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Myocardial Infarction (MI)

Clinical Subject Page

Myocardial Infarction (MI)

Also called

Heart Attack

ICD-10

I50.30

Specialty

Cardiology

Onset

Acute

Reviewed

June 2026

On This Page

Overview

A myocardial infarction (MI), or heart attack, occurs when blood flow to part of the heart muscle is blocked long enough to cause ischemic necrosis (death of heart muscle tissue).

Etiology & Risk Factors

The main causes for Myocardial Infarction (MI) include:

  • Coronary artery disease (CAD) – the most common cause
  • Coronary artery vasospasm (e.g., Prinzmetal angina, cocaine use)
  • Coronary artery dissection (e.g., spontaneous coronary artery dissection [SCAD])
  • Coronary artery embolism (e.g., from atrial fibrillation or a prosthetic heart valve)
  • Takotsubo cardiomyopathy
  • Myocarditis
  • Thrombophilia (e.g., polycythemia vera)
  • Vasculitis (e.g., polyarteritis nodosa, Kawasaki syndrome)
  • Myocardial oxygen supply-demand mismatch (Type 2 MI), such as:
    • Hypotension
    • Severe anemia
    • Hypertrophic cardiomyopathy
    • Severe aortic stenosis

Risk Factors ;

  • Coronary vasospasm: cocaine use
  • Spontaneous coronary artery dissection (SCAD):
    • Pregnancy
    • Fibromuscular dysplasia
    • Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome)
    • Inflammatory disorders
    • Hormonal therapy
    • Physical or emotional stress
    • Stimulant drug use (e.g., cocaine, amphetamines)

Pathophysiology

  • Atherosclerotic plaque rupture (Type 1 MI): An unstable, lipid-rich plaque with a thin fibrous cap ruptures. Macrophages release matrix metalloproteinases, weakening the fibrous cap and promoting rupture.
  • Thrombus formation: Rupture exposes the highly thrombogenic lipid core, causing platelet activation and thrombus formation, which partially or completely occludes the coronary artery.
  • Myocardial ischemia: Coronary artery occlusion reduces myocardial blood flow, producing an oxygen supply-demand mismatch and ischemia.
  • Myocardial necrosis: If ischemia persists without reperfusion, irreversible death of myocardial cells (ischemic necrosis) occurs.
    • Partial occlusion → Subendocardial infarction (NSTEMI)
    • Complete occlusion → Transmural infarction (STEMI)
  • Type 2 MI: Occurs without plaque rupture when myocardial oxygen supply is inadequate or oxygen demand is increased (e.g., hypotension, anemia, bradycardia, sustained tachyarrhythmia, vasospasm, or coronary dissection).

Clinical Presentation

  1. Typical Symptoms

    • Acute retrosternal chest pain lasting >20 minutes
    • Dull, squeezing, or pressure-like chest discomfort
    • Pain may radiate to the left arm, shoulder, neck, jaw, chest, or epigastrium
    • Often precipitated by physical exertion or emotional stress
    • Dyspnea
    • Diaphoresis (profuse sweating)
    • Nausea and vomiting
    • Pallor
    • Dizziness, lightheadedness, or syncope
    • Anxiety

    Physical Findings

    • Tachycardia or arrhythmias
    • Signs of heart failure (e.g., pulmonary edema, orthopnea)
    • Signs of cardiogenic shock (e.g., hypotension, cold extremities)
    • New heart murmur (e.g., S4)

    Atypical Presentation

    More common in older adults, women, and patients with diabetes:

    • Little or no chest pain (silent Myocardial Infarction MI)
    • Sharp or stabbing chest pain
    • Predominantly autonomic symptoms (e.g., nausea, diaphoresis)

    Inferior Wall Myocardial Infarction (MI)

    • Epigastric pain
    • Bradycardia
    • Right ventricular infarction may present with:
      • Hypotension
      • Elevated jugular venous pressure (JVP)
      • Clear lung fields

Types of Myocardial Infarction (MI)

Myocardial Infarction · Universal Classification (4th Universal Definition 2018)

MI = Rise and/or fall of cardiac troponin with at least one value above the 99th percentile URL, combined with evidence of acute myocardial ischaemia (symptoms, ECG changes, imaging, or coronary thrombus). Type determines management.
1
Atherosclerotic plaque rupture
Spontaneous MI from plaque disruption with coronary thrombus
2
Supply-demand mismatch
Ischaemia without plaque rupture — other cause
3
MI causing death
Cardiac death before biomarkers available
4
PCI-related MI
4a: peri-PCI • 4b: stent thrombosis • 4c: restenosis
5
CABG-related MI
Perioperative MI following bypass surgery
Type Mechanism ECG findings Troponin Coronary angiography Treatment
Type 1
Spontaneous		 Atherosclerotic plaque rupture or erosion → coronary thrombus → partial or complete occlusion

