ECG criteria
- New ST elevation at the J point in ≥2 contiguous leads; thresholds depend on the lead, sex, and age. Anatomical localization by wall is used additionally for description, but does not replace the criterion of lead contiguity
- In V2–V3: ≥2.5 mm in men <40 years, ≥2 mm in men ≥40 years, ≥1.5 mm in women (any age) per AHA/ACCF/HRS 2009 and ESC guidelines
- In other standard leads (I, II, aVL, aVF, V4–V6): ≥1 mm in men and women
- In V7–V9 (posterior wall): ≥0.5 mm is sufficient to diagnose a STEMI equivalent
- In V3R–V4R (suspected right ventricular infarction): ST elevation from approximately 0.5 mm in the appropriate clinical context, specific threshold according to the applied guideline
- ST morphology (convex upward, upsloping with hyperacute T) is an ancillary sign, not a mandatory criterion
- Reciprocal ST depression in leads of the opposite wall increases specificity
- Temporal dynamics: development of pathological Q and/or negative T waves in subsequent hours to days is possible, but not mandatory
What it looks like on ECG
The key change is persistent ST-segment elevation from the isoelectric line. For STEMI criteria, elevation is measured at the J point; if its determination is technically difficult, a validated method of the specific standard is used and changes are compared with adjacent complexes and temporal dynamics. The elevation may be convex upward ("domed", "tombstoning" sign in severe ischemia) or upsloping transitioning into a hyperacute T wave — ST morphology helps in assessment, but by itself is not a mandatory diagnostic criterion.
The formal criterion is ST elevation in two or more contiguous leads; thresholds depend on the lead, sex, and age. Anatomical correlation with the myocardial wall is used additionally to describe localization, rather than as a replacement for the contiguity criterion:
| Wall | Leads |
|---|---|
| Septal | V1–V2 |
| Anterior | V3–V4 |
| Lateral | I, aVL, V5–V6 |
| Inferior | II, III, aVF |
| Posterior | V7–V9 (mirror image in V1–V3 — ST depression, tall R) |
| Right ventricle | V3R–V4R |
Threshold values for ST elevation in V2–V3 depend on sex and age (see criteria) — this is established in the 2009 AHA/ACCF/HRS recommendations for ECG standardization and used in ESC. In most other standard leads, the threshold is uniform at 1 mm, but separate, lower thresholds apply to right and posterior leads.
Often, simultaneous reciprocal ST depression is visible in vectorially opposite leads (e.g., depression in I, aVL during inferior STEMI) — this increases confidence in the ischemic nature of ST elevation rather than benign variants.
Over time (minutes to hours), T-wave inversion and development of a pathological Q wave may occur, but this is not a mandatory stage: the outcome depends on time, infarct size, and timely reperfusion. With rapid restoration of blood flow, early ST normalization and early appearance of negative T waves without Q-wave formation are possible.
Mechanism
STEMI is an ECG category, not proof of a specific anatomical substrate: ST elevation reflects acute ischemia (usually subepicardial or transmural), but can also occur with incomplete or transient occlusion, spasm, embolism, or dissection, and complete thrombotic occlusion is not always accompanied by classic ST elevation. In severe ischemia, ischemic cardiomyocytes lose their resting membrane potential and shorten their action potential unevenly across the wall thickness, creating an injury current between the epicardium and endocardium — this shifts the ST vector toward the affected epicardium, forming ST elevation in leads facing the ischemic zone and reciprocal depression in opposite leads. The magnitude and extent of ST elevation may correlate with the volume of ischemic myocardium, but also depend on the site of the lesion, coronary anatomy, collateral development, time from occlusion onset, already established reperfusion, and the electrical axis of the heart — therefore, ST height does not allow direct quantitative assessment of the area or depth of injury.
Causes
- Atherothrombotic coronary artery occlusion (plaque rupture/erosion with thrombosis) is the primary cause
- Coronary spasm (Prinzmetal's angina)
- Coronary embolism
- Coronary artery dissection (including spontaneous, SCAD)
- Stent thrombosis
- Pronounced supply-demand mismatch of oxygen in critical stenosis (Type 2 MI, rarely with ST elevation)
Differential diagnosis
- Early repolarization syndrome — concave ST elevation, stable over time, often with a notch on the descending limb of R, without reciprocal depression or dynamics
- Pericarditis on ECG — diffuse concordant ST elevation (not limited to a single wall), PR-segment depression; reciprocal ST depression in most leads is absent, but opposite changes in aVR and frequently in V1 (ST and PR depression) are typical
- Takotsubo cardiomyopathy — diffuse ST-T changes, deep negative T waves, mismatch with the blood supply zone of a single artery, absence of obstructive coronary occlusion on angiography (concomitant coronary disease is possible); diagnosis requires imaging and clinical context
- Hyperkalemia on ECG — tall peaked narrow T waves are typical, followed by PR prolongation, reduction/disappearance of P, and QRS widening; pseudoinfarct ST elevation is possible, but not a typical sign
- Infarction in left bundle branch block — Sgarbossa and modified Sgarbossa (Smith) criteria are used, as baseline QRS/ST morphology is altered
- Brugada type 1 pattern — domed ST elevation in V1–V2, but without reciprocal changes and without ACS clinical presentation
- Left ventricular hypertrophy with systolic overload — secondary ST-T changes, but ST elevation is usually minimal and discordant to deep S waves
Clinical significance and management
STEMI is an indication for immediate reperfusion: primary percutaneous coronary intervention (PCI) within 120 minutes from diagnosis to guidewire crossing. If such a delay is expected to exceed 120 minutes, symptoms typically started ≤12 hours ago, and there are no contraindications to fibrinolysis, immediate fibrinolysis is performed with mandatory transfer to a PCI center and a pharmacoinvasive strategy. With persistent ischemia, cardiogenic shock, or life-threatening arrhythmias, invasive reperfusion may be indicated even later than 12 hours from symptom onset.
