By Dr. Abdolghader Pakniyat, peer reviewed by Dr. Sabrina Berdouk
ST-segment elevation is an ECG finding—not a diagnosis.
The ST elevation differential diagnosis includes acute coronary occlusion, electrolyte disorders, conduction abnormalities, inflammatory disease and other ECG patterns. This guide uses the ELEVATIONS mnemonic and a practical emergency department approach to identify important clues without delaying urgent treatment.
The ST segment represents the period when most ventricular myocardial cells are uniformly depolarized during phase 2 of the action potential. Because their membrane voltages are normally similar, there is little net electrical gradient, so the ST segment appears approximately isoelectric.
ST elevation occurs when something creates a voltage difference between myocardial regions. This may result from:
- Myocardial injury, such as acute coronary occlusion, myocarditis or pericarditis.
- Abnormal ventricular activation, such as left bundle branch block, ventricular pacing or ventricular hypertrophy.
- Altered action-potential physiology, such as hyperkalemia, hypercalcemia, hypothermia, early repolarization or Brugada syndrome.
These different processes can produce similar-looking ECGs despite requiring completely different treatments.
An important modern update: STEMI is not synonymous with coronary occlusion
The 2025 ACC/AHA acute coronary syndromes guideline retains the STEMI/NSTE-ACS framework. Conventional STEMI criteria require new or presumed-new J-point elevation in at least two anatomically contiguous leads: ≥1 mm outside V2–V3; in V2–V3, ≥2 mm in men aged ≥40 years, ≥2.5 mm in men aged <40 years, and ≥1.5 mm in women. These conventional thresholds are defined in the absence of LVH or LBBB; use the relevant pattern-based assessment when LVH, LBBB or ventricular pacing affects repolarization.
However, these thresholds were designed as reperfusion activation criteria, not as a perfect biological test for coronary occlusion.
Some patients with acute coronary occlusion never meet formal STEMI criteria. Conversely, many patients who meet ST-elevation criteria do not have an acutely occluded coronary artery. Recent literature therefore emphasizes identifying occlusion myocardial infarction, or OMI, rather than relying only on the STEMI/NSTEMI label.
The OMI framework is clinically influential but has not formally replaced the STEMI/NSTE-ACS classification in major guidelines. Current guidance instead asks clinicians to recognize STEMI-equivalent or occlusion patterns such as posterior infarction, hyperacute T waves, de Winter morphology and positive modified Sgarbossa criteria.
The 2026 Fifth Universal Definition of MI also recognizes ECG patterns suggesting acute coronary occlusion without classic ST-elevation thresholds.
The practical question is therefore not simply:
“Does this ECG meet STEMI criteria?”
It is:
“Is there evidence of an acutely threatened myocardium that requires immediate reperfusion?”
ST elevation differential diagnosis: the ELEVATIONS mnemonic
E — Electrolytes
Hyperkalemia
Increasing extracellular potassium makes the resting membrane potential less negative. Initially, this accelerates repolarization, producing tall, narrow, symmetric T waves. As potassium rises further, sodium channels become progressively inactivated, slowing conduction and producing:
- PR prolongation
- P-wave flattening or disappearance
- QRS widening
- Bundle-branch or fascicular patterns
- Eventually a sine-wave appearance
A pseudo-STEMI pattern can occur, particularly in the right precordial leads, but this is rare and usually occurs with severe hyperkalemia and other conduction abnormalities.
The important clue is that the apparent ST elevation often exists within a broader picture of electrical toxicity: unusual T-wave peaking, absent P waves, QRS widening or an implausible QRS–ST–T fusion.
These ECG changes do not reliably occur in a fixed sequence, and a normal ECG does not exclude dangerous hyperkalemia. Check potassium urgently when the clinical context suggests it. The July 2026 UK Kidney Association guideline emphasizes these limitations.
Do not assume hyperkalemia and coronary occlusion are mutually exclusive. A patient with renal failure may have both.
Hypercalcemia
Calcium strongly influences phase 2, the plateau phase of the ventricular action potential. High extracellular calcium shortens this plateau, causing the ST segment and QT interval to shorten.
