The summary of atherosclerosis stages is accurate and aligns
with current medical understanding. Here's a breakdown of the key stages with
supporting details:
1. Endothelial Dysfunction & Fatty Streaks
- Endothelial
damage: Triggered by hypertension, smoking, or high LDL cholesterol,
leading to inflammation and oxidative stress
- Lipid
accumulation: Oxidized LDL particles infiltrate the damaged
endothelium, attracting monocytes that differentiate into macrophages.
These engulf lipids, forming foam cells (visible as fatty
streaks)
- Early
lesions: Fatty streaks appear as yellow patches in arteries, often
detectable by adolescence
2. Plaque Progression (Fibrous Plaque)
- Smooth
muscle cell (SMC) migration: SMCs from the tunica media migrate to the
intima, proliferate, and secrete collagen, forming a fibrous cap
- Plaque
growth: Continued lipid deposition, macrophage infiltration, and
release of matrix metalloproteinases (MMPs) weaken the cap
- Chronic
inflammation: T-cells and macrophages secrete cytokines (e.g., TNF-α,
IL-1) that sustain inflammation and inhibit collagen synthesis
3. Plaque Rupture & Complications
- Vulnerable
plaques: Thin fibrous caps with large lipid cores are prone to rupture
due to MMP activity
- Thrombosis:
Rupture exposes thrombogenic material (e.g., collagen), triggering clot
formation that may occlude arteries
- Clinical
outcomes:
- Stenosis:
Chronic narrowing reduces blood flow, causing ischemia (e.g., angina)
- Acute
occlusion: Sudden clot formation leads to myocardial infarction or
stroke
Additional Notes
- Calcification:
Advanced plaques often calcify, increasing rigidity and rupture risk
- Asymptomatic
progression: Atherosclerosis develops silently over decades, with
symptoms typically manifesting after age 65
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