- 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 depolarisation and repolarisation.
- The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia / 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.
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. They may be impossible to differentiate on the ECG.
Pericarditis causes widespread concave ST segment elevation with PR segment depression in multiple leads — typically I, II, III, aVF, aVL and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1.
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- Concave “saddleback” ST elevation in leads I, II, aVL, V4-6 with depressed PR segments.
- There is reciprocal ST depression and PR elevation in aVR.
Benign Early Repolarisation
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.
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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 with 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).
Click here to find out more about left bundle branch block.
- 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 repolarisation 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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- Severe LVH with extremely deep S waves in V1-3 producing associated ST elevation (not due to myocardial ischaemia).
- Also note the ST depression and T-wave inversion in the lateral leads I, aVL and V6 .
This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.
Click here to find out more about ventricular aneurysm.
- 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.
Click here to read more about Brugada syndrome.
- 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)
- J-waves (hypothermia, hypercalcaemia)
- Sodium-channel blocking drugs (secondary to QRS widening)
- Following electrical cardioversion
- Cardiac tumour
- Mitral valvuloplasty
- Pancreatitis / gallbladder disease
- Septic shock
Causes of ST depression
Morphology of ST depression
- ST depression can be either upsloping, downsloping, or horizontal.
- Horizontal or downsloping ST depression > 1 mm at the J-point is relatively specific for myocardial ischaemia.
- Upsloping ST depression is non-specific for myocardial ischaemia.
- Reciprocal change has a morphology that resembles “upside down” ST elevation.
- ST depression in posterior MI occurs in V1-3 and is associated with dominant R waves and upright T 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. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion.
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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Treatment with digoxin causes downsloping ST depression with a “sagging” morphology, reminiscent of Salvador Dali’s moustache.
Click here to read more about digoxin effect.
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.
Click here to read more about right ventricular hypertrophy.
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.