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Atherosclerosis and myocardial infarction — from fatty streak to scar
Atherosclerosis begins as a fatty streak of foam cells and progresses to a plaque with a lipid core and fibrous cap; rupture of a "vulnerable" plaque with a thin cap causes thrombosis and infarction, and in myocardial infarction changes appear on a fixed timetable that allows dating at autopsy.
Why it matters in the exam
The bank asks what is seen in a fatty streak, what characterises a vulnerable plaque and what is seen at each stage of infarction. A fatty streak consists of lipid-laden macrophages (foam cells) and a few smooth-muscle cells, is not raised and does not disturb flow, and is found already in children. An advanced plaque has a necrotic core with cholesterol crystals, foam cells and inflammation, and a fibrous cap of smooth-muscle cells and collagen. A vulnerable plaque has a thin cap, a large lipid core and much inflammation — not necessarily the plaque that narrows the artery most. Common sites: the abdominal aorta, coronary arteries, popliteal artery, internal carotid artery and circle of Willis.
The infarct timetable: up to about 4 hours there is no gross change, and microscopically at most wavy fibres at the margins; at 4–12 hours coagulative necrosis, oedema and haemorrhage begin, and sometimes a dark mottled area is seen; at 12–24 hours contraction bands and the first neutrophil infiltration are evident; at 1–3 days there is complete coagulative necrosis with massive neutrophil infiltration; at 3–7 days macrophages begin to remove dead cells at the margins, and the area is yellow and soft; at 7–10 days softening is maximal and granulation tissue begins at the margins; at 2–8 weeks a grey-white scar develops.
Complications relate to the stage: free-wall rupture with pericardial tamponade is most common at 3–7 days, when the tissue is softest; septal rupture and papillary muscle rupture occur in the same window; pericarditis after 2–3 days; and ventricular aneurysm and heart failure in the scar stage. Reperfusion (catheterisation or thrombolysis) changes the picture — necrosis with contraction bands and haemorrhage. At autopsy of early death, TTC (triphenyltetrazolium chloride) staining shows the necrotic area as pale, because its enzymes have been lost.
Key points
- Fatty streak: foam cells; vulnerable plaque: thin cap and large lipid core.
- Up to 4 hours no visible change; TTC helps.
- 1–3 days neutrophils; 3–7 days macrophages.
- 7–10 days granulation tissue; 2–8 weeks scar.
- Wall rupture with tamponade: 3–7 days.
Summary table
| Time from onset | Gross | Microscopy | Typical complication |
|---|---|---|---|
| Up to 4 hours | No change; TTC can show it | Wavy fibres at margins | Arrhythmia |
| 4–24 hours | Dark mottling | Coagulative necrosis, contraction bands, first neutrophils | Arrhythmia |
| 1–3 days | Mottled with yellowish centre | Many neutrophils | Pericarditis |
| 3–10 days | Yellow and soft, red margins | Macrophages, then granulation tissue | Rupture of wall, septum or papillary muscle |
| 2–8 weeks | Grey-white scar | Collagen | Ventricular aneurysm, heart failure |
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — Blood vessels — atherosclerosis; The heart — myocardial infarction
- Fourth Universal Definition of Myocardial Infarction (ESC/ACC/AHA/WHF), 2018 — Pathological definition of infarction
- Michaud K et al. Diagnosis of myocardial infarction at autopsy: AECVP reappraisal, Virchows Archiv, 2020 — Time course of morphological changes
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.