Clinical Relevance

Anterior STEMI results from occlusion of the left anterior descending artery (LAD).

Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.

A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI) found that on average, patients with anterior
MI had higher incidences of in-hospital mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and significant
ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on admission (38 vs 55%) compared to patients with inferior MI.

In addition to anterior STEMI, other high-risk presentations of anterior ischaemia include left main coronary artery (LMCA)
occlusion, Wellens syndrome and De Winters T waves.

How to Recognise Anterior STEMI

ST segment elevation with Q wave formation in the precordial leads (V1-6) the high lateral leads (I and aVL).

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

NB. The magnitude of the reciprocal change in the inferior leads is determined by the magnitude of the ST elevation in I and aVL (as these leads
are electrically opposite to III and aVF), hence may be minimal or absent in anterior STEMIs that do not involve the high lateral leads.

Patterns of Anterior Infarction

The nomenclature of anterior infarction can be confusing, with multiple different terms used for the various infarction patterns. The following is a
simplified approach to naming the different types of anterior MI.
The precordial leads can be classified as follows:

Septal leads = V1-2

Anterior leads = V3-4

Lateral leads = V5-6

The different infarct patterns are named according to the leads with maximal ST elevation:

Septal = V1-2

Anterior = V2-5

Anteroseptal = V1-4

Anterolateral = V3-6, I + aVL

Extensive anterior / anterolateral = V1-6, I + aVL

(NB. While these definitions are intuitive, there is often a poor correlation between ECG features and precise infarct location as determined by
imaging or autopsy. For an alternative approach to the naming of myocardial infarctions, take a look at this 2006 article from Circulation)
Three other important ECG patterns to be aware of:

Anterior-inferior STEMI due to occlusion of a wraparound LAD: simultaneous ST elevation in the precordial and inferior leads due
to occlusion of a variant (type III) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left
ventricle.

Left main coronary artery occlusion: widespread ST depression with ST elevation in aVR V1

Wellens syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a
warning sign of imminent anterior infarction)

De Winters T waves: upsloping ST depression with symmetrically peaked T waves in the precordial leads; a STEMI equivalent
indicating acute LAD occlusion.

ECG Examples
Example 1 Hyperacute Anteroseptal STEMI

ST elevation is maximal in the anteroseptal leads (V1-4).

Q waves are present in the septal leads (V1-2).

There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.

There are hyperacute (peaked ) T waves in V2-4.

These features indicate a hyperacute anteroseptal STEMI

Example 2(a) Hyperacute Anterior STEMI

Another example of hyperacute STEMI:

There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of R wave height.

The rhythm is sinus with 1st degree AV block.

There are premature atrial complexes (beat 4 on the rhythm strip) and multifocal ventricular ectopy (PVCs of two different types),
indicating an irritable myocardium at risk of ventricular fibrillation.

Example 2 (b) Evolving Anterior STEMI

A ECG of the same patient taken around 40-50 minutes later:

There is progressive ST elevation and Q wave formation in V2-5

ST elevation is now also present in I and aVL.

There is some reciprocal ST depression in lead III.

This is an acute anterior STEMI this patient needs urgent reperfusion!

Example 3 Extensive Anterolateral STEMI (acute)

ST elevation in V2-6, I and aVL.

Reciprocal ST depression in III and AVF.

Example 4 Extensive Anterior STEMI (acute)

ST elevation in V1-6 plus I and aVL (most marked in V2-4).

Minimal reciprocal ST depression in III and aVF.

Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4.

There is a premature ventricular complex (PVC) with R on T phenomenon at the end of the ECG; this puts the patient at risk for
malignant ventricular arrhythmias.

Example 5 Prior Anteroseptal / Lateral MI

Deep Q waves in V1-3 with markedly reduced R wave height in V4.

Residual ST elevation in V1-3 (left ventricular aneurysm morphology).

Biphasic/inverted T waves in V1-5.

Poor R wave progression (R wave height < 3mm in V3).

Abnormal Q waves and T-wave inversion in I and aVL.

The pattern indicates prior infarction of the anteroseptal and lateral walls.

Example 6 Extensive anterior MI (tombstoning pattern)

Massive ST elevation with tombstone morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL).

This pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high
likelihood of cardiogenic shock and death.

Example 7 Anterior-inferior STEMI

ST elevation is present throughout the precordial and inferior leads.

There are hyperacute T waves, most prominent in V1-3.

Q waves are forming in V1-3, as well as leads III and aVF.

This pattern is suggestive of occlusion occurring in type III or wraparound LAD (i.e. one that wraps around the cardiac apex to
supply the inferior wall)

Prediction of the Site of LAD Occlusion

The site of LAD occlusion (proximal versus distal) predicts both infarct size and prognosis.

Proximal LAD / LMCA occlusion has a significantly worse prognosis due to larger infarct size and more severe haemodynamic
disturbance.

The site of occlusion can be inferred from the pattern of ST changes in leads corresponding to the two most proximal branches of
the LAD: the first septal branch (S1) and the first diagonal branch (D1).

[This great diagram was originally featured on The Radiology Assistant follow the link for a more detailed review of coronary artery anatomy.]
Territories

S1 supplies the basal part of the interventricular septum, including the bundle branches (corresponding to leads aVR and V1)

D1 supplies the high lateral region of the heart (leads I and aVL).

Occlusion proximal to S1
Signs of basal septal involvement:

ST elevation in aVR

ST elevation in V1 > 2.5 mm

Complete RBBB

ST depression in V5

Occlusion proximal to D1
Signs of high lateral involvement:

ST elevation / Q-wave formation in aVL

ST depression 1 mm in II, III or aVF (reciprocal to STE in aVL)

ST elevation in aVR of any magnitude is 43% sensitive and 95% specific for LAD occlusion proximal to S1. Right bundle branch block in anterior
MI is an independent marker of poor prognosis; this is due to the extensive myocardial damage involved rather than the conduction disorder
itself.

More Examples
Example 8 Ostial LAD occlusion (septal STEMI)

This patients ECG shows several signs of a very proximal LAD occlusion:

There is a septal STEMI with ST elevation maximal in V1-2 (extending out to V3).

There is a new RBBB with marked ST elevation (> 2.5 mm) in V1 plus STE in aVR these features suggest occlusion proximal to
S1.

This patient came in post VF arrest and was taken straight to the cath lab where he was found to have a complete ostial occlusion of his LAD.

Example 9 Anteroseptal STEMI, likely proximal LAD occlusion

Acute anteroseptal STEMI with STE maximal in V1-4. The following signs of proximal LAD occlusion are present:

RBBB.

STE in aVR.

STE in aVL.

> 1 mm ST depression in the inferior leads.