Heart Attack ECG Localisation: Which Artery Is Blocked?

The ECG does two jobs in a suspected heart attack: classification and localisation. First it classifies: ST elevation means STEMI and immediate treatment, while its absence sends the clinician to the troponin result, which separates NSTEMI from unstable angina. Then it localises: the leads that show the change identify which coronary artery is blocked, whether the anterior, inferior, lateral or posterior wall is at risk.

Dr. Vikas Thakran, Consultant, Interventional Cardiology, BLK-Max Super Speciality Hospital, New Delhi, India, at the time of the masterclass, presented ECG reading to referring doctors as a triage tool before anything else. His rule was to look at the ECG first and let it decide what happens next. This article sets out that decision pathway, the lead patterns that point to each artery, and the subtle tracings that are easily missed. For the mechanism behind the blockage and an overview of acute coronary syndrome, see the complete guide to acute coronary syndrome; for what happens after the diagnosis, see the article on STEMI and NSTEMI treatment protocols.

STEMI vs NSTEMI vs unstable angina: the ECG flow chart

Once acute coronary syndrome is suspected, an ECG is recorded at once. Dr. Thakran described only two branches:

1. ST segment elevated. The artery is 100% blocked. Treat the patient directly, without waiting for further tests. This is ST-elevation myocardial infarction (STEMI).
2. ST segment not elevated (the ECG is normal or shows ST depression). Send the cardiac markers.

• Markers positive: non-ST-elevation myocardial infarction (NSTEMI).
• Markers negative: unstable angina.

His summary for the audience was a single line: ECG first; if ST is elevated, treat directly; if not, get markers; negative is unstable angina, positive is NSTEMI.

The cardiac marker of choice is troponin, a protein released from damaged heart muscle cells. A rise in troponin confirms that muscle has died, which is the difference between an infarction (NSTEMI) and unstable angina, in which the pain is ischaemic but no measurable damage has yet occurred. Because troponin can be normal in the first hours after symptom onset, current guidelines use high-sensitivity assays repeated over a short interval rather than relying on a single early result.

What ST elevation and ST depression mean

ST elevation means the full thickness of the heart wall is ischaemic because the artery is completely blocked; ST depression means only the inner layer of the wall is affected. The ST segment is the part of the ECG between the end of the QRS complex and the start of the T wave, the early phase of ventricular repolarisation. In a healthy heart it sits on the baseline. Ischaemia moves it.

Dr. Thakran explained the difference in terms of the heart wall:

• ST depression reflects partial involvement: the ischaemia affects only the inner layer of the muscle, not its full thickness.
• ST elevation reflects total wall involvement: the ischaemia runs through the full thickness of the wall, because the supplying artery is completely occluded.

That is why the two patterns lead to different treatment. With ST elevation, he said, clinicians do not wait: the patient goes either to the catheterisation laboratory or receives medicine for thrombolysis. With ST depression, the patient receives antiplatelets while the markers are obtained. He placed the treatment window for STEMI explicitly: it is very important to treat within the first two hours.

ECG localisation of a heart attack: which artery is blocked?

The ECG localises a heart attack, or myocardial infarction (MI), by the leads that change: V1 to V6 point to the LAD and the anterior wall, II, III and aVF to the RCA and the inferior wall, I and aVL to the lateral wall, and ST depression in the anterior leads to the LCx and the posterior wall. The coronary artery map from the pillar guide translates directly into this pattern. Dr. Thakran linked each artery to the wall it supplies: the left anterior descending (LAD) artery to the anterior wall, the right coronary artery (RCA) to the inferior wall, and the left circumflex (LCx) artery to the posterior wall. Each wall is "seen" by a particular group of leads.

Anterior wall MI: leads V1 to V6

The anterior wall is viewed by the chest leads. Dr. Thakran described the anterior leads as V2 to V6 in one tracing and V1 to V6 in summary, and he stressed that anterior infarction varies widely in how it looks. At one extreme are "devastating" ST elevations across the anterior leads, which no one misses. At the other, the change can be as subtle as a small elevation in V4 to V6. Between the two, an anterior wall infarction sometimes presents as right bundle branch block (RBBB), a conduction pattern in which the right ventricle is activated late.

The RBBB presentation is the one to respect. Current guidelines advise that a patient with ischaemic symptoms and right bundle branch block be managed with the same urgency as STEMI, because the block can conceal an occlusion of the proximal LAD.

