ECG criteria
- PQ interval < 120 ms in adults (during sinus rhythm)
- Delta wave — a slurred initial deflection of the QRS; its duration is variable and not used as an independent mandatory threshold, but in pronounced pre-excitation, it typically occupies about 20–40 ms
- QRS is usually ≥ 120 ms in noticeable pre-excitation, with an initial delta wave (fusion complex); with minimal or intermittent pre-excitation, the QRS may be of normal width
- Secondary ST-segment and T-wave changes, discordant with the direction of the delta wave and QRS
- Findings may be non-sustained (intermittent) — visible on one recording and absent on another
- Pre-excitation may be constant or intermittent; in the absence of antegrade conduction, the delta wave is not recorded. A concealed accessory pathway conducts only retrogradely and does not cause manifest pre-excitation, but it can be the substrate for AV re-entrant tachycardia. The diagnosis and properties of the pathway are assessed using serial ECGs, monitoring, and, if necessary, an EPS.
What it looks like on ECG
The classic triad: short PQ (less than 120 ms), delta wave, and wide QRS. The delta wave is a gradual, slurred transition from the P wave to the main body of the QRS, reflecting the slow propagation of excitation through the myocardium from the insertion site of the accessory pathway, as opposed to rapid conduction through the His-Purkinje system. The QRS complex represents a fusion of two wavefronts — early via the accessory pathway and normal via the AV node; therefore, its morphology and width depend on the relative contribution of both pathways. With pronounced pre-excitation, the QRS is usually widened to ≥ 120 ms; with minimal or intermittent pre-excitation, the QRS width may remain normal, and width alone is not an obligatory absolute criterion.
The ST segment and T wave are often discordant relative to the delta wave and the main QRS deflection — these are typically secondary changes; however, the presence of pre-excitation does not rule out ischemia, and clinical symptoms along with dynamic changes should be evaluated separately. The degree of pre-excitation (and the prominence of all features) can vary from cycle to cycle and depends on autonomic tone, AV nodal conduction, and the location of the accessory pathway.
| Element | Parameter |
|---|---|
| PQ | < 120 ms |
| QRS | usually ≥ 120 ms with pronounced pre-excitation, delta wave |
| ST-T | discordant with QRS, predominantly secondary |
With intermittent pre-excitation, one recording may show normal narrow complexes, while another shows overt signs of pre-excitation. Such an intermittent pattern is usually a marker of lower risk for rapid antegrade conduction via the accessory pathway during atrial fibrillation, but does not completely rule out risk.
Mechanism
Normally, the only pathway from the atria to the ventricles is the AV node, which delays the impulse and protects the ventricles from excessively frequent stimulation. In pre-excitation syndrome, there is an additional bundle of muscle fibers (accessory pathway) connecting the atrium and ventricle directly, bypassing the AV node. Conduction through it is faster, but it originates not from the specialized conduction system, but from ordinary myocardium, so early ventricular activation propagates slowly — this forms the delta wave. The rest of the ventricles are activated normally via the His-Purkinje system, and the resulting QRS is the result of the fusion of two wavefronts. The presence of an accessory pathway creates an anatomical substrate for impulse re-entry and paroxysmal tachycardias.
Causes
- Congenital presence of an accessory atrioventricular pathway (Kent bundle and its variants)
- Association with congenital heart defects — particularly characteristic of association with Ebstein's anomaly, often with multiple accessory pathways
- Pre-excitation may occur in PRKAG2 syndrome and other rare glycogen storage diseases; standard hypertrophic cardiomyopathy by itself is not considered a typical cause of multiple accessory pathways
- Familial forms (genetic variants described)
- Isolated finding in healthy individuals without structural heart disease
Differential diagnosis
- Bundle branch block — QRS is wide, but PQ is not shortened, there is no delta wave, and typical block morphology is present in V1 and V5–V6
- The historical term Lown-Ganong-Levine (CLC syndrome) is no longer considered an independent proven syndrome: a short PQ with a narrow QRS without a delta wave does not prove the presence of an accessory pathway and may be a normal variant
- Inferior or posterior myocardial infarction — the delta wave in leads II, III, and aVF is sometimes mistaken for a pathological Q wave; differentiated by the presence of a short PQ and discordant rather than ischemic ST-T changes
- Hypertrophic cardiomyopathy with pseudo-infarction Q waves — no PQ shortening
- Mahaim fibers — an atypical variant with a different location and electrophysiological properties of the accessory pathway; PQ may be normal
Clinical significance and management
The ECG finding alone (asymptomatic pre-excitation) requires risk stratification: determining whether there is a history of tachycardia or syncope episodes. WPW syndrome is manifest pre-excitation combined with symptomatic tachyarrhythmia associated with the accessory pathway (primarily AV re-entrant tachycardia or pre-excited AF); in the absence of symptoms, it is more correct to use the term asymptomatic ventricular pre-excitation pattern rather than WPW syndrome. In symptomatic arrhythmia, referral to an arrhythmia specialist is indicated for an electrophysiological study and consideration of catheter ablation of the accessory pathway. The main danger is the development of atrial fibrillation with rapid antegrade conduction over the accessory pathway: a short effective refractory period of the pathway can lead to a very high ventricular rate and transformation into ventricular fibrillation. A separate mechanism of wide-complex tachycardia is antidromic AV re-entrant tachycardia, in which the impulse travels antegradely via the accessory pathway and retrogradely through the AV node.
