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Cardiology

Myocardial Infarction on ECG: STEMI and NSTEMI Signs

WhiteCoat Pro Editorial BoardApril 11, 2026Updated April 19, 20264 min read
Contents · 12 sections
  1. 1. Definition and classification
  2. 2. Pathogenesis
  3. 3. Clinical presentation
  4. 4. ECG diagnosis
  5. 5. Biomarkers
  6. 6. Risk stratification
  7. 7. STEMI management
  8. 8. NSTEMI / unstable angina management
  9. 9. Core medications and adjunctive therapy
  10. 10. Complications
  11. 11. Secondary prevention and rehabilitation
  12. 12. FAQ

In a nutshell. Myocardial infarction (MI) is cardiomyocyte necrosis due to acute ischemia. According to the Fourth Universal Definition of Myocardial Infarction (4UDMI), the diagnosis requires ↑/↓ troponin values + clinical presentation/ECG/imaging. Types: Type 1 (atherothrombosis), Type 2 (secondary to stress/anemia), Type 3 (death before biomarkers are drawn), Type 4a/b (PCI-related), Type 5 (CABG-related). STEMI → reperfusion within 12 h (primary PCI < 120 min or thrombolysis).

1. Definition and classification

Acute coronary syndrome (ACS) is a clinical term encompassing unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). The Universal Definition of Myocardial Infarction (4UDMI, 2018) requires: a rise and/or fall of cardiac troponin values with at least one value above the 99th percentile upper reference limit + at least one of the following criteria for ischemia (symptoms, new ischemic ST-T changes, new pathological Q waves, imaging evidence of new loss of viable myocardium, or identification of an intracoronary thrombus by angiography).

Types of MI

  1. Type 1 — atherothrombotic (plaque rupture/erosion).
  2. Type 2 — myocardial oxygen supply/demand imbalance (coronary spasm, anemia, hypotension, tachyarrhythmia).
  3. Type 3 — cardiac death with symptoms suggestive of myocardial ischemia, when troponin values are not yet available.
  4. Type 4a — procedural related to PCI.
  5. Type 4b — stent thrombosis.
  6. Type 4c — restenosis.
  7. Type 5 — CABG-related.

2. Pathogenesis

The underlying mechanism of Type 1 MI is the rupture or erosion of an unstable atherosclerotic plaque → exposure of collagen and von Willebrand factor → platelet adhesion and activation → platelet-rich thrombus formation → activation of the coagulation cascade → fibrin-platelet thrombus → occlusion. Total occlusion leads to STEMI, while partial occlusion or occlusion with good collateral circulation leads to NSTEMI / unstable angina.

3. Clinical presentation

  • Pressing, squeezing retrosternal chest pain > 20 minutes, not relieved by nitroglycerin.
  • Radiation to the left arm, lower jaw, epigastrium.
  • Cold sweat, weakness, nausea, dyspnea, sense of impending doom.
  • Atypical presentations: abdominal (inferior MI), asthmatic, arrhythmic, cerebral, painless (more common in diabetics, elderly, and women).

4. ECG diagnosis

STEMI

  • ST-segment elevation in ≥ 2 contiguous leads: ≥ 1 mm in limb leads and V4–V6, ≥ 2 mm in men < 40 years and ≥ 1.5 mm in women in leads V2–V3.
  • New left bundle branch block (LBBB) in the appropriate clinical setting (Sgarbossa criteria).

NSTEMI

  • ST-segment depression ≥ 0.5 mm, T-wave inversion, or sometimes a normal ECG.
  • Evolution of changes on serial ECGs.

STEMI localization

LeadsWallArtery
V1–V4AnteriorLAD
I, aVL, V5–V6LateralLCx / diagonal
II, III, aVFInferiorRCA (80%) or LCx
V7–V9PosteriorRCA/LCx
V3R, V4RRight ventricleRCA

In inferior MI, always record leads V3R–V4R and V7–V9 to rule out right ventricular involvement and posterior wall infarction.

5. Biomarkers

  • High-sensitivity cardiac troponin I or T (hs-cTn) is the gold standard. Rises within 1–3 h, peaks at 12–24 h, and remains elevated for 10–14 days.
  • The 0/1-hour and 0/3-hour algorithms allow for rapid rule-out or rule-in of MI.
  • CK-MB, myoglobin — outdated now that troponin testing is widely available.

