ST segment elevation is one of the most critical findings on an electrocardiogram (ECG or EKG). It typically raises an immediate red flag for acute myocardial infarction (MI), particularly ST-elevation myocardial infarction (STEMI). However, not all ST elevations indicate a heart attack.
There are several non-infarction causes of ST elevation that can mimic myocardial infarction, and distinguishing between them is essential for accurate diagnosis and appropriate treatment.
To aid clinicians and students in memorizing these causes, the mnemonic "ELEVATION" offers a simple yet powerful framework:
- E – Electrolytes (e.g., hyperkalemia)
- L – Left bundle branch block
- E – Early repolarization
- V – Ventricular hypertrophy
- A – Arrhythmia / Aneurysm of LV
- T – Takotsubo cardiomyopathy / TIA
- I – Infarction (MI) / Injury
- O – Osborn waves
- N – Non-atherosclerotic vasospasm
In this article, we will explore each of these causes in detail, supported by clinical correlations and diagnostic pearls.
What Is ST Segment Elevation?
The ST segment represents the period between ventricular depolarization and repolarization on an ECG. In a normal heart rhythm, it appears as a flat, isoelectric line between the S wave and the beginning of the T wave.
ST elevation refers to a rise of the ST segment above the baseline and can suggest transmural (full-thickness) myocardial injury or other non-infarction causes that alter myocardial electrical activity.
Criteria for ST Elevation
- ≥1 mm (0.1 mV) elevation in ≥2 contiguous leads
- ≥2 mm in men and ≥1.5 mm in women in V2–V3 leads
- Should be assessed in the clinical context
E – Electrolytes (e.g., Hyperkalemia)
Electrolyte imbalances, particularly hyperkalemia, can significantly alter ECG morphology.
ECG changes in hyperkalemia:
- Peaked T waves
- Flattened or absent P waves
- Widened QRS complexes
- Sine-wave pattern in severe cases
- ST segment elevation in early stages
Mechanism:
Hyperkalemia affects membrane potential and cardiac repolarization, which can mimic ischemic changes. Prompt correction is vital to avoid cardiac arrest.
Clinical Pearls:
- Always correlate with serum potassium levels.
- Look for history of renal failure, potassium-sparing diuretics, or potassium supplements.
L – Left Bundle Branch Block (LBBB)
LBBB is a conduction abnormality that alters the usual depolarization pattern, leading to secondary ST-T wave changes, including ST elevation.
Key ECG Features of LBBB:
- Broad QRS complex (>120 ms)
- Deep S wave in V1
- Tall, notched R wave in V6
- Discordant ST segments and T waves
Challenge:
LBBB can mask or mimic signs of STEMI, especially in anterior leads. Special criteria like the Sgarbossa criteria are used to assess MI in LBBB.
E – Early Repolarization
This is a benign ECG variant, especially common in young, healthy individuals and athletes.
Features of early repolarization:
- ST elevation, typically in V2–V5
- Notched or slurred J-point (fishhook appearance)
- Concave upward ST segment
- No reciprocal changes or Q waves
Clinical Significance:
- No chest pain or cardiac symptoms
- ST changes do not evolve over time
- Normal cardiac enzymes
Important to distinguish from MI to avoid unnecessary intervention.
V – Ventricular Hypertrophy (especially LVH)
Left Ventricular Hypertrophy (LVH) due to hypertension, aortic stenosis, or cardiomyopathy can cause repolarization abnormalities known as strain patterns.
ECG features:
- High voltage QRS complexes
- ST depression and T wave inversion (strain pattern)
- Occasionally, ST elevation in right precordial leads (V1–V2) due to right ventricular hypertrophy
Clinical Note:
ST elevation in this context does not reflect infarction, but rather increased workload and oxygen demand.
A – Arrhythmia / Aneurysm of LV
Ventricular arrhythmias (e.g., VTach, VFib)
May lead to transient ST changes post-resuscitation due to myocardial stunning or injury.
Left Ventricular Aneurysm
A true aneurysm of the left ventricle forms after a transmural infarct and may cause persistent ST elevation, even weeks later.
