Clinical Notes : Cardiology

147. ECG STEMI - Lateral

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ECG - Lateral STEMI

Lateral ST Elevation Myocardial Infarction

MI is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand.

This is usually caused by occlusion in the coronary arteries. ST-elevation myocardial infarction (STEMI) is suspected when a patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.


Clinical Significance of lateral STEMI

  • The lateral wall of the LV is supplied by branches of the left anterior descending (LAD) and left circumflex (LCx) arteries.

  • Infarction of the lateral wall usually occurs as part of a larger territory infarction, e.g. anterolateral STEMI.

  • Isolated lateral STEMI is less common, but may be produced by occlusion of smaller branch arteries that supply the lateral wall, e.g. the first diagonal branch (D1) of the LAD, the obtuse marginal branch (OM) of the LCx, or the ramus intermedius.

  • Lateral STEMI is a stand-alone indication for emergent reperfusion.

  • Lateral extension of an anterior, inferior or posterior MI indicates a larger territory of myocardium at risk with consequent worse prognosis.


How to recognise a lateral STEMI


  • ST elevation in the lateral leads (I, aVL, V5-6).

  • Reciprocal ST depression in the inferior leads (III and aVF).

  • ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI.


NB. Reciprocal change in the inferior leads is only seen when there is ST elevation in leads I and aVL. This reciprocal change may be obliterated when there is concomitant inferior ST elevation (i.e an inferolateral STEMI)



Patterns of lateral infarction

Three broad categories of lateral infarction:

  • Anterolateral STEMI due to LAD occlusion.

  • Inferior-posterior-lateral STEMI due to LCx occlusion.

  • Isolated lateral infarction due to occlusion of smaller branch arteries such as the D1, OM or ramus intermedius


Example 1 : Anterolateral STEMI

  • ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6).

  • Q waves are present in both the anterior and lateral leads, most prominently in V2-4.

  • There is reciprocal ST depression in the inferior leads (III and aVF).

  • This pattern indicates an extensive infarction involving the anterior and lateral walls of the left ventricle


ST elevation in the precordial leads plus the high lateral leads (I and aVL) is strongly suggestive of an acute proximal LAD occlusion (this combination predicts a proximal LAD lesion 87% of the time).

STEMI lat - example 1.jpg

Anterolateral STEMI

Example 2 : Hyperacute Anterolateral STEMI

  • There is early ST elevation with hyperacute T waves in the anteroseptal leads (V1-4).

  • There is also subtle ST elevation in the high lateral leads (I and aVL); this may be easily missed.

  • However, the presence of reciprocal ST depression in the inferior leads (III and aVF) makes the lateral ST elevation more obvious.

  • This ECG represents the early stages of a large anterolateral infarction.

  • As with the previous case, the combination of ST elevation in the precordial and high lateral leads is indicative of proximal LAD occlusion.


Tip: ST depression localised to the inferior leads should prompt you to scrutinise the ECG for evidence of high lateral infarction

STEMI lat - example 2.jpg

Hyperacute Anterolateral STEMI

Example 3 : Inferolateral STEMI

  • There is ST elevation in the inferior (II, III, aVF) and lateral (I, V5-6) leads.

  • The precordial ST elevation extends out as far as V4, however the maximal STE is in V6.

  • ST depression in V1-3 is suggestive of associated posterior infarction (the R/S ratio > 1 in V2 is consistent with this).

  • This is an acute inferolateral STEMI with probable posterior extension.

  • This constellation of ECG abnormalities is typically produced by occlusion of the proximal circumflex artery.

STEMI lat - example 3.jpg

Inferolateral STEMI

Example 4 : Inferoposterolateral STEMI

  • ST elevation is present in the inferior (II, III and aVF) and lateral leads (I, V5-6).

  • ST depression in V1-3 with tall, broad R waves and upright T waves and a R/S ratio > 1 in V2 indicate concomitant posterior infarction (this patient also had ST elevation in the posterior leads V7-9).

  • These changes are consistent with a massive infarction involving the inferior, lateral and posterior walls of the left ventricle.

  • The culprit vessel is again very likely to be an occluded proximal circumflex artery.

STEMI lat - example 4.jpg

Inferoposterolateral STEMI

Example 5 : High Lateral ST Elevation Myocardial Infarction

  • ST elevation primarily localized to leads I and aVL is referred to as a high lateral STEMI.

  • It is usually associated with reciprocal ST depression and T wave inversion in the inferior leads.

  • Sometimes referred to as the South African Flag sign


Culprit vessels

Occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) may produce isolated ST elevation in I and aVL

Occlusion of the circumflex artery may cause ST elevation in I, aVL along with leads V5-6.

South African Flag sign

High lateral STEMI is associated with pattern of ST elevation caused by acute occlusion of the first diagonal branch of the left anterior descending coronary artery (LAD-D1).

With the 4×3 display of the 12-lead ECG, the location of the most impressive ST deviations resemble the shape of the South African flag.

  • ST Elevation: Lead I, aVL, V2

  • ST Depression: Lead III (and inferior leads)


Example 5a

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STEMI hi lat - example 1b.png

High Lateral STEMI (a)


Example 5b

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STEMI hi lat - example 2b.jpg

High Lateral STEMI (b)



Refer A+E

In OOH settings where delay in transfer to A+E is inevitable : 

  • aspirin

    • 300 mg orally immediately, followed by 75 mg once daily

  • oxygen

    • Supplemental oxygen is indicated only if oxygen saturation is less than 90%

  • morphine

    • 2-4 mg intravenously every 5-15 minutes until adequate pain control is achieved

  • glyceryl trinitrate

    • if not hypotensive :

      • 0.3 to 1 mg sublingually every 5 minutes,

      • maximum 3 doses

    • if hypertensive or heart failure

      • 5 micrograms/minute intravenously initially,

      • increase by 5-20 microgram/minute increments every 3-5 minutes according to response,

      • maximum 200 micrograms/minute

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Life in the Fast Lane

Austalian Emergency Medicine website. 


ST-elevation myocardial infarction

BMJ Best Practice

Last reviewed : March 2019

Last updated : September 2018


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