ECG criteria
- Topical interpretation is applied only after confirming diagnostically significant ST elevation according to STEMI criteria: ≥1 mm in two contiguous limb leads or in V7–V9, and in chest leads V2–V3 — taking into account sex and age (thresholds of ≥2.5 mm in men under 40, ≥2 mm in men ≥40, ≥1.5 mm in women are most commonly cited; values in different sources may slightly differ); mimics must be excluded — early repolarization, LVH, pericarditis, LBBB
- ST elevation in V1–V4 (anteroseptal leads) with reciprocal depression in II, III, aVF — anterior wall, LAD territory
- ST elevation in II, III, aVF with maximum in III > II — inferior wall, most commonly RCA
- ST elevation in II, III, aVF with maximum in II ≥ III and/or ST elevation in I, aVL — inferior wall, most commonly LCx
- In inferior MI, ST elevation ≥ 1 mm in V4R (or V3R–V4R), especially in the first hours, supports the diagnosis of right ventricular infarction and usually indicates proximal RCA occlusion; anatomical exceptions are possible
- ST depression in V1–V3 can be a reciprocal sign of posterior MI; ST elevation ≥0.5 mm in two contiguous leads V7–V9 supports posterior localization of acute ischemia/occlusion (LCx or distal RCA); the diagnosis of infarction is established based on symptoms, ECG dynamics, and troponin, rather than this sign alone
- ST elevation in I, aVL, V5–V6 — lateral wall, diagonal branch of LAD or LCx
- South African flag sign — a rare pattern of high lateral ischemia: ST elevation in I, aVL, and V2 with reciprocal depression in III; classically associated with occlusion of the first diagonal branch of the LAD; anatomical correlation is probabilistic and does not replace coronary angiography
What it looks like on ECG
The logic of topical diagnostics is built in two steps: first, diagnostically significant ST elevation is confirmed by STEMI criteria in two contiguous leads, then the wall is determined by the lead group and the probable artery, taking into account anatomical blood supply variants.
| Wall | Leads | Artery |
|---|---|---|
| Anterior/septal | V1–V4 | LAD |
| Lateral | I, aVL, V5–V6 | diagonal branch of LAD or LCx |
| Inferior | II, III, aVF | RCA (more often) or LCx |
| Posterior | reciprocally V1–V3, directly V7–V9 | LCx or distal RCA |
| Right ventricle | V3R–V4R | proximal RCA |
In inferior MI, the artery dominance sign is the ratio of ST elevation in III and II: III > II with depression in I, aVL suggests RCA; II ≥ III without depression in I, aVL suggests LCx. Diffuse ST depression, especially combined with ST elevation in aVR, indicates diffuse subendocardial ischemia and can occur with left main coronary artery disease or multivessel disease, but pertains to the differential diagnosis of ischemia without localized ST elevation rather than topical localization of infarction. Extensive anterior ST elevation in V1–V6, I, aVL increases the probability of proximal LAD occlusion; the exact level of occlusion and the affected branch (septal, diagonal) are determined by coronary angiography rather than ECG.
Mechanism
Each coronary artery supplies a specific myocardial segment that corresponds to the zone "seen" by the respective ECG leads. In acute myocardial injury, an injury current is generated in the ischemic zone, directed toward the electrodes overlying the affected area, which typically causes ST-segment elevation in these leads and reciprocal depression in the opposite ones. This mechanism should not be reduced to obligatory transmural ischemia: ST elevation can also occur with subepicardial injury without complete transmurality, and its absence does not rule out acute occlusion. Anatomical variants (RCA or LCx dominance, ramus intermedius or branching LAD patterns) explain why the "lead-to-artery" mapping is probabilistic rather than absolute.
Causes
- Atherothrombotic occlusion of an epicardial coronary artery (the main cause of STEMI)
- Coronary spasm (Prinzmetal's angina)
- Spontaneous coronary artery dissection (SCAD)
- Coronary embolism
Differential diagnosis
Pericarditis: typically diffuse ST elevation with ST depression in aVR and frequently in V1, as well as PR depression; prominent reciprocal depression in other leads points more toward a focal MI. Early repolarization syndrome: stable pattern, notch at the J point, without dynamic evolution. Left bundle branch block and pacemaker pattern: Sgarbossa criteria and modified Smith criteria are used rather than standard lead-based topography. Takotsubo cardiomyopathy: can mimic an anterior MI; imaging reveals transient wall motion abnormalities, most commonly the apical variant, though mid-ventricular, basal, and focal variants are also possible; there is no culprit coronary artery occlusion, while coexisting non-critical or even significant atherosclerosis is not excluded. Severe multi-vessel atherosclerosis without acute occlusion: diffuse ST-depression pattern with ST elevation in aVR — reflects subendocardial ischemia and occurs in multi-vessel disease, left main coronary artery (LMCA) disease, anemia, hypoxia, tachycardia, and other conditions; by itself, it does not prove either LMCA occlusion or STEMI.
