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🫀 MYOCARDIAL INFARCTION (MI)

A Complete Exam-Oriented, Clinically Practical Teaching Module

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1. DEFINITION

Myocardial Infarction is the irreversible death (necrosis) of cardiac muscle caused by prolonged ischemia, most commonly due to occlusion of a coronary artery by atherosclerotic plaque rupture with superimposed thrombosis.

Key phrase: "Time is Myocardium" - every minute of delay = more dead muscle.

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2. CAUSES (ETIOLOGY)

Common Causes

Important Risk Factors

1. Smoking (most powerful risk factor in young patients)
2. Hypertension
3. Diabetes mellitus
4. Dyslipidemia (high LDL, low HDL)
5. Obesity
6. Sedentary lifestyle

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3. TYPES / CLASSIFICATION

A. By ECG Pattern (Most Important Clinically)

STEMI + NSTEMI + UA = collectively called Acute Coronary Syndrome (ACS)

B. By Depth of Necrosis

C. By Universal Classification (for viva)

D. By Location

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4. PATHOPHYSIOLOGY

Step-by-Step Flowchart

Risk factors (HTN, DM, smoking, dyslipidemia)
        ↓
Endothelial injury → Atherosclerotic plaque formation in coronary artery
        ↓
Plaque rupture / erosion (triggered by shear stress, inflammation)
        ↓
Subendothelial collagen + plaque contents exposed to blood
        ↓
Platelet adhesion → Activation → Aggregation
(release Thromboxane A2, ADP, serotonin → vasoconstriction + more platelet aggregation)
        ↓
Coagulation cascade activated (Tissue Factor) → Fibrin clot forms
        ↓
Coronary artery OCCLUSION (thrombus complete within minutes)
        ↓
Blood flow ceases to downstream myocardium (area at risk)
        ↓
Aerobic metabolism STOPS within seconds
→ ATP production falls
→ Creatine phosphate depleted
→ Lactic acid accumulates
        ↓
Contractility LOST within <2 minutes (stunning begins)
        ↓
~20-40 minutes: IRREVERSIBLE CELL DEATH begins (necrosis)
(subendocardium first → wavefront progresses outward to epicardium)
        ↓
Sarcolemmal membrane disruption
→ Intracellular proteins leak into bloodstream
→ Troponin I, Troponin T, CK-MB detected in blood ← BASIS OF BLOOD TESTS
        ↓
6-12 hours: Necrosis becomes complete
        ↓
Inflammatory response: Neutrophils → Macrophages → Granulation tissue
        ↓
2-8 weeks: Fibrous SCAR formation (thin, non-contractile)
        ↓
Complications: Pump failure, arrhythmia, rupture, aneurysm

Key Biochemical Timeline (from Robbins):

Why the Subendocardium Dies First:

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5. CLINICAL FEATURES

Symptoms

Signs

Atypical Presentations (High-yield - don't miss!)

• Elderly: Breathlessness alone, confusion, falls
• Diabetics: "Silent MI" - no pain (autonomic neuropathy blunts pain sensation)
• Women: Fatigue, jaw pain, epigastric discomfort - often misdiagnosed
• Inferior MI: Epigastric pain + vomiting - often mistaken for peptic ulcer!

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6. KEY SYMPTOMS THAT SUGGEST DIAGNOSIS

Hallmark Symptom

Crushing central chest pain lasting >30 minutes, radiating to the left arm/jaw, NOT relieved by nitrates, accompanied by diaphoresis

Classic Clinical Clues

Red Flag Findings (Require Immediate Action)

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7. LABORATORY INVESTIGATIONS

Biomarker Timeline (High-Yield Chart)

Hours:       0    2    4    6    12   24   48   72   96   7d   10d  14d
Myoglobin:   ——RISE——PEAK——FALL—————————
CK-MB:            ———RISE——————PEAK———FALL——————————
Troponin I:             ——RISE————————PEAK(24h)————————————————FALL(7-10d)
LDH:                              ——RISE——————PEAK(3-4d)—————————————FALL(14d)

