ECG criteria
- PQ (PR) interval less than 120 ms (less than 3 mm at 25 mm/s) in an adult, measured from the onset of the P wave to the onset of the QRS complex
- QRS complex of normal duration, less than 120 ms in adults
- No signs of manifest pre-excitation: no initial delta wave, no widening or morphological changes of QRS in limb and chest leads
- In sinus or lower atrial rhythm, the P wave usually precedes each QRS; the PR interval is measured in individual complexes and its variability is assessed (physiological variability is possible, e.g., in sinus arrhythmia). Junctional rhythm with retrograde conduction to the atria is a separate cause of an unusual P-QRS relationship rather than a typical criterion for the CLC/LGL pattern; P-wave morphology and axis are used for differential diagnosis of the rhythm source, not as an independent diagnostic criterion
- The ST segment and T wave are evaluated separately: secondary ST-T changes are not mandatory either with or without pre-excitation, and are not among the diagnostic criteria
- History may include documented paroxysms of supraventricular tachycardia (not mandatory for noting the finding); if present, the historical term LGL is applicable with a caveat regarding its limited modern significance
- When in doubt, repeat the recording and analyze multiple leads to rule out intermittent or minimal pre-excitation
What it looks like on ECG
The basis of the finding is a short PQ interval: less than 120 ms (less than 3 mm at a speed of 25 mm/s). It is measured from the onset of the P wave to the onset of the QRS complex in the lead where both points are most clearly visible; this is not necessarily II or V1 — the lead is chosen based on recording quality, and when in doubt, multiple leads and a repeat ECG are compared.
The key point is the absence of signs of manifest pre-excitation on the given tracing: QRS is narrow (less than 120 ms), there is no initial delta wave (a sloping, delayed initial upstroke/downstroke), no QRS widening, and no regular morphological changes in limb and chest leads. Manifest pre-excitation usually presents with a delta wave, alteration of the initial part of QRS, and often QRS ≥ 120 ms; PR is often shortened in this case but may be normal with minimal pre-excitation. Therefore, the absence of these signs on a single ECG only indicates the absence of overt pre-excitation at the time of recording and does not rule out intermittent or minimally expressed pre-excitation.
The P wave must be assessed separately to determine the source of the rhythm. A sinus P wave is usually positive in I, II, and aVF, negative in aVR, and often biphasic in V1. This morphology argues against junctional or lower atrial rhythm, where a short PQ is explained by the proximity of the impulse source to the ventricles rather than accelerated AV conduction. Axis deviation and unusual P morphology suggest a lower atrial or other ectopic rhythm.
| Parameter | Normal | Short PQ (CLC/LGL pattern) |
|---|---|---|
| PQ | 120–200 ms | < 120 ms |
| QRS | < 120 ms | < 120 ms, no delta wave |
| P wave | present, constant morphology | requires assessment of the rhythm source |
The ST segment and T wave are unchanged in most cases, but their normal appearance is not a diagnostic criterion and does not rule out concealed pre-excitation. Outside of a tachycardia episode (if documented), the ECG may appear almost normal except for the shortened PQ.
Mechanism
Historically, the shortening of PQ in this pattern was explained by accelerated conduction through the AV node and/or the existence of nodoventricular or atrionodal fibers (specifically, hypothesized James fibers) that partially bypass the zone of physiological delay in the AV node. This hypothesis is not a proven and universally accepted mechanism: a specific anatomical substrate is not confirmed in the majority of patients with a short PQ, and nodoventricular pathways belong to separate, electrophysiologically distinct variants of pre-excitation.
In most patients, it is more correct to speak simply of a short PQ interval without signs of manifest pre-excitation, without tying it to a specific anatomical pathway. The presence of a short PQ by itself does not allow predicting the mechanism of tachycardia if it occurs: it could be AV nodal reentrant tachycardia, AV reentrant tachycardia via a concealed accessory pathway, or another form of supraventricular tachycardia. The mechanism is established by ECG during the episode and, if necessary, an electrophysiological study, rather than assumed solely from the resting PQ duration.
Causes
- Variant of normal: isolated shortening of PQ in healthy individuals without structural heart disease and without clinical manifestations
- Historically hypothesized but unproven anatomical features of AV conduction in the majority of patients (accelerated nodal conduction, nodoventricular/atrionodal fibers)
- Increased sympathetic tone, tachycardia, childhood and young adulthood — conditions where PQ is physiologically shorter
- Association with paroxysms of supraventricular tachycardia in a subset of patients (mechanism is established separately, not assumed automatically)
Differential diagnosis
- WPW syndrome (manifest pre-excitation) — typically features a delta wave, alterations in the initial part of QRS, and often a shortened PR; with minimal pre-excitation, these signs may be less pronounced, and PR and QRS may be within normal limits. A narrow QRS without a delta wave on the given tracing argues against overt pre-excitation, but does not rule out its intermittent or minimal variant.