Clinical significance and management
Topographical localization on the ECG helps predict the volume of affected myocardium, the risk of complications (AV block in inferior MI, cardiogenic shock in anterior MI), and guides the interventionalist before coronary angiography, but does not replace it — angiography remains the gold standard for identifying the culprit artery. If inferior MI is suspected, recording V3R–V4R is mandatory to assess the right ventricle: detecting an RV infarction requires hemodynamic assessment; in case of hypotension, nitrates and other preload-reducing agents are avoided, and cautious fluid administration is considered only in the absence of signs of fluid overload and under close monitoring. In case of ST depression in V1–V3 without overt elevation anywhere, record V7–V9 to rule out isolated posterior MI. The pattern of diffuse subendocardial ischemia with ST elevation in aVR is a high-risk marker; the urgency of the invasive strategy is determined by the clinical presentation (ongoing chest pain, hemodynamic instability, ECG dynamics, troponin), not by this single sign alone.
Common interpretation errors
- Drawing conclusions about the culprit artery without recording V7–V9 in the presence of isolated ST depression in V1–V3
- Forgetting V3R–V4R in inferior MI and missing right ventricular involvement
- Interpreting ST elevation in aVR with diffuse depression as proven LMCA occlusion rather than as a non-specific high-risk marker
- Applying standard topography in LBBB or pacing without Sgarbossa/Smith criteria
- Treating the lead-to-artery mapping as absolute, ignoring anatomical blood supply variants and the need to confirm the significance of ST elevation using STEMI criteria
1. ST elevation is maximal in lead III compared to lead II, with ST depression in leads I and aVL. Which artery is more likely affected?
The predominance of ST elevation in lead III over lead II with reciprocal depression in leads I and aVL is a classic sign of right coronary artery occlusion in inferior MI.
2. Which additional leads should be recorded during an inferior myocardial infarction to assess the right ventricle?
Right precordial leads V3R–V4R allow the detection of ST elevation indicating right ventricular infarction in proximal RCA occlusion.
3. How should ST elevation in aVR accompanied by diffuse ST depression in 8 or more leads be interpreted?
This pattern is non-specific for a single vessel, but indicates widespread high-risk ischemia requiring clinical evaluation and, where indicated, an urgent invasive strategy.
Frequently asked questions
Can the culprit artery be accurately determined from the ECG alone?
No, the ECG provides a probabilistic localization of the myocardial wall and the likely artery taking typical anatomy into account. Precise identification of the culprit vessel and the level of occlusion is only possible via coronary angiography.
How to differentiate RCA occlusion from LCx occlusion in inferior myocardial infarction?
The ratio of ST elevation in lead III to lead II and the presence of depression in leads I and aVL are evaluated. The predominance of lead III over lead II with depression in I and aVL points to the RCA, whereas II ≥ III without such depression points to the LCx.
Why are right precordial leads recorded in inferior myocardial infarction?
Because right ventricular infarction is frequently associated with proximal RCA occlusion and accompanies inferior MI. ST elevation ≥1 mm in V4R alters hemodynamic assessment and the approach to nitrates and fluid therapy.
What does ST-segment elevation in aVR signify in acute coronary syndrome?
ST-segment elevation in aVR accompanied by widespread ST-segment depression in most leads is a nonspecific marker of high-risk diffuse subendocardial ischemia. It may occur in left main coronary artery disease or multivessel disease, but by itself does not prove occlusion and is not an independent indication for emergency invasive management without clinical evaluation.
Are posterior leads necessary for all patients presenting with chest pain?
No, leads V7–V9 are recorded specifically when isolated posterior myocardial infarction is suspected — typically in the presence of ST-segment depression in V1–V3 without ST-segment elevation in the standard 12 leads.
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Related terms
More in the section "Ischemia and Myocardial Infarction"
Sources
- Goldberger's Clinical Electrocardiography, latest edition
- ESC Guidelines for the management of acute coronary syndromes, 2023
- Orlov V.N. Guide to Electrocardiography
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.