MBBS Year
1st Year
Subject
What Is Usually Asked
Coronary arteries and their territories
Resource HubAll Years (1st-Final)Medical Topic AuthorityMyocardial Infarction
Myocardial Infarction: Notes, PPT and PYQs for MBBS
Myocardial infarction (MI) is death of heart muscle caused by prolonged ischaemia, most often due to thrombotic occlusion of a coronary artery over a ruptured atherosclerotic plaque. It is examined in Pathology and Pharmacology in 2nd Year, and in General Medicine in Final Year, with supporting concepts from Anatomy and Physiology in 1st Year.
SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and notesQuick Summary: What You Need to Know for University Exams
- MI is part of the acute coronary syndrome (ACS) spectrum, along with unstable angina.
- It is classified clinically as ST-elevation MI (STEMI) or non-ST-elevation MI (NSTEMI).
- The commonest cause is atherosclerotic plaque rupture with superimposed thrombosis.
- Classic symptom: crushing retrosternal chest pain lasting more than 20 minutes, with sweating and breathlessness.
- Cardiac troponin is the preferred biomarker; the ECG separates STEMI from NSTEMI.
- Primary PCI is the preferred reperfusion therapy for STEMI; fibrinolysis is used when timely PCI is not available.
- Ventricular fibrillation is the main cause of early death after MI.
Myocardial Infarction Across MBBS Subjects
| MBBS Year | Subject | What Is Usually Asked |
|---|---|---|
| 1st Year | Anatomy | Coronary arteries and their territories |
| 1st Year | Physiology | Coronary circulation, ECG basics |
| 1st Year | Biochemistry | Cardiac enzymes and markers, lipoproteins |
| 2nd Year | Pathology | Pathogenesis, morphological changes over time, complications |
| 2nd Year | Pharmacology | Antiplatelets, anticoagulants, fibrinolytics, nitrates, statins |
| Final Year | General Medicine | Diagnosis, ECG changes, management, complications |
MBBS Year
1st Year
Subject
What Is Usually Asked
Coronary circulation, ECG basics
MBBS Year
1st Year
Subject
What Is Usually Asked
Cardiac enzymes and markers, lipoproteins
MBBS Year
2nd Year
Subject
What Is Usually Asked
Pathogenesis, morphological changes over time, complications
MBBS Year
2nd Year
Subject
What Is Usually Asked
Antiplatelets, anticoagulants, fibrinolytics, nitrates, statins
MBBS Year
Final Year
Subject
What Is Usually Asked
Diagnosis, ECG changes, management, complications
Definition and Classification
Definition: MI is myocardial cell death due to prolonged ischaemia. By the Fourth Universal Definition, it is diagnosed when there is a rise and/or fall of cardiac troponin with at least one value above the 99th percentile upper reference limit, together with evidence of myocardial ischaemia (symptoms, new ischaemic ECG changes, new Q waves, imaging evidence or an intracoronary thrombus).
Clinical Classification
| Type | Key Feature |
|---|---|
| STEMI | ST elevation (or new left bundle branch block) with raised troponin; usually complete occlusion of a coronary artery |
| NSTEMI | Raised troponin without ST elevation; ST depression or T inversion may be present |
| Unstable angina | Ischaemic symptoms without a rise in troponin (not an infarction, but part of ACS) |
Type
STEMI
Key Feature
ST elevation (or new left bundle branch block) with raised troponin; usually complete occlusion of a coronary artery
Type
NSTEMI
Key Feature
Raised troponin without ST elevation; ST depression or T inversion may be present
Type
Unstable angina
Key Feature
Ischaemic symptoms without a rise in troponin (not an infarction, but part of ACS)
Universal Definition Types
| Type | Description |
|---|---|
| Type 1 | Atherothrombotic event (plaque rupture or erosion) |
| Type 2 | Supply-demand mismatch without acute plaque rupture, for example severe anaemia, tachyarrhythmia or hypotension |
| Type 3 | Cardiac death with symptoms suggestive of MI before biomarkers are available |
| Type 4 | Related to percutaneous coronary intervention (PCI), including stent thrombosis |
| Type 5 | Related to coronary artery bypass grafting (CABG) |
Type
Type 1
Description
Atherothrombotic event (plaque rupture or erosion)
Type
Type 2
Description
Supply-demand mismatch without acute plaque rupture, for example severe anaemia, tachyarrhythmia or hypotension
Type
Type 3
Description
Cardiac death with symptoms suggestive of MI before biomarkers are available
Type
Type 4
Description
Related to percutaneous coronary intervention (PCI), including stent thrombosis
Type
Type 5
Description
Related to coronary artery bypass grafting (CABG)