- Isolated short PQ in an asymptomatic person — a finding without documented tachyarrhythmias; the historical term LGL was applied when combined with confirmed SVT, but in modern classifications, it is not an independent diagnosis whether tachycardia is present or absent.
- Accelerated junctional rhythm — the P wave is absent, inverted, or not linked by a constant interval to QRS, whereas in the discussed pattern during sinus or lower atrial rhythm, the P wave precedes each QRS.
- Lower atrial ectopic rhythm — short PQ due to the proximity of the ectopic focus to the AV node; the P wave differs in shape and axis from the sinus P wave.
- AV block with an escape junctional rhythm and retrograde atrial capture — the retrograde P wave may be located before, within, or after QRS; requires analysis of the P-QRS relationship rather than isolated measurement of the PQ interval.
Clinical significance and management
An isolated short PQ without signs of manifest pre-excitation is not an established marker of increased risk of sudden cardiac death and does not require risk stratification by analogy with WPW. This does not mean that risk is completely ruled out in any context — it is determined by the clinical picture: symptoms, family history of sudden death, presence of structural heart disease, and documented arrhythmias, rather than the mere fact of PQ shortening.
The physician should: confirm that QRS is truly narrow and contains no delta wave (when in doubt, compare with old ECGs, repeat the recording, check speed and calibration); clarify the history of paroxysmal palpitations; determine the rhythm source from P-wave morphology. In symptomatic, recurrent, or clinically significant supraventricular tachycardia, consultation with an arrhythmologist is indicated, and depending on the suspected mechanism, frequency, and impact on quality of life, discuss an electrophysiological study and catheter ablation — the decision is not made automatically based on the fact of a short PQ. An asymptomatic finding without documented tachyarrhythmias is not specifically treated and is limited to observation.
Common interpretation errors
- Using the diagnosis of "CLC syndrome" as an established nosological entity confirming a specific electrophysiological substrate.
- Equating the finding with WPW solely based on a short PQ without careful evaluation of QRS for a delta wave across multiple leads.
- Attributing an obligatory mechanism of AV nodal reentrant tachycardia to a short PQ without documenting the arrhythmia itself.
- Overlooking a lower atrial rhythm as the cause of a short PQ due to inattention to P-wave morphology and axis.
- Ignoring the possibility of intermittent or minimal pre-excitation on a single normal tracing.
1. Which feature distinguishes overt pre-excitation (WPW) from a short PQ interval without pre-excitation?
Overt pre-excitation produces a delta wave and QRS widening due to direct ventricular involvement via an accessory pathway; in its absence, the QRS remains narrow regardless of the PQ duration.
2. What is the threshold value of the PQ interval for defining its shortening in an adult?
Normal PQ in adults is 120–200 ms; shortening is defined as a value less than 120 ms (less than 3 mm at 25 mm/s).
3. What determines the clinical risk in a patient with an isolated short PQ without signs of overt pre-excitation?
Isolated PQ shortening without signs of pre-excitation is not a proven independent risk marker; the entire clinical context matters, including documented tachyarrhythmias.
Frequently asked questions
How does a short PQ with a narrow QRS (LGL) differ from WPW?
With a typical overt pre-excitation pattern (WPW), there is a delta wave, alterations of the initial part of the QRS, and often a shortened PR; with minimal pre-excitation, these signs may be subtle. With a short PQ and no delta wave, there are no signs of overt pre-excitation on the given ECG, though this does not rule out an intermittent variant, and the historical term LGL does not confirm the existence of a separate mechanism or conduction pathway.
Is «LGL syndrome» dangerous?
Isolated short PQ without signs of overt pre-excitation is generally not associated with indications for sudden death prevention, unlike WPW. Clinical risk is assessed comprehensively: taking into account symptoms, structural heart disease, and documented arrhythmias, rather than PQ duration alone.
Should an incidentally discovered short PQ without symptoms be treated?
No, an incidental finding without documented tachyarrhythmias is not treated; observation and patient education are sufficient.
What mechanism underlies PQ shortening in this pattern?
Historically, accelerated AV nodal conduction and/or the presence of nodoventricular or atrionodal fibers were hypothesized, but a specific substrate has not been proven in most patients. It is more accurate to refer to a short PQ without signs of overt pre-excitation, without attributing it to a specific anatomical pathway.
What to do if a patient with a short PQ has episodes of palpitations?
It is necessary to document tachycardia on an ECG during an episode, determine its mechanism (AVNRT, AVRT via a concealed pathway, or another form of SVT), and in case of symptomatic or recurrent arrhythmia, refer the patient for an arrhythmologist consultation to consider an electrophysiological study and catheter ablation.
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Related terms
More in the section «Ventricular pre-excitation»
Sources
- Orlov, V.N. «Electrocardiography Guide»
- Hampton J.R. «The ECG Made Easy»
- Surawicz B., Knilans T. «Chou's Electrocardiography in Clinical Practice»
- AHA/ACCF/HRS Recommendations for the Standardization of the Electrocardiogram, 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.