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ECG Reference · Ischemia and Myocardial Infarction

Occlusion Myocardial Infarction (OMI) on ECG

Occlusion MI · OMI, NOMI, OMI paradigm

Occlusion myocardial infarction (occlusion MI, OMI) is a working clinical and angiographic concept defined as a suspicion of acute coronary occlusion based on a combination of clinical presentation, ECG dynamics, and other data, rather than a separate validated diagnostic category with a single ECG criterion. The core premise is that a proportion of acute occlusions do not meet the formal voltage criteria for STEMI and can be missed if assessment is restricted to ST-segment elevation thresholds in millimeters.

8 min readFor medical students and physiciansUpdated 18.10.2026
Prepared by WhiteCoat Pro editorial teamCriteria verified against guidelines by two independent reviewers

ECG criteria

  1. Dynamic ST-T changes on serial ECGs in an appropriate clinical context warrant urgent reassessment and consultation, but do not constitute an independent, specific OMI criterion
  2. Hyperacute T waves: symmetrical, broad, tall, disproportionate to the QRS complex, and localized to specific leads — assess in dynamics and correlate with electrolyte levels and clinical presentation
  3. Reciprocal ST depression in leads opposite to the suspected ischemia zone (e.g., depression in II, III, aVF when lateral ischemia is suspected)
  4. de Winter pattern: upsloping ST depression at the J point, typically ≥1 mm in leads V2–V6 (frequently involving V3–V4) with tall, symmetrical T waves, possibly accompanied by minor ST elevation in aVR — a pattern suspicious for acute occlusion/critical proximal LAD lesion in the appropriate clinical context, but not independent proof of occlusion
  5. Horizontal ST depression, maximal in V1–V3 (occasionally extending to V4), particularly with a tall R wave and positive T wave — suspicion of posterior MI; confirmed by ST elevation in V7–V9, typically ≥0.5 mm in two contiguous leads
  6. ST elevation in aVR ≥ elevation in V1 in the setting of diffuse ST depression across most leads — a marker of high-risk extensive subendocardial ischemia, potential left main coronary artery or multivessel disease, but not independent proof of occlusion
  7. Aslanger pattern (a rare associated sign, not an independent diagnostic criterion): predominant ST elevation in lead III without elevation in lead II, combined with ST depression in V4–V6 (often with a positive terminal T wave component) in acute inferior MI with concomitant ischemia in another territory — requires expert evaluation, do not use in isolation
  8. The absence of formal STEMI voltage criteria does not rule out significant occlusion in the presence of a compelling clinical picture and a combination of highly specific signs
Risktransmural ischemia and risk of myocardial necrosis are possible if the presentation is underestimated
Where to lookall 12 leads + V7–V9, V3R–V4R when suspected
Key signhyperacute T waves, reciprocal ST depression, highly specific occlusion equivalents
Managementurgent interventional cardiology consultation in the presence of a compelling clinical picture and specific signs

What it looks like on ECG

OMI is not a distinct ECG pattern, but an approach: suspecting acute coronary occlusion based on a constellation of signs, even when formal STEMI criteria are not met. STEMI criteria (per AHA/ACCF/HRS and ESC): ST-segment elevation ≥1 mm in two contiguous limb leads; in leads V2–V3, thresholds are stratified by sex and age — in women ≥1.5 mm, in men aged 40 years and older ≥2 mm, in men younger than 40 years ≥2.5 mm; in all other precordial leads ≥1 mm. In the presence of LBBB, ventricular pacing, and marked LV hypertrophy, standard thresholds are less reliable because baseline ST-T morphology is altered: in these cases, Sgarbossa criteria or modified (Smith) criteria are applied alongside comparison with a prior ECG. New RBBB is not in itself a sufficient criterion for occlusion, but if ischemic symptoms persist, it requires urgent evaluation. Pre-existing ST-segment elevation (e.g., in LV aneurysm) is evaluated by comparing dynamics with previous tracings rather than relying on absolute values.