Includes: STEMI, NSTEMI, UA		 STEMI: ST elevation ≥1mm in ≥2 contiguous leads or new LBBB
NSTEMI: ST depression, T-wave inversion, or normal 		Elevated Rise & fall pattern above 99th percentile URL Obstructive CAD with culprit lesion; thrombus visible STEMI: Primary PCI <90 min (or thrombolysis if PCI unavailable)
NSTEMI: Anticoagulation, antiplatelet, early invasive strategy
Type 2
Secondary		 Supply-demand mismatch without plaque rupture:
• Coronary spasm
• Embolism
• Tachyarrhythmia
• Severe anaemia
• Hypertensive crisis
• Respiratory failure 		ST depression, T-wave changes, or diffuse ST changes depending on cause; may be non-specific Elevated Often modest rise; correlates with degree of ischaemia Normal or non-obstructive coronaries (<50% stenosis) in many cases; no culprit thrombus Treat underlying cause (arrhythmia, anaemia, hypoxia). Antiplatelet ± anticoagulation based on context
Type 3
Fatal MI		 Presumed MI causing sudden cardiac death before biomarkers or ECG can be obtained. Autopsy may confirm coronary thrombus or plaque rupture. ECG may show new ST changes or LBBB before death; often unavailable Unavailable Patient dies before blood drawn or results returned Post-mortem angiography or autopsy findings CPR / ACLS. Post-mortem diagnosis. Family counselling and genetic screening if inherited cause suspected.
Type 4a
Peri-PCI		 MI occurring within 48h of PCI due to: side branch occlusion, slow/no reflow, dissection, embolisation of atherosclerotic debris New ST changes or new LBBB post-procedure Elevated cTn >5× 99th percentile URL with rise from normal baseline, or >20% rise if already elevated Post-PCI: may show side branch loss, dissection, or no-reflow phenomenon GP IIb/IIIa inhibitors, intracoronary vasodilators (adenosine), thrombectomy; IABP if haemodynamically compromised
Type 4b
Stent thrombosis		 Acute, subacute, late, or very late stent thrombosis confirmed angiographically or at autopsy. Risk: dual antiplatelet non-adherence, stent underexpansion Acute STEMI pattern in stented territory Elevated Same as Type 1 criteria Thrombus within previously placed stent confirmed on angiography Emergency PCI; aspiration thrombectomy; optimise DAPT (prasugrel/ticagrelor preferred)
Type 4c
Restenosis		 In-stent restenosis or restenosis at balloon angioplasty site causing ischaemia — intimal hyperplasia, not thrombosis ST depression or T-wave changes in territory of prior PCI Elevated Meets MI criteria in setting of prior PCI Luminal narrowing at stent site without thrombus; no new culprit lesion Repeat PCI with drug-eluting balloon or new DES; CABG if anatomy unfavourable
Type 5
CABG-related		 Perioperative MI within 48h of CABG: graft occlusion, inadequate myocardial protection, coronary spasm, air embolism New Q waves ≥0.02s or new LBBB post-operatively Elevated cTn >10× 99th percentile URL from normal baseline; or >20% rise if already elevated Graft occlusion or native vessel disease on post-op angiography; diffuse ischaemia on imaging Urgent re-angiography; surgical revision if graft occluded; IABP / mechanical support; optimise antiplatelet
Troponin interpretation — key rules
Rise & fall pattern (acute MI)
Peak at 12–24h; draw at 0h, 1h (hs-cTn), and 3h
>20% relative rise within 1–3h = acute MI (hs-cTn protocols)
Single high value alone is insufficient — dynamic change required
Non-ischaemic causes of elevated troponin
Myocarditis, pericarditis, Takotsubo CM
PE, pulmonary hypertension, right HF
Sepsis, CKD, stroke, rhabdomyolysis
Cardioversion, cardiac contusion
High-sensitivity troponin (hs-cTn) thresholds
Rule OUT MI: hs-cTnT <5 ng/L at 0h (ESC 0h/1h algorithm)
Rule IN MI: hs-cTnT ≥52 ng/L at 0h OR Δ≥6 ng/L at 1h
Observe zone: values between rule-in and rule-out thresholds → 3h sample

ECG Changes In Myocardial Infarction (MI)

