## Pathophysiology of Acute Atherosclerotic Thrombosis **Key Point:** Rupture or erosion of the fibrous cap with exposure of the thrombogenic lipid-rich necrotic core is the primary mechanism of acute coronary thrombosis in unstable atherosclerotic plaques. ### Vulnerable Plaque Characteristics The plaque that ruptured in this patient demonstrates the hallmark features of a **vulnerable (high-risk) plaque**: | Feature | Significance | |---------|-------------| | Thin fibrous cap | Prone to rupture under hemodynamic stress | | Large lipid-rich necrotic core | Highly thrombogenic when exposed | | Increased macrophage infiltration | Produces metalloproteinases that degrade collagen | | Neovascularization | Prone to intraplaque hemorrhage | | Active inflammation | Weakens cap integrity | ### Mechanism of Thrombosis 1. **Plaque rupture** occurs due to: - Hemodynamic stress (hypertension in this patient) - Inflammatory weakening of the fibrous cap - Smoking-induced endothelial dysfunction 2. **Exposure of tissue factor (TF)** and phosphatidylserine in the lipid core activates the extrinsic coagulation cascade 3. **Platelet adhesion and aggregation** on the denuded surface 4. **Thrombus formation** leads to acute luminal occlusion and myocardial infarction **Clinical Pearl:** The presence of ST elevation in inferior leads (II, III, aVF) with elevated troponin confirms acute transmural MI from acute thrombotic occlusion—not gradual stenosis. **High-Yield:** Plaque rupture (not erosion) accounts for ~70% of acute coronary syndromes. The lipid core is the most thrombogenic component because it contains tissue factor and phosphatidylserine. **Mnemonic: RUPTURE** — **R**ich lipid core, **U**nstable fibrous cap, **P**roliferation of macrophages, **T**issue factor exposure, **U**ncontrolled inflammation, **R**emodeling of extracellular matrix, **E**ndothelial erosion. ### Why Gradual Narrowing Does Not Cause Acute Thrombosis Smooth muscle cell proliferation causes **stable angina** through gradual luminal narrowing, not acute thrombosis. Stable plaques have thick fibrous caps and minimal inflammation.
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