240 ms at an electrophysiology study, marks a pathway that can lead to ventricular fibrillation.
Clinical impact
- Usually harmless alone: the pattern is found in 1 to 3 people per 1000, and the risk of sudden death with the pattern alone is about 0.1% a year.
- Tachycardia: the same pathway can carry a re-entrant tachycardia, usually narrow and regular (orthodromic AVRT). With symptoms it is WPW syndrome, and the risk of sudden death is about 0.8% a year.
- Sudden death: atrial fibrillation conducted down a fast pathway can reach the ventricles at over 250 per minute and degenerate into ventricular fibrillation. It can be the first sign.
Management
The pattern alone, no symptoms: assess the risk
Observation is reasonable. An exercise test that shows abrupt, persistent loss of the delta suggests a low-risk pathway; an electrophysiology study is reasonable for those in high-risk occupations or competitive sport, and ablation if the pathway proves high-risk.
Symptoms: ablate the pathway
Catheter ablation is the first choice for WPW syndrome: success is over 94% and complications under 1%. It removes both the re-entry circuit and the danger in atrial fibrillation.
Pre-excited atrial fibrillation: keep away from the AV node
No adenosine, verapamil, diltiazem, beta-blocker or digoxin: blocking the node sends more impulses down the pathway. Intravenous amiodarone is no longer recommended either: it can speed conduction down the pathway, and ventricular fibrillation has followed it. Give intravenous ibutilide or procainamide, with flecainide or propafenone as alternatives.
Unstable: synchronised cardioversion
Whenever a pre-excited tachycardia is poorly tolerated, or the diagnosis is uncertain.
Differential
Also a tall R in V1 with a wide QRS, but the PR is normal and the width is at the end: a late R′ and a broad terminal S in I and V6. In WPW the PR is short and the width is at the start.
A right-sided pathway gives an LBBB-like shape. The PR and the start of the QRS tell them apart: LBBB has a normal PR and no slur before a QRS that is slow throughout.
Ordinary atrial fibrillation is irregular and narrow. Conducted down an accessory pathway it is irregular, wide and very fast, and the QRS changes width from beat to beat.
Pre-excited atrial fibrillation is often called VT. VT is regular with one QRS shape; pre-excited atrial fibrillation is irregular and its complexes vary.
References
- Wolff-Parkinson-White syndrome: Diagnostic and management strategies — Cleveland Clinic Journal of Medicine, 2025
- 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia — Circulation, 2016
- 2019 ESC Guidelines for the management of patients with supraventricular tachycardia — European Heart Journal, 2020
- PACES/HRS Expert Consensus Statement on the Management of the Asymptomatic Young Patient with a Wolff-Parkinson-White (WPW, Ventricular Preexcitation) Electrocardiographic Pattern — Heart Rhythm, 2012
- Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome — Journal of Cardiovascular Electrophysiology, 1998