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8. DIFFERENTIAL DIAGNOSIS

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9. SHORT CLINICAL CASES

Case 1 - Classic STEMI

"A 58-year-old male smoker with known hypertension presents to the ER with crushing central chest pain of 2 hours duration radiating to the left jaw and arm, associated with profuse sweating and nausea. BP 95/60, HR 108, RR 22. ECG shows 3mm ST elevation in leads II, III, and aVF. Troponin-I is markedly elevated. Pulses are equal bilaterally."

• ST elevation in II, III, aVF = inferior wall = RCA territory
• Classic crushing chest pain >30 min + diaphoresis
• Nausea and bradycardia tendency = vagal activation (inferior MI hallmark)
• Hypotension = may indicate RV involvement or early cardiogenic shock
• Positive troponin = myocardial necrosis confirmed
• Equal BP in both arms = rules out aortic dissection

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Case 2 - NSTEMI / Diabetic Silent Presentation

"A 67-year-old diabetic female presents with a 12-hour history of severe fatigue, mild jaw discomfort, and breathlessness. No obvious chest pain. ECG shows 2mm ST depression in V4-V6. High-sensitivity troponin-T is 0.08 ng/mL (elevated) with a 3-hour repeat of 0.14 ng/mL (significant rise)."

• Atypical presentation (fatigue, jaw pain) - classic in women and diabetics
• No ST elevation → not STEMI; troponin positive → not unstable angina → NSTEMI
• Rising troponin (delta troponin >20% rise) confirms active necrosis
• ST depression in V4-V6 = lateral ischemia
• Diabetic autonomic neuropathy blunts classic chest pain

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10. TREATMENT

A. Non-Pharmacological Treatment

1. Immediate rest - reduce myocardial oxygen demand
2. Oxygen - only if SpO2 <90% (routine oxygen is NOT recommended if SpO2 normal - it causes vasoconstriction)
3. IV access - two large-bore cannulas
4. Cardiac monitoring - continuous ECG, pulse oximetry
5. Reperfusion (the most important treatment):
   • Primary PCI (percutaneous coronary intervention) = Drug of Choice for STEMI if available within 120 min (target: door-to-balloon <90 min)
   • Thrombolysis (fibrinolytic therapy) = if PCI not available within 120 min (give within 30 min of arrival - "door-to-needle time")
   • CABG (coronary artery bypass graft) = for multi-vessel disease, failed PCI, left main disease
6. Cardiac rehabilitation after discharge
7. Lifestyle modification: Smoking cessation, diet, exercise, weight loss

B. Pharmacological Treatment

Summary - Drug Priority

MONA mnemonic (Emergency Initial Therapy)

M - Morphine (pain relief) O - Oxygen (if SpO2 <90%) N - Nitrates (sublingual GTN) A - Aspirin (300mg chewed)

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11. CLINICAL PEARLS

Bedside Clues

• A patient with crushing chest pain + diaphoresis + new S4 = MI until proven otherwise
• Inferior MI loves to cause bradycardia and vomiting (vagal effect - RCA supplies SA node + vagal fibers)
• A new pansystolic murmur 2-5 days post-MI = papillary muscle rupture (MR) or VSD - surgical emergency
• RV infarction triad: hypotension + elevated JVP + clear lungs (no pulmonary oedema) - occurs with inferior STEMI; give IV fluids, avoid nitrates!
• Dressler syndrome = pericarditis 2-6 weeks post-MI (immune-mediated) - treat with NSAIDs/aspirin

