Pre-excitation Syndromes, WPW Pattern – ECG

1. Overview: what is ventricular pre-excitation?

Ventricular pre-excitation occurs when an electrical impulse reaches part of the ventricular myocardium earlier than it would through the normal atrioventricular (AV) conduction system. In the usual Wolff–Parkinson–White (WPW) substrate, an accessory atrioventricular pathway provides a direct connection between atrial and ventricular myocardium, allowing some activation to bypass the AV node and His–Purkinje system.

WPW pattern describes the characteristic resting ECG appearance of manifest pre-excitation. WPW syndrome is generally used when manifest pre-excitation is accompanied by a documented or clinically relevant tachyarrhythmia. The terms should not be treated as interchangeable when describing an asymptomatic ECG finding.

Core ECG recognition: a short PR interval, a slurred initial QRS upstroke or downstroke (delta wave), and a widened or otherwise altered QRS complex in a patient with manifest pre-excitation. The degree of QRS widening depends on how much ventricular activation occurs through the accessory pathway versus the normal conduction system.

Pre-excitation may be persistent, intermittent, subtle, or absent on a particular tracing. A normal sinus-rhythm ECG does not exclude a concealed accessory pathway, which conducts only retrogradely and may still participate in AV re-entrant tachycardia (AVRT).

2. Electrophysiology and accessory-pathway physiology

Normal AV conduction versus pre-excitation

In normal conduction, atrial impulses pass through the AV node, His bundle, bundle branches, and Purkinje network before activating the ventricles. AV nodal conduction produces the physiological delay represented by the PR interval. An accessory pathway (AP) is a separate myocardial connection that bypasses some or all of this AV nodal delay.

Normal conduction

Atrial activation is followed by AV nodal delay and then rapid, coordinated ventricular activation through the His–Purkinje system. The PR interval and QRS morphology are usually within normal limits.

Manifest pre-excitation

Early activation spreads from the ventricular insertion of the AP into adjacent myocardium. This initial, relatively slow myocardial activation produces the delta wave; subsequent activation through the normal conduction system fuses with it.

Accessory-pathway conduction properties

Bidirectional: conducts antegradely from atrium to ventricle and retrogradely from ventricle to atrium; many pathways have this property.
Retrograde-only (concealed): does not pre-excite the ventricles during sinus rhythm, so the resting ECG may be normal; it can nevertheless form the retrograde limb of orthodromic AVRT.
Antegrade-only: conducts towards the ventricle but not retrogradely; this is uncommon.

Pathways may be left-sided, right-sided, septal, or multiple. Their location and conduction properties influence the degree and direction of initial ventricular activation, the surface ECG appearance, and the potential re-entry circuit.

Why tachycardia occurs

In AVRT, the AV node–His–Purkinje system and the accessory pathway form a re-entry circuit. In orthodromic AVRT, conduction travels antegradely through the AV node and His–Purkinje system and returns retrogradely through the AP; the tachycardia QRS is usually narrow unless aberrant conduction is present. In antidromic AVRT, antegrade conduction travels down the AP and retrograde conduction returns through the AV node or another pathway; the tachycardia is typically wide-complex and fully pre-excited.

Atrial fibrillation may also conduct rapidly to the ventricles through an antegradely conducting AP. Because the AP may lack the rate-limiting properties of the AV node, very short ventricular cycle lengths can occur and may precipitate ventricular fibrillation.

3. Characteristic ECG features in sinus rhythm

Interpret the three core findings together rather than diagnosing WPW from a short PR interval alone.

ECG feature	Typical finding	Interpretation
Rhythm	Often sinus rhythm	Sinus P waves usually precede the pre-excited QRS complexes; pre-excitation can also coexist with other atrial rhythms.
PR interval	Short, typically ≤120 ms	Part of ventricular activation begins before the usual AV nodal–His pathway would activate it.
Delta wave	Slurred initial upstroke or downstroke of QRS	Represents early, relatively slow myocardial activation through the AP.
QRS duration	Usually widened; ESC description uses >120 ms	Fusion of early AP-mediated activation with later normal conduction alters the QRS onset and overall duration.
ST segment and T wave	Often secondary, discordant repolarization changes	May be directed opposite to the dominant QRS vector and can mimic primary ST–T pathology.

