ECG criteria
- In I, II, aVL, aVF, V4–V6: Q wave width ≥ 0.03 s and depth ≥ 0.1 mV (1 mm), or a QS complex in two contiguous leads (AHA/ACCF/HRS 2009)
- In V2–V3: a Q wave duration ≥ 0.02 s or a QS complex is considered pathological; the criterion is applied taking into account correct electrode placement and clinical context
- A QS complex in V1 is often nonspecific and may be a normal variant; by itself, it is not a criterion for prior MI
- Historical criterion (less standardized): Q depth ≥ 25% of the R wave amplitude in the same complex — used as an additional reference point, does not replace absolute thresholds
- Poor R wave progression in the chest leads is a nonspecific pattern sometimes seen after MI, but it is not an independent criterion for a scar: it requires comparison with previous ECGs, echocardiography, or MRI
- The ST segment is isoelectric; persistent ST elevation in leads with Q weeks to months after MI may indicate a post-infarction aneurysm or LV dyskinesia, but the diagnosis is confirmed by imaging
- The T wave may be inverted, flattened, or already normalized — by itself, it does not rule out a prior MI
- Changes are stable when comparing serial ECGs (distinguishing from the evolution of the acute stage)
What it looks like on ECG
The basis of diagnosis is a pathological Q wave (pathological Q) or a QS complex in leads reflecting the infarcted myocardial area. Quantitative criteria depend on the lead group:
| Lead | Criterion for pathological Q |
|---|---|
| I, II, aVL, aVF, V4–V6 | width ≥ 0.03 s and depth ≥ 1 mm, or QS, in two contiguous leads |
| V2–V3 | Q duration ≥ 0.02 s, or QS |
| V1 | A QS complex is possible as a normal variant and has no independent diagnostic weight |
A QS complex in V2–V3 or contiguous leads is a sign compatible with prior MI, but not direct proof of a transmural scar: an identical pattern can be caused by incorrect electrode positioning, bundle branch blocks, and other conditions.
Scar localization is approximate and determined much like in acute MI: anteroseptal — V1–V4, lateral — I, aVL, V5–V6, inferior — II, III, aVF, posterior — reciprocal changes in V1–V3 (tall R, ST depression) or direct signs in V7–V9. The exact correspondence of the Q wave to the anatomical zone is limited — interpretation depends on neighboring leads, the cardiac axis, and recording quality.
In an uncomplicated course, the ST elevation present in the acute phase usually diminishes and may eventually normalize completely, but the exact timeline is unpredictable: it depends on the size and localization of the MI, reperfusion, and the presence of dyskinesia or an aneurysm. Persistent ST changes require evaluation over time, correlation with clinical findings and imaging, rather than tying to a fixed timeframe. The T wave may remain inverted for years (chronic post-infarction inversion) or normalize — this does not change the diagnosis of prior MI if the Q wave persists. Sometimes the Q wave decreases or disappears over time (especially with small non-transmural necrosis, successful reperfusion, or hypertrophy of the opposite wall), so the absence of a Q wave does not rule out a history of prior MI.
Mechanism
The necrotic myocardial area is replaced by connective tissue (a scar), which is electrically inert and does not generate a depolarization vector. As a result, an electrode placed over the scar records not the local R wave, but potentials from the opposite (healthy) heart wall directed away from the electrode, creating an initial negative deflection — the pathological Q wave. The Q wave reflects a change in the sequence of depolarization and can be associated with a scar, but it does not reliably indicate transmurality and infarct size: pathological Q/QS waves occur with scars of various sizes and depths, and a Q wave may be absent in large transmural necrosis (especially after early reperfusion) and, conversely, appear in subendocardial damage or entirely non-ischemic conditions. The presence or absence of a Q wave is not used as a reliable way to differentiate between transmural and non-transmural infarction — imaging (echocardiography, MRI) is required to assess the size and depth of the damage.
Causes of pathological Q/QS and pseudo-infarction pattern
- Pathological Q waves may persist after any type of MI (ST-elevation and non-ST-elevation); their presence does not reliably determine the type of prior MI, transmurality, or necrosis size
- Post-infarction cardiosclerosis of any localization
- Myocarditis resulting in focal fibrosis (pseudo-infarction Q waves)
- Cardiomyopathies with prominent fibrosis (hypertrophic, dilated, infiltrative)
- Left ventricular aneurysm following a transmural anterior MI
- Mimics: surgical myocardial scars after cardiac surgery or ablation, incorrect electrode placement, bundle branch blocks, WPW syndrome — are not signs of prior MI, but produce a similar Q/QS pattern
Differential diagnosis
- Physiologic septal Q in I, aVL, V5–V6 — narrow (< 0.03 s) and shallow, reflects normal septal depolarization, does not grow over time
- Isolated QS or Q in III — a frequent normal variant in a vertical heart position; pathology is assessed using quantitative criteria, the electrical axis, and neighboring leads, rather than the formal presence or absence of Q in II
- WPW syndrome — the delta wave can mimic a Q wave due to a negative initial vector
- Hypertrophic cardiomyopathy — deep, narrow "pseudo-infarction" Q waves in inferolateral leads without a history of coronary artery disease
- Left bundle branch block — the absence of a normal septal R wave makes Q wave interpretation unreliable; Sgarbossa criteria are needed if acute ischemia is suspected
- Acute stage of MI — not always accompanied by overt ST/T evolution on available recordings; differentiation requires serial ECGs, clinical picture, and troponin, not just Q-wave stability
- Poor R wave progression without a distinct Q wave — a nonspecific pattern that may occur after MI, but is often related to electrode position, ventricular hypertrophy or dilation, COPD, conduction abnormalities, and other causes; it does not prove a scar and requires correlation with previous ECGs, echocardiography, or MRI
Clinical significance and management
A pathological Q/QS wave in the corresponding leads supports the diagnosis of prior MI, but is not exclusively specific for a scar: similar patterns are caused by cardiomyopathies, myocarditis, conduction disturbances, and technical recording artifacts, so the finding must be correlated with history, clinical presentation, and imaging data (echocardiography, MRI if necessary). When a Q wave is newly discovered without a known history of MI, the physician must: correlate with clinical findings and previous tracings, order an echocardiography to assess regional contractility and rule out an aneurysm, and consider an ischemic origin (history, risk factors) versus non-ischemic causes of the scar.
