ECG criteria
- New or presumably new horizontal or downsloping ST depression ≥ 0.5 mm (0.05 mV) at the J point, measured relative to the isoelectric line (typically the TP segment; if that is altered, use a stable PR/PQ segment), in two contiguous leads; this criterion is non-specific and must be correlated with clinical presentation and prior ECGs.
- New symmetrical T-wave inversion ≥ 1 mm in leads with a dominant R wave supports ischemia (can be the only abnormality); T-wave flattening and asymmetrical inversion are non-specific and should only be evaluated in context and via serial changes.
- ST-T changes can be transient—appearing during pain/exertion and regressing at rest or after nitrates; this increases the probability of acute ischemia, but is not mandatory and does not differentiate unstable angina from NSTEMI.
- Comparison with a previous or pain-free ECG is mandatory in the diagnostic process—evolution is important, but its absence does not rule out the diagnosis.
- Persistent diagnostic ST elevation, typical of STEMI, is usually absent; transient ST elevation is possible and is a high-risk sign requiring immediate assessment for occlusion. Old pathological Q waves and preexisting intraventricular conduction disturbances do not rule out unstable angina; new conduction abnormalities require clinical-ECG evaluation, serial troponin testing, and a search for signs of acute occlusion.
- Deep symmetrical T-wave inversion in V2–V4 (Wellens' pattern) is a high-risk marker of probable proximal LAD lesion even without chest pain at the time of recording; it requires urgent expert evaluation and coronary angiography, but is not independent proof of anatomical stenosis.
- Widespread ST depression (often ≥ 6 leads) with ST elevation in aVR and/or V1 is a non-specific high-risk pattern of widespread subendocardial ischemia; it requires ruling out left main coronary artery disease, multivessel disease, and non-cardiac causes of oxygen supply/demand mismatch, rather than being considered an independent diagnostic criterion.
What it looks like on ECG
The primary sign is horizontal or downsloping ST-segment depression. There is no strict "lead = ischemic zone" mapping for ST depression: unlike ST elevation, depression can be diffuse, reciprocal, or reflect posterior wall ischemia. In widespread ST depression across multiple leads, especially when combined with ST elevation in aVR, it is necessary to evaluate the context, look for reciprocal changes, and record posterior leads V7–V9 if posterior ischemia is suspected. The magnitude of displacement is assessed at the J point relative to the isoelectric line—typically the TP segment; if altered, a stable PR/PQ segment can be used as a reference. Upsloping ST depression is less specific for ischemia, but not always benign: De Winter's pattern (upsloping ST depression with tall, symmetrical T waves in precordial leads) is a high-risk pattern of acute LAD occlusion and a potential equivalent of occlusive myocardial infarction; in the setting of ACS symptoms, it requires immediate contact with emergency invasive services and should not be interpreted as a routine variant of unstable angina.
The second frequent sign is new symmetrical T-wave inversion in leads with a dominant R wave; T-wave flattening and asymmetrical inversion are non-specific on their own and are evaluated only in context and through serial changes. Wellens' pattern deserves separate mention: a deep symmetrical negative T wave (Type B) or biphasic T wave (Type A) in V2–V4 with a preserved R wave and minimal ST elevation, recorded in the asymptomatic period following a pain episode, is a high-risk marker of likely proximal LAD disease.
ST-T evolution associated with pain increases the likelihood of acute ischemia and has prognostic value, but is not mandatory for diagnosis: changes may persist between episodes, and the ECG can be normal even in NSTEMI. Therefore, a single resting ECG recorded outside of an episode does not rule out the diagnosis, and comparing serial tracings is mandatory.
| Sign | Typical picture |
|---|---|
| ST | horizontal/downsloping depression ≥ 0.5 mm |
| T | inversion, flattening, biphasic |
| Dynamics | may be associated with pain, but is not mandatory |
| ST elevation | no persistent diagnostic elevation, transient elevation is possible |
Mechanism
A frequent mechanism is the rupture or erosion of an unstable atherosclerotic plaque with incomplete or transient thrombotic coronary occlusion, without sustained cessation of flow; dynamic spasm, embolism, and ischemia secondary to myocardial oxygen supply/demand mismatch without plaque rupture are also possible. The subendocardium is most vulnerable to reduced perfusion because it is the last to be supplied with blood and functions under the highest intramyocardial pressure. Subendocardial ischemia shifts the repolarization vector, which manifests as ST depression. The distinction between unstable angina and non-ST-segment elevation myocardial infarction is established not by the ECG pattern, but by serial high-sensitivity troponin testing: in unstable angina, there is no acute rise/fall above the 99th percentile, whereas in NSTEMI this dynamic is present alongside clinical or ECG signs of ischemia.
Causes
- Rupture or erosion of an unstable atherosclerotic plaque with mural thrombosis without total occlusion
- Dynamic coronary spasm in the setting of stenosing atherosclerosis
- Mismatch between oxygen demand and supply in the presence of fixed stenosis (severe anemia, tachyarrhythmia, hypertensive crisis, aortic stenosis): if such secondary ischemia is accompanied by an acute rise/fall in troponin, myocardial infarction is diagnosed—type 2 is assigned if the cause is a supply/demand mismatch without acute atherothrombosis.