When the T wave begins very early after the QRS, it may appear as though the ST segment is elevated. The characteristic clue is therefore:
Apparent ST elevation plus a short or nearly absent ST segment and shortened QT interval.
True hypercalcemia-associated pseudo-STEMI is uncommon and generally occurs with marked hypercalcemia.
L — Left bundle branch block and ventricular-paced rhythm
LBBB and right ventricular pacing activate the ventricles through an abnormal route. Because repolarization normally proceeds in the opposite direction to depolarization, abnormal depolarization produces secondary ST–T abnormalities.
This creates appropriate discordance:
- A predominantly negative QRS is followed by some ST elevation.
- A predominantly positive QRS is followed by some ST depression.
The question is therefore not whether discordance exists, but whether the ST deviation is unexpectedly concordant or excessively discordant.
Smith-modified Sgarbossa criteria
Acute coronary occlusion is strongly suggested if any of the following is present:
- Concordant ST elevation ≥1 mm in a lead with a positive QRS.
- Concordant ST depression ≥1 mm in V1–V3.
- Discordant ST elevation ≥1 mm that is at least 25% of the preceding S-wave depth—an ST/S ratio of ≤−0.25 when the S-wave amplitude is entered as a negative value.
These criteria can be applied to LBBB and ventricular-paced rhythms with the relevant secondary ST–T changes. A positive result requires urgent assessment for coronary occlusion; a negative result cannot exclude it. Interpret the actual QRS morphology in newer conduction-system pacing rather than applying a paced-rhythm label alone. See the ACC chest-pain pathway and the ventricular-paced-rhythm validation study.
A new or presumed-new LBBB by itself is no longer considered an automatic STEMI equivalent.
E — Early repolarization
The term early repolarization has been used broadly for stable, usually concave ST elevation in healthy people. Contemporary consensus defines the early-repolarization ECG pattern more specifically by end-QRS notching or slurring in inferior or lateral leads; ST elevation is not required. An ECG pattern alone does not establish early-repolarization syndrome, which requires an appropriate arrhythmic clinical context.
Typical findings include:
- J-point notching or slurring—the “fish-hook” appearance
- Concave ST elevation
- Prominent, concordant upright T waves
- Preserved R-wave progression
- Relative stability on previous or serial ECGs
- Absence of convincing reciprocal ST depression, except in aVR
It is commonly seen in younger, healthy people, although it may also persist later in life.
Important correction to traditional teaching
Normal-variant anterior ST elevation and inferior or inferolateral early-repolarization patterns should not be treated as interchangeable labels. A concave ST segment does not safely exclude acute coronary occlusion. Syncope, documented ventricular arrhythmia or a family history of sudden unexplained death warrants further assessment, even when the tracing resembles an early-repolarization pattern. See the ECG definition consensus and 2026 J-wave consensus.
The most reassuring evidence is not the shape alone—it is the combination of a compatible clinical setting, proportional ST elevation, stable morphology, normal reciprocal leads and an unchanged previous ECG.
V — Ventricular hypertrophy
A hypertrophied ventricle produces larger depolarization forces and abnormal repolarization.
In left ventricular hypertrophy:
- Deep S waves in V1–V3 may be followed by discordant anterior ST elevation.
- Tall R waves in I, aVL, V5 and V6 may be followed by lateral ST depression and asymmetric T-wave inversion—the LVH “strain” pattern.
The ST deviation is generally related to the preceding QRS amplitude. Disproportionate change is a warning sign, but do not transfer the modified Sgarbossa rule directly to LVH; it was developed for LBBB and subsequently studied in ventricular pacing.
A few millimetres of ST elevation after a very deep S wave may therefore be normal for LVH. The same amount of elevation after a small S wave may be disproportionate and concerning.
Look for:
- Voltage criteria for hypertrophy
- Asymmetric rather than symmetric T-wave inversion
- Stable changes on an old ECG
- Lack of new reciprocal changes
- Lack of dynamic evolution
LVH does not protect the patient from OMI. New, disproportionate or dynamic changes must not automatically be dismissed as “strain.”
