A 58-year-old man from Delhi presents with acute anterior wall myocardial infarction. Coronary angiography reveals a critical stenosis (>90%) in the left anterior descending artery with an irregular, ulcerated plaque. Histopathology of the culprit lesion shows a lipid-rich core with a thin fibrous cap infiltrated by macrophages and T lymphocytes. Which of the following best describes the pathological classification of this atherosclerotic plaque?

Explanation

## Atherosclerotic Plaque Classification **Key Point:** The morphological features described—lipid-rich core, thin fibrous cap, and inflammatory infiltrate (macrophages and T lymphocytes)—define a **vulnerable (high-risk) plaque**, which is prone to rupture and thrombosis. ### Pathological Features of Vulnerable Plaques | Feature | Vulnerable Plaque | Stable Plaque | |---------|-------------------|---------------| | **Lipid core** | Large, lipid-rich | Small, minimal | | **Fibrous cap** | Thin (<65 μm) | Thick (>65 μm) | | **Inflammation** | Abundant macrophages, T cells | Sparse inflammatory cells | | **SMC content** | Minimal | Abundant | | **Clinical outcome** | Rupture → acute thrombosis | Gradual luminal narrowing | **High-Yield:** Vulnerable plaques are responsible for **acute coronary syndromes (ACS)** despite not always causing severe stenosis. The thin cap is mechanically weak and prone to rupture, exposing the thrombogenic lipid core to circulating blood. ### Histological Hallmarks 1. **Thin fibrous cap** (<65 μm) — poor collagen organization 2. **Large necrotic lipid core** — cholesterol crystals, cellular debris 3. **Inflammatory infiltrate** — CD68+ macrophages, CD4+ T cells 4. **Reduced smooth muscle cells** — less structural support 5. **Ulceration/erosion** — surface disruption **Clinical Pearl:** The **thin cap macrophage-rich (TCMR) plaque** is the morphological substrate of plaque rupture. Angiographic features (irregular, ulcerated appearance) correlate with histological vulnerability. **Mnemonic:** **LIPID** = **L**arge necrotic core, **I**nflammatory cells, **P**oor cap integrity, **I**nstability, **D**angerous rupture-prone. ### Why This Matters in the Clinical Context The patient presented with **acute MI**, not stable angina. This acute presentation is explained by plaque rupture with superimposed thrombosis—a hallmark of vulnerable plaque pathology. Stable, fibrocalcific plaques typically cause chronic, predictable angina due to fixed stenosis. [cite:Robbins 10e Ch 11]