ECG Changes in Myocardial Infarction · Systematic Guide

Minutes (Hyperacute)
Tall, peaked T waves
Hyperacute T waves — earliest sign; often missed. Broad-based, asymmetric, taller than normal.
Hours 1–6 (Acute)
ST elevation
ST elevation ≥1mm in ≥2 contiguous leads. Tombstone pattern in severe STEMI. T wave merges with ST.
Hours 6–24 (Evolving)
Q waves + T inversion
Pathological Q waves begin forming. T waves invert as ST starts to resolve. Sign of transmural necrosis.
Days 1–3 (Subacute)
ST resolves, deep T inversion
ST returns toward baseline. Deep symmetrical T-wave inversion (Wellens pattern). Q waves persist.
Weeks–months (Chronic)
Persistent Q waves
Q waves become permanent markers of old MI. T waves may normalise. ST usually isoelectric.
Territory Artery (culprit) Leads with ST elevation Reciprocal ST depression Clinical notes
Inferior MI RCA (80%) or LCx (20%)
II III aVF
I aVL
Most common STEMI. Check RV involvement with V4R. Hypotension may indicate RV infarct — avoid nitrates.
Lateral MI LCx or diagonal branch of LAD
I aVL V5 V6
II III aVF
High lateral (I, aVL) — often from small diagonal. Low lateral (V5, V6) — LCx territory. May be subtle.
Anterior MI LAD (proximal)
V1 V2 V3 V4
II III aVF
Largest territory — worst prognosis. Proximal LAD occlusion → anteroseptal + lateral involvement. Risk of LBBB, CHB.
Septal MI LAD (septal perforators)
V1 V2
— Isolated septal MI uncommon. Often part of anteroseptal MI. Risk of complete heart block and VSD.
Posterior MI RCA or LCx (dominant) No ST elevation in standard leads
V1 V2 V3
ST depression + tall R + upright T in V1–V3 = posterior STEMI equivalent
 Must use posterior leads V7–V9 to confirm — ST elevation ≥0.5mm in V7–V9 is diagnostic. Frequently missed.
RV MI Proximal RCA
V1 V4R
Right-sided leads V3R–V6R
 — Always consider with inferior STEMI (II,III,aVF). Triad: hypotension + JVD + clear lungs. Nitrates & diuretics CONTRAINDICATED.
ECG waveform evolution
Hyperacute T
Tall T
ST Elevation
ST↑
Q + T inversion
Q T↓
Chronic / Old MI
Q persists
STEMI equivalents — no ST elevation but needs immediate cath lab
New LBBB
Any lead with new LBBB pattern
New LBBB in the context of chest pain = STEMI equivalent. Use Sgarbossa criteria to identify superimposed ischaemia (concordant ST elevation ≥1mm, concordant ST depression ≥1mm V1–V3, excessively discordant ST elevation ≥5mm).
DeWinter T waves
V1–V6
Upsloping ST depression (≥1mm) at J-point in V1–V6 + tall, symmetric, peaked T waves. No ST elevation. Represents proximal LAD occlusion. Seen in ~2% of LAD occlusions. Do NOT wait — activate cath lab.
Wellens Syndrome
V2–V3 (pain-free)
Type A: Biphasic T waves (positive-then-negative) in V2–V3.
Type B: Deep symmetric T inversion in V2–V3.
Seen after chest pain resolves. Indicates critical proximal LAD stenosis. Stress test CONTRAINDICATED — can precipitate massive MI.
Reciprocal changes — confirms true STEMI (not pericarditis)
Inferior STEMI
↑ ST in II, III, aVF
↓ ST in I, aVL
Anterior STEMI
↑ ST in V1–V4
↓ ST in II, III, aVF
Lateral STEMI
↑ ST in I, aVL, V5–V6
↓ ST in II, III, aVF, V1
Posterior STEMI
↑ ST in V7–V9
↓ ST + tall R in V1–V3

Investigations

  • 1. Electrocardiogram (ECG) – First-line Investigation

    • 12-lead ECG should be performed immediately.
    • Findings:
      • ST-segment elevation (STEMI)
      • ST-segment depression or T-wave inversion (NSTEMI)
      • Pathological Q waves (myocardial necrosis)
    • Repeat serial ECGs if initial ECG is nondiagnostic.

    2. Cardiac Biomarkers

    • Cardiac troponin I or T (most sensitive and specific marker)
      • High-sensitivity assays: rise in 1–3 hours
      • Peak: 12–24 hours
      • Remain elevated for 7–10 days
    • CK-MB
      • Rise: 4–9 hours
      • Returns to normal in 2–3 days
      • May help detect reinfarction.

    3. Laboratory Tests

    • CBC
    • Renal function and electrolytes
    • CRP and WBC
    • Coagulation profile
    • BNP/NT-proBNP (if heart failure is suspected)

    4. Coronary Angiography

    • Gold standard for identifying coronary artery occlusion.
    • Confirms diagnosis and allows percutaneous coronary intervention (PCI).

