- The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.
- It represents the interval between ventricular depolarization and repolarization.
- The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.
Causes of ST Segment Elevation
Morphology of the Elevated ST segment
Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.
ST Segment Morphology in Other Conditions
Patterns of ST Elevation
Acute ST elevation myocardial infarction (STEMI)
Causes ST segment elevation and Q-wave formation in contiguous leads, either:
There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + aVL typically produces reciprocal ST depression in lead III (see example below).
Follow the links above to find out more about the different STEMI patterns.
Coronary Vasospasm (Prinzmetal’s angina)
This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. It may be impossible to differentiate these two conditions based on the ECG alone.
Pericarditis causes widespread concave (“saddleback”) ST segment elevation with PR segment depression in multiple leads, typically involving I, II, III, aVF, aVL, and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1. Spodick’s sign — a downward sloping TP segment — may also be seen.
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- Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments.
- There is reciprocal ST depression and PR elevation in aVR.
- Spodick’s sign is present.
Benign Early Repolarization
BER causes mild ST elevation with tall T-waves mainly in the precordial leads. Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern. The ST changes may be more prominent at slower heart rates and disappear in the presence of tachycardia.
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- There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)
Left Bundle Branch Block
In left bundle branch block, the ST segments and T waves show “appropriate discordance” — i.e. they are directed opposite to the main vector of the QRS complex. This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).
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- Note the ST elevation in leads with deep S waves — most apparent in V1-3.
- Also note the ST depression in leads with tall R waves — most apparent in I and aVL.
Left Ventricular Hypertrophy
LVH causes a similar pattern of repolarization abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).
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- Deep S waves with ST elevation in V1-3
- ST depression and T-wave inversion in the lateral leads V5-6
- Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to associated left posterior fascicular block.
This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It is associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.
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- There is ST elevation with deep Q waves and inverted T waves in V1-3.
- This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.
This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.
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- There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.
Ventricular Paced Rhythm
Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.
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Raised Intracranial Pressure
Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave inversions (“cerebral T waves”).
Click here to find out more about the ECG changes seen with raised intracranial pressure.
- Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.
Less Common Causes of ST segment Elevation
- Pulmonary embolism and acute cor pulmonale (usually in lead III)
- Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
- Sodium-channel blocking drugs (secondary to QRS widening)
- J-waves (hypothermia, hypercalcaemia)
- Following electrical cardioversion
- Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease
Causes of ST Depression
Morphology of ST Depression
- ST depression can be either upsloping, downsloping, or horizontal.
- Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
- Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD.
- Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
- Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.
ST segment morphology in myocardial ischaemia
|ST elevation in III||Reciprocal change in aVL|
ST segment morphology in posterior MI
Patterns of ST depression
ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.
NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.
ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads:
Posterior Myocardial Infarction
Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.
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De Winters T Waves
This pattern of upsloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.
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Treatment with digoxin causes downsloping ST depression with a “sagging” morphology, reminiscent of Salvador Dali’s moustache.
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Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.
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Right ventricular hypertrophy
RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.
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Right Bundle Branch Block
RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.
Click here to read more about right bundle branch block.
Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment.
- Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
- Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002 Apr 20;324(7343):963-6. Review. PubMed PMID: 11964344; PubMed Central PMCID: PMC1122906. Full text.
- Phibbs BP. Advanced ECG: Boards and Beyond (second edition). Elsevier 2006.
- Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg Med. 2005 May;23(3):279-87. PubMed PMID: 15915398.
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.