One of his example tracings was an anterior Q-wave infarction. Pathological Q waves are deep, broad initial downward deflections that indicate heart muscle that has already died, so their presence signals an infarction that is established rather than evolving.

Inferior wall MI: leads II, III and aVF

An occlusion of the right coronary artery produces ST elevation in the inferior leads, II, III and aVF, which view the heart from below. The inferior pattern carries a treatment implication that Dr. Thakran raised separately when discussing drugs: nitrates should be used with care, and may not be appropriate, in inferior wall STEMI. The reason is that an RCA occlusion often extends to the right ventricle, which then depends on adequate filling pressure; nitrates reduce that pressure and can cause profound hypotension. Right-sided chest leads, particularly V4R, are recorded to detect right ventricular involvement. The treatment article covers nitrate use in detail.

Lateral wall MI: leads I and aVL

In lateral infarction, Dr. Thakran pointed to ST elevation in lead I and lead aVL, the high lateral leads. The lower lateral leads, V5 and V6, are frequently involved as well. Lateral changes can be small and are among the easiest to overlook, which is one reason the territory table above is worth committing to memory.

Posterior MI on the ECG: look at the back

The posterior wall is easily missed, because no standard lead faces it. Dr. Thakran made the point directly: in posterior infarction, the classical ST elevation may be absent. Instead the standard ECG shows ST depression in the anterior chest leads, the mirror image of what is happening on the back of the heart. Because the LCx is the posterior wall artery, an LCx occlusion can present this way.

The established pattern is horizontal ST depression in the right precordial leads, V1 to V3, often with tall R waves in the same leads. His practical tip was the remedy: place leads on the back of the patient. Posterior leads (V7 to V9) placed there show the ST elevation that the standard ECG cannot. For a referring doctor, the habit to build is simple: anterior ST depression in a patient with chest pain should prompt posterior leads before the case is labelled NSTEMI, because a posterior STEMI needs immediate reperfusion.

Wellens syndrome: the warning ECG in a pain-free patient

Wellens syndrome is a pattern of deep or biphasic T waves in the anterior chest leads that warns of a critical narrowing of the proximal LAD, often in a patient who looks stable. Dr. Thakran called one such tracing, with deep T-wave inversions in the anterior leads, "interesting". In his words, such a patient, though apparently stable, is likely to have a big anterior wall infarction in the coming two weeks, in up to 80% of patients.

The narrowing behind the pattern has temporarily reopened. The T-wave changes typically appear in leads V2 and V3, either as deep symmetrical inversion or as a biphasic T wave, and they are often recorded when the patient is pain-free, with normal or only mildly raised troponin. That combination is what makes it dangerous: the patient appears well enough to send home.

The established management follows from the anatomy. Exercise stress testing is avoided, because the added demand can precipitate the very infarction the pattern predicts, and the patient is referred for early coronary angiography.

Suspected heart attack ECG checklist for referring doctors

For doctors managing chest pain without immediate specialist support, Dr. Thakran's guidance condenses into a short checklist:

1. Record the ECG first. A single tracing is enough to start STEMI treatment.
2. ST elevation: treat now. The artery is fully blocked. Arrange PCI or give thrombolysis without waiting for blood results, ideally within the first two hours.
3. No ST elevation: send troponin and give antiplatelets. Positive means NSTEMI; negative means unstable angina.
4. Localise the territory. Anterior (V1 to V6), inferior (II, III, aVF), lateral (I, aVL) or posterior (ST depression in the anterior leads, elevation in back leads).
5. Look for the subtle patterns. Small elevation in V4 to V6, RBBB, anterior ST depression that may be posterior STEMI, and the deep anterior T-wave inversions of Wellens syndrome.
6. Check the inferior wall before giving nitrates. Inferior STEMI calls for caution.

Dr. Thakran shared annotated ECGs with the audience for each territory, with explanatory captions, so that the patterns could be studied after the session. The questions doctors asked him, including how PCI is performed and the role of defibrillation, are answered in the session's Live Discussion, and his background is on his doctor profile. For a broader account of heart attack diagnosis, including troponin, CK-MB and echocardiography, see Dr. Rohit Goel's article on diagnosing a heart attack. More heart care content is on the cardiology specialty page.