A 58-year-old man from Delhi presents with acute onset chest pain radiating to the left arm for 2 hours. He has a 15-year history of hypertension and type 2 diabetes mellitus, both poorly controlled. On examination, BP is 145/92 mmHg, HR 102/min. ECG shows ST elevation in leads II, III, aVF. Troponin I is elevated at 2.8 ng/mL (normal <0.04). Coronary angiography reveals a 95% stenosis of the right coronary artery with a thrombus overlying an eccentric plaque. Which of the following pathological features of atherosclerotic plaque best explains the acute thrombotic occlusion in this patient?

Explanation

## Pathophysiology of Acute Atherosclerotic Thrombosis ### Plaque Rupture Mechanism **Key Point:** Rupture of the fibrous cap is the most common trigger for acute thrombotic occlusion in atherosclerotic coronary artery disease, accounting for approximately 70–80% of acute coronary syndromes. The clinical presentation of acute ST-elevation myocardial infarction (STEMI) with elevated troponin and angiographic evidence of thrombus overlying an eccentric plaque is pathognomonic for **plaque rupture**. ### Vulnerable Plaque Features | Feature | Significance | |---------|-------------| | Lipid-rich necrotic core | Large, poorly organized lipid accumulation; weakens fibrous cap | | Thin fibrous cap | <65 μm; prone to rupture under hemodynamic stress | | Eccentric plaque morphology | Asymmetric growth; creates stress concentration at cap shoulders | | Macrophage infiltration | Secretes MMPs and collagenases; degrades cap collagen | | Angiographically eccentric lesion | Indicates active remodeling and vulnerability | **High-Yield:** The combination of **eccentric morphology + thrombus + elevated troponin** is diagnostic of plaque rupture with superimposed thrombosis. This is the acute coronary syndrome pathway. ### Contrast with Chronic Atherosclerosis **Clinical Pearl:** Gradual concentric narrowing (option B) produces **stable angina** — it develops slowly, allowing collateral formation and is hemodynamically significant but not acutely thrombotic. Calcification (option C) stabilizes plaques and is associated with chronic, stable lesions. Endothelial erosion (option D) is less common (~20% of ACS) and typically occurs in younger patients with less lipid-rich disease. ### Triggers for Cap Rupture 1. Hemodynamic stress (shear forces at plaque shoulders) 2. Inflammation (macrophage-derived proteases degrade collagen) 3. Intraplaque hemorrhage (from vasa vasorum rupture) 4. Vasospasm (superimposed on fixed stenosis) **Mnemonic:** **VLIM** = **V**ulnerable plaque + **L**ipid core + **I**nflammation + **M**echanical rupture → acute thrombosis. [cite:Robbins 10e Ch 11]