    5. Transthoracic Echocardiography

    • Detects regional wall motion abnormalities
    • Assesses left ventricular function (LVEF)
    • Identifies complications (e.g., mitral regurgitation, ventricular aneurysm, pericardial effusion, free wall rupture)

Diagnosis of Myocardial Infarction (MI)

1. Electrocardiogram (ECG) – First-line Investigation

  • 12-lead ECG should be performed immediately when Myocardial Infarction (MI) is suspected.
  • Findings:
    • ST-segment elevation (STEMI)
    • ST-segment depression or T-wave inversion (NSTEMI)
    • Pathological Q waves (myocardial necrosis)
  • Repeat serial ECGs if initial ECG is nondiagnostic.

2. Cardiac Biomarkers

  • Cardiac troponin I or T (most sensitive and specific marker)
    • High-sensitivity assays: rise in 1–3 hours
    • Peak: 12–24 hours
    • Remain elevated for 7–10 days
  • CK-MB
    • Rise: 4–9 hours
    • Returns to normal in 2–3 days
    • May help detect reinfarction.

3. Laboratory Tests

  • CBC
  • Renal function and electrolytes
  • CRP and WBC
  • Coagulation profile
  • BNP/NT-proBNP (if heart failure is suspected)

4. Coronary Angiography

  • Gold standard for identifying coronary artery occlusion.
  • Confirms diagnosis and allows percutaneous coronary intervention (PCI).

5. Transthoracic Echocardiography

  • Detects regional wall motion abnormalities
  • Assesses left ventricular function (LVEF)
  • Identifies complications (e.g., mitral regurgitation, ventricular aneurysm, pericardial effusion, free wall rupture)
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Management of Myocardial Infarction (MI)

Initial Management for All ACS Patients

Monitoring

  • • Continuous telemetry
  • • Serial ECGs
  • • Serial troponins

Oxygen

  • • Supplement oxygen as needed to maintain saturation ≥ 90%

Antiplatelet Therapy

  • • Aspirin
  • • P2Y12 inhibitor
  • • Dual antiplatelet therapy (DAPT)

Anticoagulation

  • • Parenteral anticoagulation (e.g., UFH)

Additional Medical Therapy

  • • Statins
  • • Beta blockers
  • • RAAS inhibitors
  • • Analgesia for chest pain

MONA-BASH Mnemonic

LetterTherapy
MMorphine
OOxygen
NNitroglycerin
AAntiplatelet drugs
BBeta blockers
AACE inhibitors
SStatins
HHeparin

Complications of Myocardial Infarction (MI)

    • Early (0–24 hours)

      • Arrhythmias (especially ventricular fibrillation) – common cause of early death
      • Sudden cardiac death
      • Acute heart failure → pulmonary edema
      • Cardiogenic shock

      1–3 days

      • Early fibrinous pericarditis (usually self-limiting)

      3–14 days

      • Papillary muscle rupture → acute mitral regurgitation
      • Ventricular septal rupture → acute VSD
      • Left ventricular free wall rupture → cardiac tamponade
      • Ventricular pseudoaneurysm

      Weeks to months

      • True ventricular aneurysm → mural thrombus
      • Dressler syndrome (post-MI autoimmune pericarditis)
      • Mural thrombus → systemic thromboembolism (e.g., stroke)
      • Arrhythmias
      • Congestive heart failure
      • Reinfarction

Prognosis of Myocardial Infarction (MI)

      • Early reperfusion therapy reduces the extent of myocardial necrosis and helps prevent complications such as early pericarditis.
      • Early infarct-associated pericarditis is usually self-limiting.
      • Prevention of recurrent MI and complications includes:
        • Dual antiplatelet therapy
        • Statin therapy
        • Beta blockers and/or ACE inhibitors
        • Management of modifiable cardiovascular risk factors

Key Points / Clinical Pearls of Myocardial Infarction (MI)

  • MI = ischemic necrosis of heart muscle, most commonly due to coronary artery disease.
  • Diagnosis is based on:
    • Typical symptoms
    • ECG changes
    • Elevated cardiac biomarkers
    • Cardiac catheterization confirms the diagnosis and enables treatment.
  • Emergency revascularization should be considered in suspected acute coronary syndrome.
  • Remember the timing of major complications:
    • 0–24 h: Arrhythmias, cardiogenic shock, heart failure
    • 1–3 d: Pericarditis
    • 3–14 d: Papillary muscle rupture, VSD, free wall rupture
    • Weeks–months: Ventricular aneurysm, Dressler syndrome, heart failure, reinfarction
  •