Characteristics of LV aneurysm:
- ST elevation that remains unchanged
- Presence of Q waves
- Often seen in the anterior leads
T – Takotsubo Cardiomyopathy / TIA
Takotsubo Cardiomyopathy (Stress-Induced)
Also called "broken heart syndrome", this mimics MI with chest pain and ST elevation but has normal coronary arteries on angiography.
ECG Findings:
- ST elevation in anterior leads
- QT prolongation
- T wave inversion after 24–48 hours
Triggered by emotional or physical stress. More common in post-menopausal women.
TIA (Transient Ischemic Attack):
Though rare, TIAs may co-exist with cardiac stress or atrial fibrillation, indirectly influencing ECG.
I – Infarction (MI) / Injury
This is the most critical and common cause of ST elevation, requiring immediate intervention.
ECG features of STEMI:
- ST elevation in contiguous leads
- Reciprocal ST depression
- Evolving Q waves
- Hyperacute T waves early on
Location clues:
- Inferior MI: II, III, aVF
- Anterior MI: V1–V4
- Lateral MI: I, aVL, V5–V6
- Posterior MI: Tall R in V1, ST depression V1–V3
Immediate reperfusion therapy is vital.
O – Osborn Waves (J waves)
Osborn waves are characteristic of hypothermia, but can also be seen in hypercalcemia and brain injury.
ECG Features:
- Positive deflection at the J point
- Seen best in V3–V6
- Can mimic ST elevation
Clinical clues:
- Low body temperature (<35°C)
- Bradycardia
- History of exposure or CNS injury
N – Non-Atherosclerotic Vasospasm
This includes Prinzmetal’s (variant) angina, where transient coronary artery spasm causes temporary ST elevation, typically at rest or during early morning hours.
ECG Changes:
- ST elevation during pain episodes
- Reversible after nitroglycerin or CCBs
- No troponin rise unless prolonged spasm
Triggers include:
- Cold exposure
- Emotional stress
- Smoking
- Cocaine use
Summary Table: ELEVATION Mnemonic for ST Elevation Causes
| Letter | Cause | Key ECG Features / Clues |
|---|---|---|
| E | Electrolytes (Hyperkalemia) | Peaked T, wide QRS, ST elevation |
| L | Left bundle branch block (LBBB) | Broad QRS, discordant ST-T waves |
| E | Early repolarization | Concave ST, J-point notch, young athletes |
| V | Ventricular hypertrophy | High QRS, ST elevation in V1–V2 |
| A | Arrhythmia / LV Aneurysm | Persistent ST elevation post-MI |
| T | Takotsubo / TIA | ST elevation + emotional trigger, normal coronaries |
| I | Infarction (MI) / Injury | ST elevation + reciprocal changes, troponin rise |
| O | Osborn waves | J wave with hypothermia |
| N | Non-atherosclerotic vasospasm | Reversible ST elevation, normal coronaries |
Differentiating STEMI from Non-Infarction ST Elevation
| Feature | STEMI | Non-Ischemic ST Elevation |
|---|---|---|
| Chest Pain | Typical, crushing | Often absent or vague |
| Evolution on Serial ECGs | Dynamic changes | Static or minimal changes |
| Reciprocal Changes | Present | Usually absent |
| Troponin Elevation | Markedly elevated | Normal or mildly elevated |
| Response to Nitroglycerin | Variable | Often complete resolution |
Frequently Asked Questions (FAQ)
What is the first step when ST elevation is seen on ECG?
Always assess the clinical context. If chest pain and ST elevation are present, treat as STEMI unless proven otherwise. Initiate emergency care.
Can ST elevation occur in healthy people?
Yes. Early repolarization, especially in athletes or young adults, can cause benign ST elevation. This is not associated with chest pain or troponin rise.
How is Takotsubo cardiomyopathy different from MI?
Takotsubo presents like MI with chest pain and ST elevation but has normal coronary arteries on angiography and typically resolves over days to weeks.
What are Osborn waves and when should I suspect them?
Osborn waves are positive deflections at the J point seen in hypothermia. Suspect them in a cold, bradycardic patient with altered sensorium.
Can vasospastic angina mimic a heart attack?
Yes. Prinzmetal’s angina can cause transient ST elevation and chest pain at rest, but angiography reveals no obstructive coronary disease.
