How plaque forms
- The retention model
The artery is lined by a thin active layer, the endothelium. Where blood flow is turbulent (branch points, curves) it becomes leaky and inflamed, and ApoB-carrying particles (LDL and its relatives) pass into the wall and get trapped — the 'response-to-retention' model, the initiating step. Trapped particles are oxidised, which the body reads as danger.
- The inflammatory loop
Oxidised particles recruit immune cells (monocytes) that become macrophages, which gorge on the trapped cholesterol and turn into foam cells — the earliest visible lesion (a 'fatty streak', present in many people by their 20s). Foam cells die, spilling a soft lipid/necrotic core; smooth-muscle cells lay a fibrous cap over it. The whole thing is self-amplifying: more particles in the blood means more retained, more inflammation, more plaque. Evidence ●●●●●