The term used to describe the buildup of fatty ‘plaques’ on arterial walls; it is the pathological basis for angina, ACS, PAD, AAA and some strokes

Aetiology

Modifiable risk factors

• Smoking
• Hypertension
• Obesity
• Hypercholesterolemia
• Diabetes
• Alcohol consumption (→ hypertension)

Non-modifiable risk factors

• Family history
• Male
• ↑ age

Pathophysiology

1. Primary endothelial injury e.g. due to smoking, hypertension etc.
2. Uptake of LDL from the blood into the intima of artery, where it is oxidized to become OXLDL
3. Macrophages migrate across the endothelium into the intima where they take up OXLDL and become foam cells → form a fatty streak
4. Activated macrophages release cytokines and growth factors, particularly PDGF, which result in proliferation of the smooth muscle layer and deposition of collagen
5. As the plaque enlarges blood flow is compromised → angina, PAD
6. Unstable angina/MI results when a large enough plaque ruptures, the clotting cascade is activated, and the thrombus occludes the artery