Rapid Review·Cardiovascular
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PATHOLOGY
T2High yieldEvolution Of Myocardial Infarction
p308
Focus on
A timeline where each histologic stage predicts a specific, lethal complication.
Key takeaways
The infarct
Commonly occluded coronary arteries
LAD > RCA > circumflex.Symptoms
diaphoresis, nausea, vomiting, severe retrosternal pain, pain radiating to the left arm or jaw, shortness of breath, fatigue.The timeline, stage by stage
0 to 24 hours
on the MI at 0 to 24 hours figure.- Wavy fibers at 0 to 4 hours (grossly nothing yet), then early coagulative necrosis at 4 to 24 hours, with cell contents released into blood, plus edema and hemorrhage; grossly, dark mottling.
- Tetrazolium stain: healthy tissue stains dark, infarcting tissue stains pale.
- Reperfusion injury: free radicals and calcium influx cause hypercontraction of myofibrils, giving contraction band necrosis, the dark eosinophilic stripes. A CK that rises after reperfusion is this injury.
1 to 3 days
on the MI at 1 to 3 days figure: extensive coagulative necrosis, with neutrophils infiltrating the surrounding tissue. Grossly, hyperemia with yellow pallor.3 to 14 days
on the MI at 3 to 14 days figure: macrophages, then granulation tissue (type III collagen) at the margins. Grossly, central yellow-brown softening with a hyperemic border. This is the weakest the wall ever is, and therefore the rupture window.2 weeks to several months
on the MI at 2 weeks to months figure: contracted scar complete (type I collagen), grossly a gray-white scar.| Time | Gross | Light microscopy | Complications |
|---|---|---|---|
| 0 to 24 hours | Tetrazolium: infarct stains pale; dark mottling after 4 hours | Wavy fibers, then early coagulative necrosis; reperfusion gives contraction bands | Ventricular arrhythmia, heart failure, cardiogenic shock (massive infarct), papillary muscle dysfunction with mitral regurgitation |
| 1 to 3 days | Hyperemia, yellow pallor | Extensive coagulative necrosis, neutrophils | Postinfarction fibrinous pericarditis |
| 3 to 14 days | Central yellow-brown softening with hyperemic border | Macrophages, then granulation tissue (type III collagen) | Free wall rupture causing tamponade; papillary muscle rupture causing MR; septal rupture causing a left-to-right shunt; LV pseudoaneurysm |
| 2 weeks to months | Gray-white scar | Contracted scar complete (type I collagen) | Postcardiac injury syndrome, heart failure, arrhythmia, true ventricular aneurysm with mural thrombus |
| Mechanism | Consequence |
|---|---|
| Macrophage-mediated structural degradation | The wall is at its weakest |
| Free wall ruptures | Cardiac tamponade |
| Papillary muscle ruptures | Acute mitral regurgitation |
| Septum ruptures | Left-to-right shunt, an acquired VSD |
| Feature | Coagulative necrosis | Contraction band necrosis |
|---|---|---|
| Cause | Ischemia itself | Reperfusion |
| Mechanism | Loss of nuclei with preserved architecture | Free radicals and calcium influx cause hypercontraction |
| Appearance | Pale, anucleate fibers | Dark eosinophilic stripes |
A reperfused STEMI patient's biopsy shows dark eosinophilic stripes across the myocytes. What are they, and what caused them?
Contraction band necrosis: the signature of reperfusion, not of the ischemia itself. Free radicals and calcium influx make the myofibrils hypercontract.
How it's tested
Free wall rupture, papillary muscle rupture, and septal rupture all fall in the 3-to-14-day window for one reason: macrophages have digested the necrotic tissue and the wall is at its weakest before the scar forms. If you know that single mechanism, you can place every mechanical complication without memorising dates. Contraction band necrosis with dark eosinophilic stripes is the signature of reperfusion, not of the ischemia itself, so it appears in the patient who was successfully treated.
Go deeper
First Aid 2026 — CV/Pathology (p.308) · B&B — MI histology timeline · Mehlman — HY Cardio (neutrophils vs macrophages, rupture timeline)
High-yield images4
Flashcards for this page
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Generation of (...) and increased (...) influx → Hypercontraction of (...)
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