Persistent ST elevation in leads with an old MI may indicate a post-infarction aneurysm or dyskinesia, but this is an ECG presumption rather than an independent diagnostic criterion — confirmation requires imaging, primarily echocardiography; in the event of new symptoms (pain, shortness of breath, worsening heart failure), acute ischemia must be ruled out.
The mere fact of a prior MI does not require emergency actions, but serves as an occasion to assess LV ejection fraction and the ischemic etiology of the lesion. The decision to implant an ICD is made not based on the presence of a Q wave, but according to established criteria: LV ejection fraction value, heart failure symptoms, documented ventricular arrhythmias, time elapsed since MI, and adequacy of optimal medical therapy.
Common interpretation errors
- Mistaking a physiologic septal Q in I, aVL, V5–V6 for pathology without evaluating its width
- Automatically considering an isolated Q/QS in III as normal without evaluating duration, depth, axis, and clinical picture, or conversely — requiring an obligatory Q in II to recognize pathology in III and aVF
- Failing to account for the fact that the disappearance of a Q wave on repeat ECGs does not rule out a prior MI (remodeling, reperfusion)
- Confusing persistent ST elevation over an old Q wave (possible aneurysm) with an acute MI — evaluation of dynamics, clinical picture, and imaging is needed
- Interpreting Q in LBBB without additional criteria, although septal R is physiologically absent there
- Concluding about transmurality, MI type, or necrosis size based solely on the presence and depth of Q, as well as equating poor R-wave progression to a proven scar
1. Which ECG sign is most characteristic of a prior myocardial infarction?
Pathological Q in the appropriate leads, stable over time, supports the diagnosis of prior MI, although pseudoinfarction causes (cardiomyopathies, myocarditis, conduction abnormalities) must be ruled out and correlated with history and imaging.
2. Persistent ST elevation over the old pathological Q zone months after an infarction primarily requires:
Persistent ST elevation over the scar may be associated with LV aneurysm or dyskinesia, but it is not an independent diagnostic criterion—confirmation requires imaging, and acute ischemia must be ruled out if new symptoms appear.
3. How should an isolated Q wave in lead III be correctly interpreted?
Q in III is common with a vertical heart position, but the conclusion of pathology is made based on quantitative criteria and clinical context; the combination of pathological Qs in III and aVF may meet the criterion of two contiguous inferior leads even without Q in II.
Frequently asked questions
How to distinguish prior infarction from acute infarction on ECG?
In prior MI, the ST segment is usually on the isoelectric line and changes are stable when compared with serial tracings, which supports the diagnosis of an old scar. However, acute MI does not always produce noticeable ST/T dynamics on available recordings, and negative T waves are not specific to the acute stage alone. When an acute event is suspected, serial ECGs, high-sensitivity troponin with dynamic assessment, and the clinical picture are necessary.
Can the Q wave disappear after an infarction?
Yes, especially in small non-transmural necrosis or successful early reperfusion. The disappearance of Q over time is not uncommon and does not rule out a history of prior MI.
Is the pathological Q wave itself dangerous?
The Q wave itself is not dangerous; it is the electrical footprint of a scar. The danger is associated with reduced contractility, the risk of arrhythmias, and, in persistent ST elevation, a potential left ventricular aneurysm, which requires imaging confirmation.
Is treatment required when an old Q wave is discovered without symptoms?
No emergency measures are required, but echocardiography is needed to assess contractility and, if risk factors are present, further cardiological evaluation and arrhythmia risk stratification.
How do Q criteria in V2–V3 differ from other leads?
In V2–V3 the threshold is lower: a Q wave with a duration of ≥ 0.02 s or a QS complex is considered pathological, whereas most other leads (I, II, aVL, aVF, V4–V6) require a width of ≥ 0.03 s and a depth of ≥ 1 mm, or a QS complex, in two contiguous leads.
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Related terms
More in the section "Ischemia and Myocardial Infarction"
Sources
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
- Orlov V.N. Guide to Electrocardiography
- Hampton J. The ECG in Practice
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.