In AF with pre-excitation, adenosine, digoxin, verapamil, diltiazem, beta-blockers, and intravenous amiodarone are contraindicated — these drugs slow conduction through the AV node and facilitate conduction through the accessory pathway. The physician must recognize such AF (irregular wide QRS with changing morphology and high heart rate). In hemodynamic instability, immediate synchronized cardioversion is indicated; in stability, a drug acting on the accessory pathway (e.g., procainamide according to local protocol) or cardioversion is indicated.
Common interpretation errors
- Missing the delta wave due to low amplitude or intermittent pre-excitation
- Interpreting the delta wave in inferior or lateral leads as a pathological Q wave (pseudo-infarction pattern)
- Diagnosing a bundle branch block in wide QRS without evaluating the PQ interval
- Prescribing AV node-blocking drugs in AF with pre-excitation due to failure to recognize the wide irregular rhythm as such AF
- Confusion with the historical CLC syndrome, where true ventricular pre-excitation is not proven
1. Which interval is shortened in ventricular pre-excitation syndrome?
The accessory pathway bypasses the delay in the AV node, so the ventricles are activated prematurely — the PQ interval is shortened.
2. What forms the delta wave on the ECG?
The accessory pathway inserts into the ordinary ventricular myocardium, where conduction is slower than through the specialized conduction system, producing a gradual onset of the QRS.
3. Which medications are contraindicated in atrial fibrillation with pre-excitation?
AV nodal blockade can increase the proportion of conduction through the accessory pathway and sharply accelerate the ventricular response, increasing the risk of ventricular fibrillation.
Frequently asked questions
What is the difference between pre-excitation syndrome and WPW syndrome?
Pre-excitation syndrome is an ECG finding (short PQ, delta wave, wide QRS) regardless of symptoms. WPW syndrome refers to manifest pre-excitation combined with symptomatic tachyarrhythmia associated with the accessory pathway; without symptoms, the term "asymptomatic ventricular pre-excitation pattern" is used.
Is asymptomatic pre-excitation dangerous?
The risk is lower than in the symptomatic variant, but not zero. The decision on further evaluation (including assessment of accessory pathway properties) is made by an arrhythmologist, taking into account age, profession, and comorbid factors.
How to distinguish a delta wave from a pathological Q wave?
In pre-excitation, the PQ interval is shortened, and the initial deflection of QRS is slurred, merging into the main complex without a clear border. In myocardial infarction, the PQ interval is normal, and pathological Q/QS waves are evaluated by duration, depth, ratio to R in adjacent leads, and ST-T dynamics. When in doubt, comparison with previous ECGs, imaging methods, and clinical context are helpful.
Why shouldn't AV nodal blocking drugs be administered in AF with pre-excitation?
These drugs slow conduction through the AV node, but not through the accessory pathway. This can increase the proportion of conduction via the accessory pathway and sharply accelerate the ventricular response, increasing the risk of progression to ventricular fibrillation.
Can pre-excitation disappear on different ECGs of the same patient?
Yes, this is called intermittent pre-excitation and reflects the variable contribution of the accessory pathway depending on autonomic tone and AV nodal conduction. This is usually a marker of a lower risk of rapid antegrade conduction during AF, but does not completely rule it out.
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Related terms
More in the section «Ventricular pre-excitation»
Sources
- Goldberger's Clinical Electrocardiography, latest edition
- Surawicz, Knilans. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- AHA/ACCF/HRS Recommendations for the Standardization of ECG, 2009
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.