Threshold note: the supplied LITFL educational article describes QRS prolongation as greater than 110 ms, whereas the 2019 ESC SVT guideline describes the typical WPW ECG as PR ≤120 ms, a delta wave, and QRS >120 ms. Use the full morphology and clinical context; do not make the diagnosis depend on a borderline QRS-duration value alone.

Pseudo-infarction and pseudo-hypertrophy patterns

Abnormal initial ventricular activation can produce negative delta waves that resemble pathological Q waves, or prominent R waves in right precordial leads. Secondary repolarization changes may resemble ventricular hypertrophy or ischemia. These appearances are sometimes termed pseudo-infarction or pseudo-hypertrophy patterns. They should prompt careful evaluation of the entire ECG and clinical context rather than an automatic diagnosis of infarction or chamber hypertrophy.

Actual ECG examples from the supplied PDF

TYPE A · ADULT ECG

Figure 1. Type A WPW pattern with a dominant R wave in V1

Original 12-lead ECG, type A WPW: short PR, delta waves, broad QRS, dominant R in V1, right precordial T-wave inversion — Source: *Pre-excitation syndromes(1).pdf*, page 6 (Example 1; original LITFL ECG image reproduced in the supplied PDF).

Interpretation: the tracing is described in the source as sinus rhythm with a very short PR interval, broad QRS complexes, and a slurred initial QRS upstroke. A dominant R wave in V1 supports the historical type A pattern, commonly associated with a left-sided AP.

Additional clues: right precordial T-wave inversion may reflect secondary repolarization, while a negative delta wave in aVL can simulate a lateral infarction Q wave. Do not diagnose RV hypertrophy or prior infarction from these features in isolation.

TYPE A · SECOND EXAMPLE

Figure 2. Another type A pre-excitation tracing

Original 12-lead ECG showing type A WPW with dominant R in V1 and right precordial T-wave inversion — Source: *Pre-excitation syndromes(1).pdf*, page 7 (Example 2).

Interpretation: the supplied source identifies a left-sided accessory pathway pattern, with a dominant R wave in V1 and right precordial T-wave inversion. Compare the QRS onset across multiple leads to identify the delta wave rather than relying on a single lead.

TYPE B · ADULT ECG

Figure 3. Type B WPW pattern with a dominant S wave in V1

Original 12-lead ECG showing type B WPW, short PR interval, delta waves and dominant S wave in V1 — Source: *Pre-excitation syndromes(1).pdf*, page 7 (Example 3).

Interpretation: the source describes a short PR interval, delta waves, and a dominant S wave in V1, historically called type B WPW and associated with a right-sided AP pattern. Inferior-lead and lateral precordial repolarization changes can mimic LV hypertrophy.

TYPE B · SECOND EXAMPLE

Figure 4. Right-sided AP pattern with pseudo-infarction Q waves

Original ECG demonstrating right-sided accessory pathway pattern and negative delta waves in leads III and aVF — Source: *Pre-excitation syndromes(1).pdf*, page 8 (Example 4).

Interpretation: negative delta waves in leads III and aVF are described as simulating Q waves of a prior inferior myocardial infarction. The historical type A/type B labels are broad pattern descriptions, not a substitute for a validated accessory-pathway localization algorithm or electrophysiology study.

Paediatric ECGs: subtle pre-excitation

Pre-excitation may be less obvious in children. QRS duration may not look markedly prolonged, and age-related QRS patterns can complicate pathway-side inference. Assess the PR interval in an age-appropriate context and look carefully for slurring at the beginning of the QRS in several leads.

PAEDIATRIC · 5 YEARS

Figure 5. Subtle WPW features in a 5-year-old child

Original paediatric ECG from a 5-year-old showing subtle short PR and delta waves — Source: *Pre-excitation syndromes(1).pdf*, page 9 (Example 5).

Source-described findings: the PR interval is short for age; QRS complexes are not strikingly broad, but the upstroke of R waves is slurred, particularly in II, III, aVF and V4. The source notes that RSR′ with T-wave inversion in V1–V2 may be age-related and that aVL pseudo-infarction Q waves can occur.

PAEDIATRIC · 7 YEARS

Figure 6. Pre-excitation in a 7-year-old child

Original paediatric ECG from a 7-year-old child showing mild QRS widening, delta waves and a pseudo-infarction pattern — Source: *Pre-excitation syndromes(1).pdf*, page 10 (Example 6).