In the presence of symptoms or equivalents of acute ischemia and diagnostic ECG changes, reperfusion is initiated immediately; a fixed duration of pain is not mandatory — shorter episodes, atypical presentations, and painless forms are possible. Troponin confirms acute myocardial infarction, but its result should not delay reperfusion.
Posterior and right ventricular infarction with corresponding ECG patterns (ST depression in V1–V3 with elevation in V7–V9; ST elevation in V3R–V4R) are considered STEMI equivalents. The de Winter pattern and other OMI patterns (occlusion myocardial infarction without classic ST elevation) require immediate evaluation and often urgent coronary angiography, but OMI is not a formal STEMI category in all current guidelines, and equating it to STEMI unconditionally is incorrect. Diffuse ST depression with ST elevation in aVR in multivessel disease is a marker of severe subendocardial ischemia and high risk; ESC 2023 treats this pattern as requiring urgent evaluation and often early/emergency invasive strategy in signs of very high risk, but it does not prove left main coronary artery disease and does not equal the formal STEMI criterion. Non-ST-elevation patterns, such as Wellens syndrome, belong to non-ST-elevation ACS with an indication for an early invasive strategy (rather than the primary PCI <120 min window applicable to STEMI).
It is important for the physician to: record a 12-lead ECG within the first 10 minutes of presentation, in case of suspected inferior MI — additionally record V3R–V4R and V7–V9, repeat serial ECGs if the initial tracing is non-diagnostic and symptoms persist.
Common interpretation errors
- Failing to account for different sex- and age-specific ST-elevation thresholds in V2–V3 — in young men, an overestimated threshold of 2.5 mm may mask true STEMI if the general 2.0 mm criterion is incorrectly applied in the opposite direction
- Mistaking early repolarization or pericarditis for STEMI without evaluating dynamics and reciprocal changes, relying solely on ST morphology
- Forgetting to record V7–V9 and V3R–V4R in isolated ST depression in V1–V3 or inferior STEMI
- Failing to apply Sgarbossa/Smith criteria in left bundle branch block, leaving STEMI unrecognized
- Measuring ST-segment elevation not at the J-point, but arbitrarily along the segment, which distorts the evaluation in tachycardia and baseline wander
1. What is the minimum ST-segment elevation in leads V2–V3 required to diagnose STEMI in a woman of any age?
According to the 2009 AHA/ACCF/HRS criteria, the threshold in V2–V3 for women is 1.5 mm regardless of age.
2. What ECG finding increases the specificity of a STEMI diagnosis when ST-segment elevation is present in the inferior leads?
Reciprocal ST-segment depression in leads with opposing vectors to the ischemic zone (I, aVL in inferior myocardial infarction) confirms the ischemic origin of the ST-segment elevation.
3. What management is indicated in STEMI if the expected time from diagnosis to wire crossing exceeds 120 minutes, symptoms are of recent onset, and there are no contraindications?
When the expected delay to primary PCI exceeds 120 minutes, symptoms are generally ≤12 hours, and there are no contraindications, immediate fibrinolysis followed by a pharmacoinvasive strategy is indicated.
Frequently asked questions
How to distinguish STEMI from early repolarization syndrome?
In early repolarization, ST-segment elevation is concave, stable over time, often accompanied by a J-point notch, without reciprocal ST depression and without the clinical picture of acute ischemia. STEMI exhibits ST-T dynamics over hours and reciprocal changes.
Is ST-segment elevation in aVR dangerous?
ST-segment elevation in lead aVR combined with diffuse ST depression in other leads is a marker of severe subendocardial ischemia and high risk. The 2009 ESC guidelines consider this pattern as requiring urgent evaluation and often emergency invasive management, although it is not specific for left main coronary artery disease and is not formally a STEMI criterion.
Should troponin be awaited before performing reperfusion in STEMI?
No. The diagnosis of STEMI is established based on the ECG combined with symptoms or equivalents of acute ischemia; the decision for primary PCI or fibrinolysis is made immediately without waiting for biomarker results.
How does STEMI differ from non-ST-segment elevation acute coronary syndrome?
STEMI and NSTE-ACS are ECG categories of acute coronary syndrome; the presence or absence of ST-segment elevation by itself does not determine the anatomical completeness of the occlusion or the degree of transmural injury. STEMI requires immediate reperfusion (primary PCI within 120 minutes from diagnosis to wire crossing or fibrinolysis if PCI is unavailable within this timeframe), whereas NSTE-ACS involves an early invasive strategy without a rigid 120-minute window.
Why are the ST-elevation thresholds in V2–V3 different for men and women?
Healthy young men have a physiologically higher baseline ST-segment level in V2–V3, which is why the 2009 AHA/ACCF/HRS established a higher threshold (2.5 mm) for men under 40 and a lower threshold (1.5 mm) for women to avoid missing true STEMIs in women and overdiagnosing in young men.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
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Related terms
More in the section "Ischemia and Myocardial Infarction"
Sources
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the ECG, 2009
- ESC Guidelines for the management of acute coronary syndromes, 2023
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
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.