Differential diagnosis
- STEMI: persistent ST elevation ≥ 1 mm in two contiguous limb leads or specific thresholds in V2–V3 (guidelines vary by sex/age: according to some sources, ≥ 2 mm in men ≥ 40 years and ≥ 2.5 mm in men < 40 years, ≥ 1.5 mm in women); reciprocal changes support the diagnosis of STEMI, but their absence does not rule it out.
- NSTEMI: the ECG picture may be identical, with the distinction established by serial troponin—an acute rise/fall above the 99th percentile with signs of ischemia.
- Benign (early) repolarization and non-specific ST-T changes: stable over time, unrelated to pain and lacking serial evolution.
- Left ventricular hypertrophy with systolic overload: downsloping ST depression and asymmetrical negative T waves in V5–V6, I, aVL accompanying voltage criteria for hypertrophy and unchanged by pain.
- Digitalis effect on ECG: scooping ST depression ("scooped" ST segment) regardless of pain symptoms.
- T-wave pseudonormalization: temporary normalization of a previously negative T wave during acute ischemia—a pitfall in serial monitoring.
Clinical significance and management
Unstable angina is an indication for hospitalization and risk stratification using scores (GRACE and similar). Per ESC 2023: an immediate invasive strategy is indicated for very high risk, an early strategy preferably within 24 hours for high risk, and for remaining patients, an invasive strategy during hospitalization depending on risk and clinical situation; the primary PCI window of "< 120 min" applies only to STEMI and its occlusion equivalents. The clinician must: obtain an ECG within the first 10 minutes of presentation, repeat the recording when symptoms change and at follow-up intervals, compare with baseline tracings, and determine serial troponin levels. Identification of Wellens' pattern requires avoiding stress testing and referring for early coronary angiography due to the risk of acute LAD occlusion. De Winter's pattern in the setting of ACS symptoms requires immediate contact with emergency cardiac/invasive services as a potential occlusive myocardial infarction, without waiting for standard non-ST-segment elevation ACS pathways. Widespread ST depression with ST elevation in aVR increases suspicion of multivessel disease or left main coronary artery stenosis, but is a non-specific pattern—alongside a coronary cause, anemia, tachyarrhythmia, hypoxia, and other conditions with oxygen supply/demand mismatch must be ruled out.
Common interpretation errors
- Relying solely on a normal resting ECG recorded outside of chest pain and ruling out ACS
- Failing to recognize Wellens' pattern as a sign of likely critical LAD disease, mistaking it for "non-specific T-wave changes"
- Consider upsloping ST depression always benign and ignore the de Winter pattern as a possible sign of acute occlusion
- Fail to compare the current ECG with previous tracings and miss dynamic changes
- Interpret T-wave pseudonormalization as an improvement without considering the clinical pain presentation
- Differentiate unstable angina from NSTEMI based on ECG findings rather than serial troponin
1. Which type of ST-segment depression is most specific for myocardial ischemia?
Horizontal and downsloping ST depressions are considered ischemic types, unlike the less specific upsloping depression.
2. How does unstable angina differ from non-ST-segment elevation myocardial infarction (NSTEMI) given a similar ECG presentation?
With an identical ECG presentation, the key distinction is the absence of an acute rise/fall in troponin above the 99th percentile in unstable angina versus the presence of such dynamics in NSTEMI.
3. What does the Wellens pattern in V2–V4 indicate?
Deep or biphasic negative T waves in V2–V4 with preserved R waves, recorded during an asymptomatic period, are a high-risk marker for probable proximal LAD disease.
Frequently asked questions
How does the ECG in unstable angina differ from NSTEMI?
The ECG picture can be identical: ST depression and/or T-wave inversion. The distinction is established via laboratory testing: in unstable angina, serial high-sensitivity troponin does not show an acute rise/fall above the 99th percentile, whereas in NSTEMI, there is acute myocardial injury with such dynamics alongside clinical, ECG, or imaging signs of ischemia.
Can the ECG be normal in unstable angina?
Yes, outside of a pain episode, the ECG often normalizes. A normal tracing does not rule out the diagnosis of either unstable angina or NSTEMI, which is why serial tracings correlated with the clinical pain presentation and troponin are essential.
What is the Wellens pattern and why is it important?
This is a specific pattern of deep or biphasic negative T waves in V2–V4 with a preserved R wave, recorded during an asymptomatic period following a pain episode. It indicates a probable critical lesion of the proximal left anterior descending (LAD) artery and requires early coronary angiography without stress testing.
Is primary PCI within 120 minutes required for unstable angina, as it is for STEMI?
No, this time window applies to STEMI and occlusion equivalents. For unstable angina and NSTEMI, risk stratification is applied: an immediate invasive strategy for very high risk, an early strategy within 24 hours for high risk, and for others, an invasive strategy during hospitalization based on the clinical situation.
What depth of ST depression is considered significant?
New or presumed new horizontal or downsloping ST depression ≥ 0.5 mm (0.05 mV) at the J-point relative to the isoelectric line in two contiguous leads is a suspicious but nonspecific sign of myocardial ischemia; it requires correlation with clinical presentation, previous ECGs, and the exclusion of alternative causes (hypertrophy, digitalis, chronic ST depression).
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Related terms
More in the section "Ischemia and Myocardial Infarction"
Sources
- Hampton J. The ECG in Practice, 6th ed.
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice, 6th ed.
- ESC Guidelines for the management of acute coronary syndromes, 2023
- Clinical Guidelines of the Russian Ministry of Health on Acute Coronary Syndrome Without ST-Segment Elevation
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.