Aetiology (Causes and Risk Factors)
Causes:
- Atherosclerotic plaque rupture or erosion with thrombosis (most common)
- Coronary artery spasm
- Coronary embolism
- Coronary artery dissection
- Vasculitis and other rare causes
Risk factors for coronary artery disease:
| Non-Modifiable | Modifiable |
|---|---|
| Increasing age | Smoking |
| Male sex | Hypertension |
| Family history of premature coronary artery disease | Diabetes mellitus |
| Genetic factors | Dyslipidaemia |
| - | Obesity and physical inactivity |
| - | Unhealthy diet and psychosocial stress |
Non-Modifiable
Increasing age
Modifiable
Smoking
Non-Modifiable
Male sex
Modifiable
Hypertension
Non-Modifiable
Family history of premature coronary artery disease
Modifiable
Diabetes mellitus
Non-Modifiable
Genetic factors
Modifiable
Dyslipidaemia
Non-Modifiable
-
Modifiable
Obesity and physical inactivity
Non-Modifiable
-
Modifiable
Unhealthy diet and psychosocial stress
Pathophysiology
Flowchart
- Atherosclerotic plaque with a thin fibrous cap develops in a coronary artery
- Plaque ruptures or erodes, exposing thrombogenic material
- Platelets adhere, activate and aggregate
- The coagulation cascade forms a thrombus that occludes the artery
- Myocardium supplied by the artery becomes ischaemic
- Aerobic metabolism stops within seconds; irreversible injury begins after roughly 20 to 40 minutes of severe ischaemia
- Necrosis spreads as a wavefront from the subendocardium towards the subepicardium
- Loss of contractile tissue leads to reduced cardiac function and electrical instability
(Examiner may ask you to draw the pathogenesis flowchart.)
Coronary Territories
| Artery | Area Supplied | ECG Leads Showing Changes |
|---|---|---|
| Left anterior descending | Anterior wall of left ventricle, anterior two-thirds of septum | V1 to V4 (anterior) |
| Left circumflex | Lateral wall of left ventricle | I, aVL, V5, V6 (lateral) |
| Right coronary artery | Inferior wall of left ventricle, right ventricle, posterior one-third of septum in most people | II, III, aVF (inferior) |
Artery
Left anterior descending
Area Supplied
Anterior wall of left ventricle, anterior two-thirds of septum
ECG Leads Showing Changes
V1 to V4 (anterior)
Artery
Left circumflex
Area Supplied
Lateral wall of left ventricle
ECG Leads Showing Changes
I, aVL, V5, V6 (lateral)
Artery
Right coronary artery
Area Supplied
Inferior wall of left ventricle, right ventricle, posterior one-third of septum in most people
ECG Leads Showing Changes
II, III, aVF (inferior)
Morphological Changes Over Time (Pathology)
| Time After Onset | Gross Appearance | Microscopic Features |
|---|---|---|
| First few hours | No visible change | Wavy fibres at the margins may be seen |
| 12 to 24 hours | Dark mottling | Coagulation necrosis begins, contraction band necrosis, early neutrophils |
| 1 to 3 days | Mottled with a yellow-tan centre | Coagulation necrosis with loss of nuclei, dense neutrophilic infiltrate |
| 3 to 7 days | Hyperaemic border, softening centre | Dead myocytes removed by macrophages |
| 7 to 10 days | Maximally yellow-tan and soft | Early granulation tissue at the margins |
| 10 to 14 days | Red-grey, depressed borders | Well-established granulation tissue |
| 2 to 8 weeks | Grey-white scar | Increasing collagen deposition |
| More than 2 months | Firm scar | Dense collagenous scar |
Time After Onset
First few hours
Gross Appearance
No visible change
Microscopic Features
Wavy fibres at the margins may be seen
Time After Onset
12 to 24 hours
Gross Appearance
Dark mottling
Microscopic Features
Coagulation necrosis begins, contraction band necrosis, early neutrophils
Time After Onset
1 to 3 days
Gross Appearance
Mottled with a yellow-tan centre
Microscopic Features
Coagulation necrosis with loss of nuclei, dense neutrophilic infiltrate
Time After Onset
3 to 7 days
Gross Appearance
Hyperaemic border, softening centre
Microscopic Features
Dead myocytes removed by macrophages
Time After Onset
7 to 10 days
Gross Appearance
Maximally yellow-tan and soft
Microscopic Features
Early granulation tissue at the margins
Time After Onset
10 to 14 days
Gross Appearance
Red-grey, depressed borders
Microscopic Features
Well-established granulation tissue
Time After Onset
2 to 8 weeks
Gross Appearance
Grey-white scar
Microscopic Features
Increasing collagen deposition
Time After Onset
More than 2 months
Gross Appearance
Firm scar
Microscopic Features
Dense collagenous scar
The 3 to 7 day period, when the infarct is softest, carries the highest risk of rupture.