Source-described findings: slight QRS widening and delta waves are more evident than in the younger child; pseudo-infarction Q waves in aVL are again noted. The source cautions that a dominant R wave in V1 may be normal for age, making left-versus-right AP inference difficult.

4. A systematic approach to the ECG

Use a repeatable sequence. Confirm the tracing is technically adequate, then establish whether the short PR and QRS morphology are truly consistent with manifest pre-excitation.

Check calibration and lead placement. Confirm standardization (commonly 25 mm/s and 10 mm/mV unless otherwise stated), inspect artefact, and verify precordial lead placement.
Determine the rhythm. Identify sinus P-wave morphology and regularity. Do not assume every pre-excited tracing is sinus rhythm.
Measure the PR interval. Measure from the onset of the P wave to the earliest onset of ventricular depolarization. A PR ≤120 ms supports pre-excitation when accompanied by a delta wave.
Inspect the first 40–60 ms of the QRS. Search for a slurred or notched initial upstroke/downstroke in more than one lead. This is the delta wave and is the key morphological clue.
Assess QRS duration and morphology. Determine whether the QRS is widened or altered by fusion. Evaluate the dominant QRS vector, including V1 and the inferior leads, but avoid overconfident pathway localization from type A/B labels.
Review ST segments and T waves. Look for secondary discordant repolarization changes. Consider whether apparent Q waves, ST–T abnormalities, or voltage criteria could be consequences of pre-excitation.
Look for intermittent pre-excitation. Compare beats and prior ECGs. Abrupt, complete loss of pre-excitation during exercise or ambulatory monitoring can be a low-risk marker, but it does not replace clinical risk assessment.
Integrate the clinical context. Ask about palpitations, syncope, documented SVT/AF, family history of sudden death, structural heart disease, and high-risk occupation or competitive sport.
Write a structured conclusion. State rhythm, presence/absence of manifest pre-excitation, the core ECG features, any secondary repolarization changes, and whether urgent clinical assessment is indicated.

Suggested reporting phrase: “Sinus rhythm with manifest ventricular pre-excitation: short PR interval, delta wave and widened/altered QRS morphology, consistent with a WPW pattern. Correlate with symptoms and arrhythmia history; consider electrophysiology assessment according to clinical risk.”

5. Accessory-pathway patterns and related entities

Historical type A and type B WPW patterns

Historical pattern	Typical surface clue described in the supplied source	Traditional association	Important limitation
Type A	Dominant R wave in V1; positive delta wave across precordial leads may be seen	Often left-sided AP	Not a definitive localization method; normal variants and fusion alter morphology.
Type B	Dominant S wave / negative delta in V1–V2	Often right-sided AP	Not a definitive localization method; use validated algorithms and EP study when clinically indicated.

Concealed accessory pathway

A concealed pathway conducts retrogradely only. Since it does not activate the ventricles early during sinus rhythm, the resting ECG does not show a delta wave or the classic WPW pattern. It may nevertheless support orthodromic AVRT. A normal resting ECG therefore does not rule out an accessory pathway in a patient with a compatible tachycardia history.

Lown–Ganong–Levine (LGL): historical and disputed terminology

The supplied PDF describes the proposed LGL pattern as a short PR interval with normal QRS morphology and no delta wave, historically attributed to James fibres. It also states that the entity's existence is disputed and that the term should not be used without paroxysmal tachycardia. In contemporary clinical practice, a short PR with a narrow QRS should be described and investigated on its own merits rather than automatically labelled as a distinct LGL syndrome.

Original ECG described in the supplied source as a possible Lown-Ganong-Levine pattern, with very short PR, narrow QRS and no delta wave — Source: *Pre-excitation syndromes(1).pdf*, page 10 (Example 7). The original source labels this as a possible LGL example.

Mahaim-type pathways

The supplied source describes right-sided pathways connecting the AV node to the ventricle, fascicles to the ventricle, or atria to fascicles. The sinus-rhythm ECG may be normal; tachycardia may show a left bundle branch block (LBBB)-like morphology. The mechanism and exact pathway anatomy require specialist electrophysiological assessment.