Findings considered suspicious for occlusion within the OMI paradigm in the appropriate clinical context include:

PatternLeadsWhat to look for
de Winter patternV2–V6 (most commonly V3–V4)upsloping ST depression at the J point with tall, symmetrical T waves, possible minor ST elevation in aVR
Posterior MI (direct and reciprocal signs)reciprocal depression in V1–V3(V4); direct elevation in V7–V9 ≥0.5 mmanterior lead ST depression as a reciprocal sign, elevation in posterior leads as a direct sign
ST elevation in aVRaVR, diffuse depression in other leadsmarker of extensive ischemia, potential left main coronary artery or multivessel disease
Aslanger patternIII (elevation without elevation in II), V4–V6 (depression)inferior MI with concomitant ischemia in another territory
Hyperacute T wavesmatching the localization of suspected ischemiatall, symmetrical, broad T waves disproportionate to QRS

The posterior component frequently coexists with inferior or lateral infarction rather than occurring in isolation; therefore, posterior leads V7–V9 are especially useful when a posterior component of an inferior or lateral MI is suspected. All of the above findings require correlation with clinical presentation (anginal chest pain) and serial ECG recordings due to the dynamic nature of the presentation.

Mechanism

Acute coronary occlusion causes myocardial ischemia and a current of injury within the perfusion zone of the affected artery; ECG manifestations reflect a complex spatial potential difference between the ischemic and intact zones, rather than a simple unidirectional shift of a single vector. The severity and morphology of changes depend on the degree and duration of occlusion, collateral development, arterial localization, spontaneous or pharmacotherapeutic reperfusion, and baseline myocardial status. Occlusion is not necessarily transmural or permanent: incomplete, transient, or spontaneously reperfused occlusion can occur, in which typical ST elevation is absent or minimal, although the risk of ischemic injury persists. In the early stages, changes may be limited to hyperacute T waves or minor ST shifts that do not reach formal criteria. Therefore, the OMI approach advocates evaluating a combination of ECG features and clinical presentation rather than relying solely on the ST-elevation threshold value.

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Causes

  • Thrombotic coronary artery occlusion due to atherosclerotic plaque rupture
  • Plaque erosion with thrombosis
  • Spontaneous coronary artery dissection (SCAD)
  • Coronary vasospasm with subtotal or total occlusion (Prinzmetal angina variant culminating in occlusion)
  • Coronary artery embolism
  • Stent thrombosis

Differential diagnosis

  • STEMI by formal criteria — an ECG category based on formal ST-elevation criteria; OMI — the concept of acute coronary occlusion. These are overlapping but non-identical categories: STEMI criteria are neither necessary nor sufficient to confirm occlusion — STEMI can occur without total occlusion, and acute occlusion may fail to produce diagnostic ST elevation.
  • NSTE-ACS without highly specific signs of occlusion — ST depression or T-wave changes without compelling equivalent patterns; managed according to the ESC NSTE-ACS risk stratification algorithm: immediate invasive strategy for very high-risk criteria, early (within 24 hours) for high risk, otherwise individualized invasive strategy.
  • Wellen's syndrome — reperfused (not occluded at the time of recording) anterior artery with biphasic or deeply inverted T waves in V2–V3; management — early NSTE-ACS invasive strategy, rather than the "<120 min" window applied to overt occlusion.
  • Early repolarization and pericarditis — diffuse concordant ST elevation without reciprocal depression and without typical ischemic dynamics.
  • LV hypertrophy with secondary ST-T changes — persistent morphology without acute dynamics, correlated with medical history and prior ECGs.

Clinical significance and management

The OMI approach emphasizes that the decision regarding the urgency of revascularization must take into account the likelihood of acute coronary occlusion based on the totality of data, rather than strict adherence to formal STEMI criteria. There is no single validated ECG algorithm for OMI; the decision for immediate angiography is made by a qualified team considering symptoms, hemodynamics, serial ECGs, troponin levels, and differential diagnosis. The physician should:

  • Evaluate ECG dynamics (repeat tracings if chest pain persists)
  • Actively search for highly specific findings: de Winter pattern, direct and reciprocal signs of posterior MI, ST elevation in aVR as a risk marker, Aslanger pattern, hyperacute T waves — correlating them with clinical presentation
  • In cases of high probability of ongoing occlusion, persistent ischemia, hemodynamic or electrical instability, or a compelling, expert-evaluated pattern (de Winter, posterior or right ventricular equivalent, overt reciprocal changes), immediately contact the regional STEMI/intervention team and consider emergency angiography; isolated nonspecific signs (e.g., isolated ST elevation in aVR or isolated Aslanger pattern without the rest of the clinical picture) do not require this on their own
  • In all other cases, manage the patient according to the NSTE-ACS risk stratification algorithm
  • For patterns without ongoing occlusion (e.g., Wellens), apply an early NSTE-ACS invasive strategy
  • Involve an experienced ECG interpreter and cardiologist when the presentation is ambiguous, without delaying consultation

Common interpretation errors

  • Refraining from suspecting occlusion solely because ST elevation did not reach the millimeter threshold, without accounting for dynamics and other signs
  • Ignoring reciprocal ST depression as a significant associated sign
  • Missing isolated ST depression in V1–V3(V4) without recording posterior leads V7–V9
  • Overinterpretation of non-specific findings (ST elevation in aVR, hyperacute T waves without dynamics, isolated Aslanger pattern) as proven left main coronary artery occlusion or STEMI equivalent
  • Single ECG evaluation without considering dynamics in the presence of ongoing clinical symptoms
Test yourselfThree exam- and accreditation-level questions with detailed explanations.

1. Which management strategy is correct for Wellens' syndrome according to the NSTE-ACS approach?

Wellens' syndrome reflects a reperfused artery without ongoing occlusion; therefore, an early NSTE-ACS invasive strategy is used rather than the strict primary PCI window.

2. Which ECG pattern is considered a finding suspicious for acute proximal LAD occlusion in suspected OMI?

The de Winter pattern is a finding suspicious for acute occlusion/critical lesion of the proximal LAD in the appropriate clinical context, but not standalone proof of occlusion.

3. How should ST elevation in aVR exceeding or equaling ST elevation in V1, in the setting of diffuse ST depression, be correctly interpreted?

This pattern is associated with extensive subendocardial ischemia and possible left main or multivessel disease, but does not in itself confirm acute occlusion and requires clinical correlation.

Frequently asked questions

How does OMI differ from STEMI?

STEMI is an ECG category based on formal voltage criteria for ST elevation. OMI is the concept of acute coronary occlusion. The categories overlap but are not identical: STEMI criteria are neither necessary nor sufficient to confirm occlusion — STEMI can occur without total occlusion, and occlusion may not produce diagnostic ST elevation.

What is NOMI?

NOMI (non-occlusive MI) is a non-standardized term not included in the standard Universal Definition of MI or ESC classifications. It should not be confused with Type 2 myocardial infarction (supply-demand mismatch, which can also occur with coronary atherosclerosis) and MINOCA (myocardial infarction with non-obstructive coronary arteries on angiography) — these are distinct, separately defined concepts.

Is emergency PCI necessary for OMI without ST elevation by STEMI criteria?

The decision is made by a qualified team taking into account the clinical presentation, dynamics, and cumulative data rather than an isolated ECG sign. In the presence of a compelling clinical presentation combined with highly specific findings (de Winter pattern, posterior or right ventricular equivalent, clear reciprocal changes, instability), emergency angiography is considered following an algorithm similar to STEMI. For non-specific or isolated findings, management remains within the framework of NSTE-ACS risk stratification.

How to suspect posterior occlusion ischemia?

By horizontal ST depression, maximal in V1–V3, sometimes extending to V4, especially with a tall R wave and positive T wave. They are confirmed by direct recording of posterior leads V7–V9 showing ST elevation, usually ≥0.5 mm in two contiguous leads.

Does the "<120 min" window apply to Wellens' syndrome?

No, Wellens' syndrome reflects a reperfused artery without active occlusion at the time of recording, so the early invasive NSTE-ACS strategy is applied, not the primary PCI window.

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Related terms

More in the section "Ischemia and Myocardial Infarction"

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Sources

  • Hampton J. The ECG in Clinical Practice
  • ESC Guidelines for the management of acute coronary syndromes, 2023
  • Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
  • Orlov V.N. Guide to Electrocardiography

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.