Clinical Features
Symptoms:
- Severe, crushing or squeezing retrosternal chest pain lasting more than 20 minutes
- Radiation to the left arm, jaw, neck or back
- Not relieved by rest or sublingual nitrates
- Sweating, nausea and vomiting
- Breathlessness, anxiety and a sense of impending doom
- Silent or atypical presentation, especially in elderly people and people with diabetes
Signs:
- Pallor, sweating and restlessness
- Tachycardia or bradycardia (bradycardia is more common in inferior MI)
- Hypotension or hypertension
- Fourth or third heart sound
- Basal crackles if left ventricular failure develops
- New murmur if a mechanical complication occurs
Killip Classification
| Class | Findings |
|---|---|
| I | No signs of heart failure |
| II | Basal crackles, third heart sound, raised jugular venous pressure |
| III | Acute pulmonary oedema |
| IV | Cardiogenic shock |
Class
I
Findings
No signs of heart failure
Class
II
Findings
Basal crackles, third heart sound, raised jugular venous pressure
Class
III
Findings
Acute pulmonary oedema
Class
IV
Findings
Cardiogenic shock
Diagnosis
ECG Changes in STEMI (Typical Sequence)
- Hyperacute (tall, peaked) T waves
- ST segment elevation in two or more contiguous leads
- Development of pathological Q waves
- T wave inversion
- ST segment returns to baseline; Q waves usually persist
Cardiac Biomarkers
| Marker | Key Points |
|---|---|
| Cardiac troponin I or T | Preferred marker; highly sensitive and specific; stays raised for several days |
| CK-MB | Rises within hours and returns to normal within about 2 to 3 days; useful to detect reinfarction |
| Myoglobin | Rises earliest but is not specific to the heart |
Marker
Cardiac troponin I or T
Key Points
Preferred marker; highly sensitive and specific; stays raised for several days
Marker
CK-MB
Key Points
Rises within hours and returns to normal within about 2 to 3 days; useful to detect reinfarction
Marker
Myoglobin
Key Points
Rises earliest but is not specific to the heart
Other Investigations
| Investigation | Purpose |
|---|---|
| Echocardiography | Regional wall motion abnormality, ejection fraction, mechanical complications |
| Chest X-ray | Pulmonary oedema, other causes of chest pain |
| Blood tests | Complete blood count, renal function, electrolytes, glucose, lipid profile |
| Coronary angiography | Defines the culprit lesion and guides PCI or CABG |
Investigation
Echocardiography
Purpose
Regional wall motion abnormality, ejection fraction, mechanical complications
Investigation
Chest X-ray
Purpose
Pulmonary oedema, other causes of chest pain
Investigation
Blood tests
Purpose
Complete blood count, renal function, electrolytes, glucose, lipid profile
Investigation
Coronary angiography
Purpose
Defines the culprit lesion and guides PCI or CABG
For reference ranges, see the normal lab values chart.
Management
Immediate Management (All ACS)
- Continuous ECG monitoring with a defibrillator available
- Oxygen only if saturation is low
- Aspirin (chewed) as early as possible
- A second antiplatelet agent (P2Y12 inhibitor such as clopidogrel, ticagrelor or prasugrel)
- Nitrates for pain, unless contraindicated (for example hypotension or right ventricular infarction)
- Analgesia, such as opioids, for severe pain
- Anticoagulation, such as heparin
Reperfusion in STEMI
| Strategy | When Used | Key Points |
|---|---|---|
| Primary PCI | Preferred when available in time | Mechanical opening of the artery with stenting |
| Fibrinolysis | When timely PCI is not available | Streptokinase, alteplase, reteplase or tenecteplase; most effective when given early |
| CABG | Selected patients | Multivessel or left main disease, or failed PCI |
Strategy
Primary PCI
When Used
Preferred when available in time
Key Points
Mechanical opening of the artery with stenting
Strategy
Fibrinolysis
When Used
When timely PCI is not available
Key Points
Streptokinase, alteplase, reteplase or tenecteplase; most effective when given early
Strategy
CABG
When Used
Selected patients
Key Points
Multivessel or left main disease, or failed PCI
Absolute contraindications to fibrinolysis (examples): any previous intracranial haemorrhage, ischaemic stroke within the past three months, active internal bleeding, suspected aortic dissection and known intracranial tumour.
NSTEMI: Fibrinolysis is not used. Treatment is antiplatelet and anticoagulant therapy with coronary angiography timed according to risk.