6. Risk stratification

  • TIMI risk score — for NSTEMI and STEMI.
  • GRACE risk score — more accurate for in-hospital and long-term mortality.
  • CRUSADE score — bleeding risk assessment prior to anticoagulation.

7. STEMI management

Primary PCI

  • The treatment of choice if it can be performed within 120 minutes of first medical contact (door-to-balloon time < 60 min).
  • Drug-eluting stent (DES) is the standard of care.
  • During the procedure: UFH or bivalirudin; GPIIb/IIIa inhibitors may be used in the presence of a high thrombus burden.

Thrombolysis

  • If primary PCI cannot be performed within 120 minutes, initiate fibrinolytic therapy within 10 minutes of diagnosis.
  • Agents: alteplase, tenecteplase (bolus administration — more convenient).
  • Reperfusion criteria: ST-segment resolution > 50% at 60–90 minutes, reperfusion arrhythmias, earlier peak of cardiac biomarkers.
  • After thrombolysis — rescue PCI in case of failure or routine coronary angiography within 2–24 h (pharmaco-invasive strategy).

8. Management of NSTEMI / unstable angina

  • Early invasive strategy (coronary angiography): in high risk (GRACE > 140, ST-segment dynamics, troponins, hemodynamics) — within 2–24 h; in very high risk (hemodynamics, arrhythmias) — < 2 h.
  • Antithrombotic therapy: ASA + P2Y₁₂ inhibitor (ticagrelor/prasugrel/clopidogrel) + parenteral anticoagulant (fondaparinux, LMWH, or UFH).

9. Essential drugs and adjunctive therapy

  • β-blockers (bisoprolol, metoprolol) — reduce mortality.
  • ACE inhibitors / ARBs — in case of reduced LVEF or anterior MI.
  • High-intensity statins (atorvastatin 80 mg, rosuvastatin 20–40 mg) — for all patients.
  • Aldosterone antagonists (eplerenone) — for LVEF < 40% + heart failure / diabetes mellitus.
  • Nitrates — symptomatically for persistent ischemia.
  • DAPT (ASA + P2Y₁₂) for 12 months, then ASA indefinitely.

10. Complications

  • Arrhythmias: ventricular fibrillation (first hours), AV blocks in inferior MI.
  • Acute heart failure, cardiogenic shock (Killip classification).
  • Mechanical complications: free wall rupture, ventricular septal rupture, papillary muscle rupture (days 3–7).
  • Pericarditis (early epistenocarditic, late — Dressler syndrome).
  • Thromboembolism (left ventricular mural thrombus).
  • Post-infarction aneurysm, remodeling.

11. Secondary prevention and rehabilitation

  • Smoking cessation, diet, physical activity.
  • Target: BP < 130/80 mmHg, LDL-C < 1.4 mmol/L, HbA1c < 7%.
  • Cardiac rehabilitation with physical exercise.
  • Influenza and pneumococcal vaccination.

12. FAQ

Can MI be diagnosed without troponins?
No. Troponin elevation is the cornerstone of the MI definition. Without laboratory confirmation, only "suspected MI" is possible.

What is MINOCA?
Myocardial infarction with non-obstructive coronary arteries. Requires investigation of the cause (spasm, embolism, myocarditis, Takotsubo).

When is the Sgarbossa criteria used?
In the presence of LBBB or paced rhythm — to confirm acute ischemia: ≥ 3 points — high probability of MI.

How long should DAPT be maintained after MI?
Standard is 12 months. In high ischemic risk and low bleeding risk — up to 36 months. In high bleeding risk — shortened to 3–6 months.

What is the rationale of the pharmaco-invasive strategy?
Following thrombolysis, regardless of its success, perform coronary angiography within 2–24 h. Improves outcomes compared to thrombolysis alone.

See also: CHF · PE · Anticoagulants · Antiarrhythmics · TIMI NSTEMI · GRACE · Cardiology Catalog

This material is educational in nature and does not replace a doctor's consultation. Verify treatment regimens and dosages with current clinical guidelines.

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