## Stable vs. Vulnerable Atherosclerotic Plaques ### Key Histological Differences **Key Point:** Vulnerable (unstable) plaques are characterized by a **thin fibrous cap** (<65 µm), **large lipid-rich necrotic core**, and **abundant macrophage infiltration** — features that predispose to rupture and acute thrombotic events. ### Comparative Table | Feature | Stable Plaque | Vulnerable Plaque | | --- | --- | --- | | Fibrous cap thickness | Thick (>200 µm) | Thin (<65 µm) | | Lipid core | Small, organized | Large, necrotic | | Macrophage content | Sparse | Abundant (foam cells) | | Smooth muscle cells | Prominent, organized | Sparse, apoptotic | | Calcification | Organized, scattered | Minimal or absent | | Clinical risk | Low | High (rupture-prone) | ### Mechanism of Vulnerability 1. **Thin fibrous cap** = reduced mechanical strength → increased shear stress concentration 2. **Large necrotic lipid core** = lipid-laden macrophages undergo apoptosis → release proteolytic enzymes (MMPs, cathepsins) 3. **Enzyme activity** = degradation of collagen and elastin → cap weakening 4. **Macrophage infiltration** = source of tissue factor (TF) → thrombotic potential if rupture occurs **High-Yield:** Vulnerable plaques are **clinically silent** on angiography (may show <50% stenosis) but cause **acute MI** when they rupture. This is why angiographically "insignificant" lesions can cause sudden cardiac death. **Clinical Pearl:** Intravascular ultrasound (IVUS) and optical coherence tomography (OCT) can identify vulnerable plaques *in vivo* by detecting thin caps and large lipid pools — emerging tools for risk stratification. ### Why Stable Plaques Do Not Rupture - Thick fibrous cap acts as a **mechanical barrier** - Smooth muscle cells synthesize collagen and maintain cap integrity - Minimal macrophage infiltration → fewer proteolytic enzymes - Calcification may actually **stabilize** the plaque (paradoxically) [cite:Robbins 10e Ch 11]
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