A — Aneurysmal left ventricle
After a large transmural infarction, scarred and dyskinetic myocardium may produce persistent localized ST elevation.
Typical clues include:
- A known previous myocardial infarction
- Persistent ST elevation in the same territory
- Mature Q or QS waves
- Relatively small T waves compared with the QRS complex
- No meaningful dynamic evolution
- An unchanged previous ECG
Physiologically, this represents chronic scar and altered ventricular geometry rather than acute ischemic injury.
The strongest diagnostic tool is an old ECG. Without one, distinguishing ventricular aneurysm from an acute anterior OMI may be difficult.
Importantly, a patient with an old ventricular aneurysm can develop a new coronary occlusion. New symptoms, reciprocal changes or dynamic ECG changes require renewed evaluation.
T — Thrombotic coronary occlusion: acute OMI
Coronary occlusion deprives myocardial cells of oxygen and ATP. Ion pumps begin to fail, extracellular potassium accumulates, resting membrane potentials become less negative and action potentials shorten.
The resulting voltage gradient between ischemic and nonischemic myocardium produces the current of injury. Leads facing the affected region may show ST elevation, while electrically opposite leads may show reciprocal ST depression.
Features increasing the probability of acute coronary occlusion include:
- A regional, anatomically coherent pattern
- Reciprocal ST depression
- Broad, bulky, symmetric hyperacute T waves that are large relative to the QRS
- Dynamic change over minutes
- Terminal QRS distortion
- New Q waves or loss of R-wave amplitude
- Posterior infarction pattern
- De Winter morphology
- Modified Sgarbossa positivity
- Symptoms, shock, pulmonary edema or ventricular arrhythmia consistent with acute ischemia
OMI may occur without diagnostic ST elevation
Important occlusion patterns include:
Posterior OMI: Horizontal ST depression in V1–V3, often with tall R waves and upright T waves. Posterior leads V7–V9 may reveal ST elevation.
De Winter pattern: Upsloping ST depression at the J point in the precordial leads followed by large, symmetric T waves, often with slight ST elevation in aVR.
Hyperacute T waves: Disproportionately large, broad and symmetric T waves, often representing the earliest stage of occlusion before substantial ST elevation develops.
Subtle ST elevation with reciprocal depression: Reciprocal depression may be easier to recognize than the small amount of primary elevation. Its absence does not exclude coronary occlusion.
A 2025 retrospective multicentre study derived and validated a quantitative hyperacute-T-wave score. In the validation subgroup without STEMI criteria, specificity was 98.4% and sensitivity was 20.7%. The study excluded QRS duration ≥110 ms, so the score should not be extrapolated to wide-QRS or paced ECGs. These findings apply to the studied score, rather than T-wave height alone; a negative score cannot exclude OMI.
Key teaching point
ST morphology alone cannot rule an occlusion in or out.
Acute OMI may be concave, subtle or initially nondiagnostic. Serial ECGs and the direction of change are often more informative than a single tracing.
I — Inflammation: pericarditis and myocarditis
Acute pericarditis
The parietal pericardium is electrically inert. ST changes reflect inflammation affecting adjacent subepicardial myocardium. When widespread, this produces an injury-current pattern that does not follow a single coronary territory.
Typical findings include:
- Widespread ST elevation
- PR-segment depression
- ST depression and PR elevation in aVR
- Sometimes similar reciprocal changes in V1
- Pleuritic or positional chest pain
- A pericardial friction rub
The ST elevation is often concave, but neither concavity nor diffuseness is sufficiently specific to establish the diagnosis.
The 2025 ESC guideline emphasizes that the classic widespread ST-elevation pattern occurs in only a proportion of patients with inflammatory myopericardial disease. Its absence therefore does not exclude pericarditis or myocarditis.
Myocarditis and myopericarditis
Myocardial inflammation may be focal rather than diffuse. It can therefore cause:
- Regional ST elevation
- Reciprocal-looking changes
- Troponin elevation
- Regional wall-motion abnormalities
- Ventricular arrhythmia or heart failure
This may be indistinguishable from OMI on the initial ECG.
The 2025 ESC guideline introduced inflammatory myopericardial syndrome as an umbrella term during the initial assessment, recognizing the frequent overlap between myocarditis and pericarditis.