High-Yield Exam Facts

• Angiography within 4 hours of MI shows thrombosis in 90% of cases
• By 12-24h, thrombosis seen in only 60% (spontaneous lysis occurs)
• 20-40 minutes = window for irreversible damage; beyond 6-12 hours = complete necrosis
• Subendocardium dies FIRST (most vulnerable zone)
• Reperfusion injury causes contraction band necrosis - characteristic microscopically
• Troponin is the GOLD STANDARD biomarker (CK-MB no longer recommended for initial NSTEMI diagnosis)
• LAD occlusion = most common (40-50%), called the "widow maker"
• Q waves on ECG = old/completed infarct (dead electrically silent tissue)
• Wellens syndrome = critical LAD stenosis; biphasic T-waves in V2-V3 even when pain-free - do NOT stress test!
• The 2025 ACC/AHA Guidelines (PMID: 40013746) update STEMI/NSTEMI management with ticagrelor preferred over clopidogrel

Viva Points

• "Why does the subendocardium infarct first?" → Last to receive blood + highest oxygen demand + compressed by systolic pressure
• "What is stunned myocardium?" → Reversible contractile dysfunction after brief ischemia; recovers in days-weeks
• "What is hibernating myocardium?" → Chronically ischemic but viable muscle with reduced function; revascularization restores function
• "Why does LDL appear falsely low in acute MI?" → Acute phase response lowers cholesterol; check lipids at admission or >6 weeks later
• "What is reperfusion injury?" → Paradoxical increase in damage when blood flow is restored; mediated by free radicals, calcium overload, mitochondrial dysfunction

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12. COMMON DIAGNOSTIC MISTAKES

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13. 5-MINUTE REVISION SUMMARY

DEFINITION
→ Irreversible death of cardiac muscle due to prolonged coronary ischemia
→ ~800,000 cases/year in USA; 1 MI every 40 seconds

CAUSES
→ 90%: Atherosclerotic plaque rupture + coronary thrombosis
→ Risk: Smoking, HTN, DM, Dyslipidaemia, Age, Male sex
→ Rare: Vasospasm, embolism, vasculitis

PATHOPHYSIOLOGY
→ Plaque rupture → Platelet aggregation → Thrombus → Coronary occlusion
→ Ischemia → ATP depleted → Contractility lost (<2 min)
→ Irreversible necrosis at 20-40 min → Complete by 6-12h
→ Subendocardium first; transmural = STEMI; subendocardial = NSTEMI
→ Proteins leak → Troponin detectable in blood (3-4 hours)

SYMPTOMS
→ Crushing central chest pain >30 min, radiates to left arm/jaw
→ Diaphoresis, nausea, breathlessness
→ Silent in diabetics and elderly!

INVESTIGATIONS
→ ECG: ST elevation (STEMI) / ST depression (NSTEMI) / Q waves (old MI)
→ Troponin: Gold standard - rises 3-4h, peaks 24h, stays 7-10 days
→ CK-MB: Useful for reinfarction
→ Echo: Wall motion abnormality (RWMA), assess LV function
→ Coronary angiography: Definitive + therapeutic (PCI)

TREATMENT
Emergency: MONA (Morphine, O2, Nitrates, Aspirin 300mg) + Anticoagulation + P2Y12
Reperfusion: Primary PCI <90 min (door-to-balloon) is DOC
              Thrombolysis if PCI unavailable within 120 min
Long-term: Aspirin + Statin (atorvastatin 80mg) + ACEi + Beta-blocker

COMPLICATIONS
Early (hours-days):
→ Arrhythmias - most common cause of EARLY death (VF = #1 killer in first hour)
→ Cardiogenic shock (>40% LV loss)
→ Acute LV failure / pulmonary oedema
→ RV infarction (with inferior MI)
→ Papillary muscle rupture → acute MR (day 2-7)
→ VSD rupture (day 3-5)
→ Free wall rupture (day 5-10) → cardiac tamponade → death

Late (weeks-months):
→ LV aneurysm (persistent ST elevation, risk of mural thrombus/VT)
→ Dressler syndrome (autoimmune pericarditis, 2-6 weeks)
→ Heart failure (chronic)
→ Reinfarction

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