Long-Term Secondary Prevention
| Drug or Measure | Purpose |
|---|---|
| Aspirin plus a P2Y12 inhibitor | Prevents further thrombotic events |
| Beta-blockers | Reduce oxygen demand and arrhythmia risk |
| ACE inhibitors or ARBs | Limit ventricular remodelling, especially with reduced ejection fraction |
| High-intensity statins | Stabilise plaques and lower LDL cholesterol |
| Lifestyle changes | Stop smoking, diet, exercise, weight control |
| Cardiac rehabilitation | Structured recovery and risk factor control |
Drug or Measure
Aspirin plus a P2Y12 inhibitor
Purpose
Prevents further thrombotic events
Drug or Measure
Beta-blockers
Purpose
Reduce oxygen demand and arrhythmia risk
Drug or Measure
ACE inhibitors or ARBs
Purpose
Limit ventricular remodelling, especially with reduced ejection fraction
Drug or Measure
High-intensity statins
Purpose
Stabilise plaques and lower LDL cholesterol
Drug or Measure
Lifestyle changes
Purpose
Stop smoking, diet, exercise, weight control
Drug or Measure
Cardiac rehabilitation
Purpose
Structured recovery and risk factor control
Revise these drug groups with the antihypertensive drugs classification chart.
Complications
| Timing | Complication | Key Points |
|---|---|---|
| Early | Arrhythmias | Ventricular fibrillation is the main cause of early death; heart block is common with inferior MI |
| Early | Left ventricular failure and cardiogenic shock | Related to the size of the infarct |
| Early | Pericarditis | Fibrinous pericarditis in the first few days |
| 3 to 7 days | Free wall rupture | Leads to haemopericardium and cardiac tamponade |
| 3 to 7 days | Ventricular septal rupture | New pansystolic murmur, left-to-right shunt |
| 3 to 7 days | Papillary muscle rupture | Acute mitral regurgitation and pulmonary oedema |
| Weeks | Mural thrombus and embolism | Can cause stroke |
| Weeks | Dressler syndrome | Autoimmune pericarditis weeks after MI |
| Late | Ventricular aneurysm | Persistent ST elevation, heart failure, thrombus |
| Late | Chronic heart failure | Due to loss of myocardium and remodelling |
Timing
Early
Complication
Arrhythmias
Key Points
Ventricular fibrillation is the main cause of early death; heart block is common with inferior MI
Timing
Early
Complication
Left ventricular failure and cardiogenic shock
Key Points
Related to the size of the infarct
Timing
Early
Complication
Pericarditis
Key Points
Fibrinous pericarditis in the first few days
Timing
3 to 7 days
Complication
Free wall rupture
Key Points
Leads to haemopericardium and cardiac tamponade
Timing
3 to 7 days
Complication
Ventricular septal rupture
Key Points
New pansystolic murmur, left-to-right shunt
Timing
3 to 7 days
Complication
Papillary muscle rupture
Key Points
Acute mitral regurgitation and pulmonary oedema
Timing
Weeks
Complication
Mural thrombus and embolism
Key Points
Can cause stroke
Timing
Weeks
Complication
Dressler syndrome
Key Points
Autoimmune pericarditis weeks after MI
Timing
Late
Complication
Ventricular aneurysm
Key Points
Persistent ST elevation, heart failure, thrombus
Timing
Late
Complication
Chronic heart failure
Key Points
Due to loss of myocardium and remodelling
Prognosis
Prognosis depends on infarct size, left ventricular function, time to reperfusion, age and complications such as heart failure and arrhythmias. Early reperfusion and consistent secondary prevention significantly improve survival.
Quick Viva Questions
Q: Which coronary artery is most commonly occluded in MI? A: The left anterior descending artery, which supplies the anterior wall of the left ventricle and the anterior septum.
Q: Why is troponin preferred over CK-MB? A: Troponin is more sensitive and specific for myocardial injury and stays raised for longer.
Q: When is the risk of myocardial rupture highest? A: About 3 to 7 days after MI, when the necrotic tissue is softest.
Q: What is the commonest cause of early death after MI? A: Ventricular fibrillation.
Q: What is Dressler syndrome? A: An autoimmune pericarditis that develops weeks after MI.
How Myocardial Infarction Appears in MBBS University Exams
Typical question styles (not attributed to specific papers or years):
- "Describe the pathogenesis and morphological changes in myocardial infarction. Add a note on its complications." (Long essay, Pathology)
- "Discuss the clinical features, diagnosis and management of acute ST-elevation myocardial infarction." (Long essay, General Medicine)
- "Write a short note on cardiac biomarkers." (Short note, Medicine or Biochemistry)
- "Write a short note on fibrinolytic agents." (Short note, Pharmacology)
- "Enumerate the complications of myocardial infarction." (Short answer)
Frequently Asked Questions
What is the difference between STEMI and NSTEMI?
Both involve myocardial necrosis with raised troponin. STEMI shows ST elevation (or new left bundle branch block) and usually reflects complete coronary occlusio
Which is the best biomarker for myocardial infarction?
Cardiac troponin (I or T) is the preferred biomarker because it is highly sensitive and specific for myocardial injury. CK-MB is useful for detecting reinfarction because it returns to normal sooner.
Can I download the myocardial infarction PPT for my presentation?
Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.
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