Cardiac magnetic resonance is central to diagnosing myocardial inflammation, but coronary angiography may still be required when acute coronary occlusion cannot be safely excluded.
O — Osborn waves and hypothermia
An Osborn or J wave is a positive deflection at the junction between the QRS complex and ST segment.
Hypothermia creates temperature-dependent differences in early repolarization between myocardial layers, producing the J wave.
Associated findings may include:
- Bradycardia
- Prolonged PR, QRS and QT intervals
- Atrial fibrillation
- Shivering artifact
- Progressive conduction slowing
- Ventricular irritability and ventricular fibrillation
Osborn waves often become more prominent as temperature falls, but the relationship is not sufficiently precise to estimate temperature from the ECG.
They are not pathognomonic for hypothermia. J waves can also occur with hypercalcemia, early repolarization, Brugada phenotypes, myocardial ischemia and some neurologic conditions.
N — Neurogenic ECG abnormalities
Subarachnoid hemorrhage, severe intracranial injury and raised intracranial pressure can produce dramatic ECG abnormalities.
A sudden sympathetic discharge and catecholamine surge may cause:
- Myocardial stunning
- Subendocardial injury
- Takotsubo physiology
- QT prolongation
- Deep, symmetric T-wave inversion
- ST depression or elevation
- Ventricular arrhythmias
Deep “cerebral” T waves and marked QT prolongation are more characteristic than isolated ST elevation, but the full range of ischemia-like patterns can occur.
The clinical history is essential, particularly in an unconscious patient. Witness or EMS information about sudden headache, seizure, focal deficit or collapse may be decisive.
Neurologic disease and ACS can coexist. An abnormal neurologic examination should prompt urgent neuroimaging, but it should not automatically invalidate an ischemic ECG.
S — Sudden death syndromes: Brugada pattern
Brugada syndrome is an inherited arrhythmic disorder associated with abnormal electrical behavior, particularly in the right ventricular outflow tract.
Type 1 Brugada pattern
The diagnostic ECG pattern consists of:
- Coved J-point/ST elevation of at least 2 mm
- In V1 or V2
- Recorded in the second, third or fourth intercostal spaces
- Followed by a negative T wave
Other causes of a similar appearance, including reversible Brugada phenocopies, must be excluded. A spontaneous type 1 pattern has different diagnostic weight from a fever- or drug-provoked pattern. A provoked pattern requires specialist interpretation alongside the clinical and family history before assigning the syndrome diagnosis, as emphasized in the 2026 J-wave consensus.
Type 2 pattern
The saddleback Type 2 pattern is suggestive but not diagnostic of Brugada syndrome. It should lead to careful review, high-right-precordial lead placement and specialist evaluation rather than an immediate definitive label.
The pattern may be unmasked or intensified by:
- Fever
- Sodium-channel-blocking drugs
- Cocaine
- Excessive alcohol
- Electrolyte disturbances
Syncope, nocturnal agonal breathing, documented ventricular arrhythmia or a family history of sudden unexplained death substantially increases concern.
Fever should be treated promptly in a patient with known or suspected Brugada syndrome.
Important causes outside the mnemonic
The ELEVATIONS mnemonic is helpful but not exhaustive.
Takotsubo syndrome
Takotsubo syndrome causes transient ventricular dysfunction and is associated with sympathetic activation; its mechanisms are not fully resolved. The ECG may show ST elevation, followed by deep T-wave inversion and QT prolongation. When the presentation suggests STEMI, suspected Takotsubo syndrome should not delay urgent coronary angiography to exclude acute coronary occlusion. See the international Takotsubo diagnostic consensus.
Aortic dissection
A dissection extending into a coronary ostium can cause a genuine coronary occlusion and ST-elevation pattern. This is not simply a “mimic”; it is a different mechanism of myocardial infarction with critically different treatment implications. Giving fibrinolysis in unrecognized dissection can be catastrophic.
Pulmonary embolism
Pulmonary embolism more commonly causes tachycardia, right-axis deviation, right bundle branch block or anterior T-wave inversion. Rarely, severe right ventricular strain can produce ST elevation.
