OverviewSignificance of ST elevationPossible causes of ST elevation


Usually, the ST segment (between the S wave and T wave) is isoelectric, i.e. there is no deviation from baseline. This segment should be at the same level as the other isoelectric parts of the ECG, such as the segment between the T and P waves. While an elevated ST segment could be a normal variant (e.g. “high take off”), it could also be a medical emergency (e.g. myocardial infarction), so it is not to be ignored. Although ST-Elevated Myocardial Infarction (STEMI) is a textbook presentation, there are several other possible diagnoses that require consideration. Finally, a normal ECG (without ST elevation) does not exclude the possibility of myocardial infarction.

Figure 1: Elevation of the ST segment, between the S wave and the T wave. This segment is elevated above the baseline, when is should be isoelectric.

Significance of an ST elevation

Recall that the T-wave is a bit of a paradox itself, being an upward deflection during repolarisation, not depolarisation and that this is due to the way in which the pattern of repolarisation occurs, from the outside inwards, making a current that looks like depolarisation. Ischaemic myocardium is slightly depolarised at rest and repolarises a little more quickly, so that a potential difference between the injured and uninjured myocardium occurs. A so-called injury current runs between the healthy and damaged tissues.

If the ischaemic zone extends through the full thickness of the wall of the ventricle, the injury current travels outwards around the infarction. This causes an upward deflection of the ECG before the normal ventricular repolarisation: an ST segment elevation. If the damaged region is smaller, and in the subendocardium, the injury current passes in the other direction, causing ST depression (non-STE acute coronary syndromes). This is why a serious infarction is more often associated with ST elevation, and why more transient ischaemia (such as unstable angina) more often produces ST depression. These are not absolutes rules though, and monitoring cardiac markers is an important part of diagnosis and treatment. It is possible to have a myocardial infarction without significant ST elevation (non-STEMI).

Changes in the ST segment do not occur in all ECG leads, but are observed in those leads that “look” in the direction of the affected part of the heart. So, for example, an inferior infarction will show up in leads II, III and aVF. In ST elevation, reciprocal ST depression should be seen in leads looking at the heart from the opposite direction.

Figure 2: Each ECG lead produces a different view of the heart. Where ST elevation is most prominent determines the likely location of an infarction. Reciprocal ST depression will be most prominent in those leads “looking” at the heart from a near-opposite perspective. (For this illustration a normal ECG has been used. See here for an example of a STEMI ECG.)

Possible causes of ST elevation

Acute coronary syndrome
Acute coronary syndromes (ACS) are medical emergencies. Diagnosis is by history, examination and observation of the ECG. ACS are divided into two categories:

  • ST-elevated myocardial infarction (STEMI)
  • Non-ST-Elevated-ACS (unstable angina or non-STEMI) [Coming soon]

Normal (“high take-off”) variant
In this normal variant, ST elevation represents early repolarisation of the ventricle. It is generally seen in the anterior chest leads (V3-V4). Because there is no damage to the myocardium, reciprocal ST depressions are not seen in other leads. A clear S wave will be present, rather than partially obscured as in STEMI.

Figure 3: "High take-off". This normal variant of the ECG represents early repolarisation. There a no reciprocal ST depressions in other leads.

Left ventricular aneurysm
Ventricular aneurysm - secondary to infarction - occurs in about 10% of survivors and can usually be seen as a bulge on an echocardiogram. This produces a persistent ST elevation. It may be noted during an examination for another condition (“Oh, I see you’ve had an MI at some stage”).

Prinzmetal’s angina (coronary artery vasospasm)
Stable and unstable angina are usually associated ST depression (or no ECG change), so this is an unusual form of angina. It results from vasospasm, which is presumably so widespread that it causes ischaemia through the entire ventricular wall and ST elevation (see above) with reciprocal depressions in the expected leads. Vasospasm is most common in the right coronary artery and is transient. Chest pain and ST elevation will resolve simultaneously. This is in contrast to STEMI, where the ST elevation evolves over hours to days.

Brugada syndrome
This inherited condition results from a mutation of the cardiac Na+ channel and can lead to ventricular fibrillation and sudden death. Although it is associated with permanent ST elevations in leads V1-V3, these do not reflect ischaemia or infarction.

Left bundle branch block
In left bundle block [coming soon] the delay in depolarisation of the left ventricle (and subsequent widening of the QRS complex) creates apparent ST elevations in leads V1-V3. These can make diagnosis of myocardial infarction difficult. New (i.e. no prior history) left bundle branch block can be a sign of an myocardial infarction.

Because pericarditis affects the whole heart, ST elevation is seen in most leads, with reciprocal depression in aVR and V1. Pericarditis chest pain tends to be sharper and more pleuritic that the more crushing, generalised and radiating pain of myocardial infarction. A friction rub is pathognomonic (a specific sign).

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