Myocardial Infarction (MI)

 

Myocardial Infarction (MI) – High-Yield Guide

Definition:
Myocardial infarction (MI) refers to ischemic necrosis of heart muscle, most commonly caused by coronary artery disease (CAD).

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Types of MI

• Type 1 MI: Plaque rupture → thrombosis → coronary occlusion

• Type 2 MI: Oxygen supply-demand mismatch (e.g., hypotension, vasospasm)

  
  
  

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Epidemiology

• More common in males than females

• Data mostly from the United States

  
  
  

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Causes / Etiology

1. Coronary Artery Disease

• Atherosclerotic plaque rupture (Type 1 MI)

2. Coronary Vasospasm

• Prinzmetal angina

• Cocaine use

3. Supply-Demand Mismatch (Type 2 MI)

• Severe anemia

• Hypotension

• Tachyarrhythmias

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Pathophysiology

Coronary Occlusion:

Occlusion	Myocardial involvement	Clinical manifestation
Partial	Subendocardial	NSTEMI, unstable angina
Complete	Transmural	STEMI

Plaque Disruption (Type 1 MI):

• Unstable plaques: lipid-rich, thin fibrous cap

• Macrophages → matrix metalloproteinases → fibrous cap rupture → thrombosis → myocardial necrosis

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Clinical Features

Classic Symptoms:

• Retrosternal chest pain: dull, squeezing, radiates to left arm, jaw, neck, epigastrium

• Dyspnea, pallor, diaphoresis, nausea, vomiting, anxiety

• Signs of CHF or cardiogenic shock: hypotension, tachycardia, pulmonary edema

Atypical Presentations:

• Elderly, diabetics, women

• Silent MI (polyneuropathy in diabetes)

• Autonomic symptoms: nausea, diaphoresis

• Epigastric pain, bradycardia

  

  

  
  
  
  

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Diagnosis

ECG Findings:

Leads	Infarct location	Vessel
V1–V2	Septal	LAD
V3–V4	Anteroapical	Distal LAD
V5–V6, I, aVL	Anterolateral	Diagonal branch of LAD / LCX
II, III, aVF	Inferior	RCA / distal LCX
V7–V9, V3R–V6R	Posterior	PDA from RCA or LCX

Mnemonic: “SAL” → Septal (V1–2), Apical (V3–4), Lateral (V5–6)

Cardiac Biomarkers:

Marker	Rise	Peak	Normalization	Notes
Troponin I/T	1–8 h	12–24 h	7–10 days	Most specific; correlates with infarct size
CK-MB	4–9 h	12–24 h	2–3 days	Useful for reinfarction; rarely used now
Myoglobin	1 h	4–12 h	24 h	Nonspecific; rarely used

Coronary Angiography:

• Diagnostic and therapeutic (PCI)

• Most occluded arteries: LAD > RCA > LCX

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Histopathology of MI

Time	Microscopic	Macroscopic
0–24 h	Wavy fibers, early coagulative necrosis	Dark mottling (12–24 h)
1–3 days	Extensive necrosis, neutrophilic infiltrate	Hyperemia, yellow pallor
3–14 days	Macrophage infiltration, granulation tissue, angiogenesis	Hyperemic border, soft yellow-brown center
2 wks–months	Dense collagenous scar	Gray-white fibrosis, ventricular remodeling

Reperfusion injury:

• After PCI or thrombolysis >3 h post-occlusion

• Contraction band necrosis, ROS-mediated myocyte injury

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Treatment

Immediate / Acute Management:

• Revascularization: PCI for STEMI

• MONA-BASH Therapy:

  • M: Morphine

  • O: Oxygen (if SpO₂ <90%, cyanosis, or severe dyspnea)

  • N: Nitroglycerin (avoid if hypotension or PDE5 inhibitors)

  • A: Antiplatelets (Aspirin + P2Y12 inhibitor)

  • B: Beta blockers (avoid if hypotension, HF, shock)

  • A: ACE inhibitors

  • S: Statins (high-intensity, early initiation)

  • H: Heparin

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Complications of MI

Time post-MI	Complication	Notes
0–24 h	Arrhythmia, SCD, acute HF, cardiogenic shock	Wavy fibers, ventricular fibrillation
1–3 days	Fibrinous pericarditis	Neutrophilic infiltration
3–14 days	Papillary muscle rupture → acute MR	Holosystolic murmur, pulmonary edema, shock
3–5 days	Ventricular septal rupture → VSD	Left-to-right shunt, new murmur, acute RHF
5–14 days	LV free wall rupture	Cardiac tamponade, sudden death
2 wks–months	LV aneurysm, mural thrombus, Dressler syndrome	Heart failure, thromboembolism, arrhythmia, autoimmune pericarditis

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✅ High-Yield Takeaways:

• Early recognition of STEMI vs NSTEMI is critical.

• Troponin is the most reliable biomarker.

• PCI / Revascularization is lifesaving.

• Monitor for acute and delayed complications, including rupture, arrhythmias, and post-MI pericarditis.