Coronary vasospasm
Epicardial coronary spasm can cause transient regional ST elevation and myocardial ischemia, sometimes with infarction or ventricular arrhythmia. Resolution of pain or ST elevation does not by itself exclude an acute coronary syndrome. Continue urgent clinical assessment and obtain serial ECGs; see the COVADIS diagnostic criteria.
Other uncommon causes
Pneumothorax, pre-excitation, post-cardioversion changes, sodium-channel-blocker toxicity and mechanical cardiac compression can occasionally produce ST-elevation patterns.
A practical ED approach to ST elevation
1. Begin with the patient, not the tracing
Immediately assess for:
- Ongoing ischemic discomfort
- Shock or hypotension
- Pulmonary edema
- Malignant ventricular arrhythmia
- Cardiac arrest
- Severe autonomic symptoms
- Aortic, neurologic or pulmonary warning features
Obtain and interpret a 12-lead ECG within 10 minutes of first medical contact when ACS is suspected. An unstable patient with a plausible occlusion pattern requires immediate reperfusion-system involvement. A patient with a convincing STEMI pattern also needs immediate activation even if blood pressure is initially normal.
2. Confirm the ECG is technically reliable
Check:
- Correct lead placement
- Calibration and paper speed
- Motion or shivering artifact
- Limb-lead reversal
- Previous ECGs
3. Examine the entire ECG
Do not focus exclusively on the elevated segment. Look for:
- Reciprocal ST depression
- Hyperacute T waves
- Q waves
- Loss of R-wave amplitude
- Terminal QRS distortion
- PR-segment abnormalities
- QRS width and morphology
- QT shortening or prolongation
- J-point notching
- Proportionality between ST deviation and QRS voltage
4. Ask whether the pattern is dynamic
Serial ECGs over short intervals are recommended when symptoms persist, suspicion remains high or the patient deteriorates.
A changing ECG strongly favors an acute process. A stable ECG may support a chronic or constitutional pattern, although it does not completely exclude ischemia.
5. Record additional leads when appropriate
- V7–V9 when posterior infarction is suspected.
- V3R–V4R in inferior infarction, particularly with hypotension or suspected right ventricular involvement.
- High V1–V2 positions when Brugada syndrome is suspected.
6. Use laboratory and imaging data without allowing them to delay reperfusion
Check electrolytes, temperature and serial high-sensitivity troponin. Troponin elevation indicates myocardial injury, not its cause. Bedside echocardiography may identify regional dysfunction, tamponade or right ventricular strain. Reliable wall-motion assessment requires adequate images and an experienced reader; abnormalities may also reflect previous infarction or myocarditis.
However:
A single early normal troponin does not exclude acute coronary occlusion.
A limited or apparently normal bedside echocardiogram cannot exclude coronary occlusion. Do not delay indicated reperfusion for troponin results, repeat ECGs or echocardiography.
7. When uncertainty remains, prioritize the diagnosis with the greatest immediate harm
If acute coronary occlusion remains plausible—particularly with persistent symptoms, instability, reciprocal changes or dynamic ECG evolution—obtain immediate expert review and consider emergent coronary angiography rather than waiting for the ECG to satisfy a rigid millimetre threshold.
Final take-home messages
- ST elevation is a voltage pattern produced by several different physiological mechanisms.
- The ELEVATIONS mnemonic organizes the differential, but it is not exhaustive.
- Concave ST elevation does not rule out acute coronary occlusion.
- Reciprocal changes, proportionality, hyperacute T waves and dynamic evolution are often more useful than ST shape alone.
- New LBBB is not automatically a STEMI equivalent; apply modified Sgarbossa criteria and clinical judgment.
- Type 2 saddleback Brugada morphology is suggestive, not diagnostic.
- Typical widespread ST elevation is not present in every case of pericarditis or myocarditis.
- Some patients have OMI without meeting STEMI thresholds. The ECG must be interpreted as a whole and in its clinical context.
- When the cost of missing acute coronary occlusion is high, do not wait for perfect ECG criteria, a positive troponin or textbook morphology.
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