6. Differential diagnosis

Alternative	Potential overlap	Clues against manifest WPW
Isolated short PR / enhanced AV nodal conduction	PR interval ≤120 ms	No convincing delta wave and no characteristic pre-excited QRS morphology. Assess rhythm and clinical context.
Junctional rhythm	Short or absent PR interval	Absent, inverted, or retrograde P waves; does not produce the typical delta wave from an atrioventricular AP.
Bundle branch block	Wide QRS complex	Usually lacks the short PR plus slurred initial QRS onset combination; look for characteristic BBB morphology.
Ventricular ectopy or ventricular rhythm	Wide QRS and abnormal initial forces	Premature timing, absent/independent P waves, capture/fusion beats, or rhythm context may distinguish it from sinus pre-excitation.
Prior myocardial infarction	Q-wave-like initial negative forces	Negative delta waves may mimic Q waves. Correlate with symptoms, serial ECGs, biomarkers and imaging rather than diagnosing infarction from morphology alone.
Ventricular hypertrophy	Prominent R waves or repolarization abnormalities	Pre-excitation itself can alter voltage and ST–T morphology; assess independent voltage/strain criteria and imaging when indicated.

In a wide-complex tachycardia, consider pre-excited tachycardia and ventricular tachycardia in the differential. A patient with known WPW can still develop VT; do not assume every wide-complex rhythm is supraventricular.

7. Clinical presentation and risk assessment

Patients may be asymptomatic or present with episodic palpitations, rapid regular tachycardia, dizziness, presyncope, syncope, or, rarely, cardiac arrest. The most concerning arrhythmia is atrial fibrillation conducting rapidly over an antegrade accessory pathway, potentially leading to ventricular fibrillation.

Features that warrant careful assessment

Documented symptomatic tachyarrhythmia, especially pre-excited AF.
Syncope suspected to be arrhythmic, or resuscitated cardiac arrest.
Very rapid pre-excited ventricular response during AF.
Competitive athletes or people in occupations where sudden incapacitation would endanger others (for example, professional pilots or drivers).
Family history or associated clinical features raising concern for inherited or structural disease.

Electrophysiological risk markers

The 2019 ESC guideline identifies high-risk invasive EP features including a shortest pre-excited RR interval during AF (SPERRI) ≤250 ms, accessory-pathway effective refractory period ≤250 ms, multiple accessory pathways, and inducible AP-mediated tachycardia. Abrupt and complete loss of pre-excitation during exercise testing or intermittent loss on ECG/ambulatory monitoring can indicate a lower-risk pathway, but non-invasive findings must be interpreted in context.

Clinical red flag — irregular wide-complex tachycardia: suspect pre-excited AF when an irregular, often very rapid rhythm has wide QRS complexes with beat-to-beat variation in morphology. This is a potentially life-threatening emergency and requires immediate monitored assessment by an appropriately trained team.

8. Clinical management principles

Management depends on symptoms, documented arrhythmia, pathway risk, and haemodynamic status. The following is an educational summary, not a patient-specific treatment protocol.

Symptomatic WPW or documented AP-mediated tachycardia

Refer for cardiology/electrophysiology assessment. In suitable patients, catheter ablation of the accessory pathway is a definitive treatment option and is recommended for pre-excited AF in the 2023 ACC/AHA/ACCP/HRS AF guideline.
Assess for associated structural or inherited disease when clinical findings suggest it; most pathways occur in otherwise structurally normal hearts, but associations exist.
Discuss the risks and benefits of EP study and ablation, including pathway location and procedural risks.

Pre-excited atrial fibrillation

Do not give AV-nodal blocking drugs in pre-excited AF. The 2023 ACC/AHA/ACCP/HRS guideline lists verapamil, diltiazem, amiodarone, digoxin, adenosine, and beta-blockers as contraindicated in AF with antegrade accessory-pathway conduction because they may promote preferential conduction over the pathway and precipitate ventricular fibrillation or haemodynamic deterioration.

Haemodynamic instability: immediate synchronized electrical cardioversion is recommended.
Haemodynamically stable: intravenous procainamide or ibutilide is recommended as a pharmacological cardioversion option in the 2023 AF guideline; management should occur with continuous monitoring and expert input.
Definitive prevention: electrophysiology study and accessory-pathway catheter ablation are recommended for patients with pre-excited AF.

Do not extrapolate the AV-nodal blocker prohibition to every rhythm in every patient with WPW. The acute rhythm diagnosis matters: treatment of a regular narrow-complex orthodromic AVRT is not the same as treatment of irregular pre-excited AF. If the rhythm is uncertain, seek expert support and manage the patient according to haemodynamic status and emergency protocols.

