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

Overview
Etiology & Risk Factors

Etiology & Risk Factors
Pathophysiology

Pathophysiology
Clinical Presentation

Clinical Presentation
Types of MI

Types of MI
ECG Changes In MI

ECG Changes In MI
Investigations

Investigations
Diagnosis

Diagnosis
Management

Management
Complications

Complications
Prognosis

Prognosis
Key Points / Clinical Pearls

Key Points / Clinical Pearls

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).

Teaching point The most common cause of Myocardial Infarction (MI) is coronary artery disease, usually from rupture of an unstable plaque that blocks a coronary artery (type 1 MI)

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 Myocardial Infarction (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 Myocardial Infarction (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

-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 of Myocardial Infarction (MI)

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

Important Note Chest pain typically lasts >20 minutes and is retrosternal, dull, squeezing, or pressure-like, Always Think about Myocardial Infarction (MI)

Types of Myocardial Infarction (MI)

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

Atherosclerotic plaque rupture

Spontaneous MI from plaque disruption with coronary thrombus

Supply-demand mismatch

Ischaemia without plaque rupture — other cause

MI causing death

Cardiac death before biomarkers available

PCI-related MI

4a: peri-PCI • 4b: stent thrombosis • 4c: restenosis

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

ST Elevation

Q + T inversion

Chronic / Old MI

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 in Myocardial Infarction (MI)

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)

Home Home Clinical Cases Cardiovascular System Clinical Cases Myocardial Infarction (MI)

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

Letter	Therapy
M	Morphine
O	Oxygen
N	Nitroglycerin
A	Antiplatelet drugs
B	Beta blockers
A	ACE inhibitors
S	Statins
H	Heparin

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 Myocardial Infarction (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)

Myocardial Infarction (MI) = ischemic necrosis of heart muscle, most commonly due to coronary artery disease.
Diagnosis of Myocardial Infarction (MI) 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 Myocardial Infarction (MI).
Remember the timing of major complications of Myocardial Infarction (MI):
- 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

National Center for Biotechnology Information (NIH). Myocardial Infarction, StatPearls.
Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Eur Heart J. 2019;40:237-269. PMID: 30154043.
Bhatt H, Ludhwani D. National Center for Biotechnology Information (NIH). Acute ST-Segment Elevation Myocardial Infarction (STEMI), StatPearls.
MedlinePlus, National Library of Medicine (NIH). Heart Attack: Health Topic.
Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation. 2025;151:e771-e862. doi: 10.1161/CIR.0000000000001309.