• 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

• Acute myocardial infarction
• Coronary vasospasm (Printzmetal’s angina)
• Pericarditis
• Benign early repolarisation
• Left bundle branch block
• Left ventricular hypertrophy
• Ventricular aneurysm
• Brugada syndrome
• Ventricular paced rhythm
• Raised intracranial pressure

Morphology of the Elevated ST segment

Myocardial infarction

Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.

ST segment morphology in other conditions

Pericarditis	BER	LBBB	LV aneurysm	Brugada

Patterns of ST elevation

Acute ST elevation myocardial infarction (STEMI)

Causes ST segment elevation and Q-wave formation in contiguous leads, either:

• Septal (V1-2)
• Anterior (V3-4)
• Lateral (I + aVL, V5-6)
• Inferior (II, III, aVF)
• Right ventricular (V1, V4R)
• Posterior (V7-9)

There is usually reciprocal ST depression in the electrically opposite leads.

Follow the links above to find out more about the different STEMI patterns.

Anterolateral STEMI

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.

Prinzmetal's angina

Pericarditis

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.

Click here to find out more about pericarditis. 

• 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.

Click here to find out more about benign early repolarisation.

Benign Early Repolarisation

• 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).

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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).

Click here to find out more about LVH. 

Left Ventricular Hypertrophy

• 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 .

Ventricular Aneurysm

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.

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.

Brugada Syndrome

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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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 isappropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.

Click here to read more about paced rhythms. 

Sequential atrial and ventricular pacing

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. 

ST elevation due to traumatic brain injury

• 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)
• Hyperkalaemia
• Sodium-channel blocking drugs (secondary to QRS widening)
• Following electrical cardioversion
• Cardiac tumour
• Mitral valvuloplasty
• Pancreatitis / gallbladder disease
• Myocarditis
• Septic shock
• Anaphylaxis

Transient ST elevation after DC cardioversion from VF

J waves in hypothermia simulating ST elevation

Causes of ST depression

• Myocardial ischaemia / NSTEMI
• Reciprocal change in STEMI
• Posterior MI
• Digoxin effect
• Hypokalaemia
• Supraventricular tachycardia
• Right bundle branch block
• Right ventricular hypertrophy
• Left bundle branch block (see above)
• Left ventricular hypertrophy (see above)
• Ventricular paced rhythm (see above)

 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 depression: upsloping (A), downsloping (B), horizontal (C)

ST segment morphology in myocardial ischaemia

Reciprocal change

ST elevation in III	Reciprocal change in aVL

ST segment morphology in posterior MI

Patterns of ST depression

Myocardial Ischaemia

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 furtherhere.

Widespread subendocardial ischaemia due to LMCA occlusion

Reciprocal Change

ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads:

• Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
• Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
• Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).

Reciprocal ST depression in aVL with inferior STEMI

Reciprocal ST depression in III and aVF with high lateral STEMI

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.

Click here to read more about posterior MI. 

Posterior MI

Digoxin Effect

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

Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.

Click here to read more about hypokalaemia. 

Hypokalaemia

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 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. 

Right bundle branch block

Supraventricular tachycardia

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.

AV-nodal re-entry tachycardia

Further Reading

• ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
• ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
• ECG Reference Sites on the WEB – the best of the rest

Author Credits

References

• 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),