Asymptomatic pre-excitation

Risk stratification may include history, 12-lead ECG, ambulatory monitoring, exercise testing, and EP study. The 2015 ACC/AHA/HRS SVT guideline considers observation reasonable in selected asymptomatic patients; EP study and ablation may be reasonable in selected patients based on pathway risk and occupational context. Decisions should be individualized through shared decision-making.

9. Common pitfalls and diagnostic limitations

Calling any short PR “WPW”: a delta wave and altered QRS morphology are essential parts of the typical manifest pattern.
Missing subtle pre-excitation: inspect the earliest QRS deflection in multiple leads, particularly when QRS widening is mild.
Over-interpreting type A/type B: these are historical surface-pattern labels and do not reliably define the exact pathway location.
Misreading secondary repolarization: ST depression, T-wave inversion, and pseudo-Q waves may be secondary to abnormal activation, but acute coronary disease must still be considered when clinically suspected.
Assuming a normal ECG excludes an AP: concealed pathways and intermittent pre-excitation may not be visible on a single resting tracing.
Assuming intermittent loss proves zero risk: it can be reassuring, but risk assessment should incorporate the clinical scenario and the quality of the observed loss.
Misclassifying a tachycardia: distinguish regular orthodromic AVRT from irregular pre-excited AF; their acute management differs substantially.
Relying on automated interpretation: computer statements may miss subtle delta waves or mislabel pseudo-infarction patterns. Confirm manually.

10. ECG interpretation practice

Choose the best answer. The explanation appears only after you select an option.

Case 1 — Short PR and slurred QRS onset

A patient in sinus rhythm has a PR interval of 90 ms, a slurred initial QRS upstroke, and a QRS duration of 130 ms. Which interpretation best fits the ECG?

Case 2 — Irregular wide-complex tachycardia in a patient with WPW

A patient with a known WPW pattern develops a very rapid, irregular wide-complex rhythm with beat-to-beat variation in QRS morphology. Which acute approach is most appropriate?

Case 3 — Short PR without a delta wave

A resting ECG shows a short PR interval but a narrow QRS without a visible delta wave. Which statement is most accurate?

11. Summary and quick reference

Question	Key point
What defines typical manifest WPW pattern?	Short PR (≤120 ms), delta wave, and widened/altered QRS morphology.
What causes the delta wave?	Early ventricular activation through an accessory atrioventricular pathway.
What is WPW syndrome?	Manifest pre-excitation associated with clinically relevant tachyarrhythmia.
Can the resting ECG be normal with an AP?	Yes: concealed retrograde-only pathways and intermittent pre-excitation may not show a resting delta wave.
What is the major acute danger?	Pre-excited AF with rapid antegrade pathway conduction and potential degeneration to VF.
What must be avoided in pre-excited AF?	AV-nodal blockers, including adenosine, beta-blockers, diltiazem, verapamil, digoxin, and amiodarone.
What is definitive therapy for high-risk/symptomatic pathways?	EP assessment and catheter ablation when indicated.

Clinical take-home: diagnose manifest pre-excitation from the combination of a short PR, delta wave, and altered QRS. Recognize that pathway-mediated arrhythmias can be dangerous, especially pre-excited AF. Correct rhythm identification is essential because AV-nodal blocking drugs are contraindicated in pre-excited AF.

12. References and further reading

1. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. European Heart Journal. 2020;41(5):655–720. doi: 10.1093/eurheartj/ehz467.

2. Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Circulation. 2024;149:e1–e156. doi: 10.1161/CIR.0000000000001193. See recommendations on WPW and pre-excitation syndromes.

3. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Journal of the American College of Cardiology. 2016;67(13):e27–e115. doi: 10.1016/j.jacc.2015.08.856.

4. Burns E, Buttner R. Pre-excitation syndromes. Life in the Fast Lane (LITFL) ECG Library. Published March 1, 2021. Supplied PDF source used for the educational ECG examples and source-specific descriptions: Pre-excitation syndromes(1).pdf.

Image provenance: Figures 1–7 are unmodified ECG image assets extracted from the user-supplied PDF. The PDF appears to reproduce LITFL material. Attribution is retained, but possession of the PDF does not itself grant public redistribution rights; confirm the original image licence/permission before publishing these image assets on a public website.