From endothelial injury to fatty streak
Atherosclerosis begins at the inner lining of arteries. When the endothelium is injured or dysfunctional, often from high LDL cholesterol, high blood pressure, smoking, or high blood sugar, it becomes more permeable and adhesive. LDL particles infiltrate the artery wall and become oxidized, prompting monocytes to enter and mature into macrophages. These macrophages engulf the modified LDL and turn into lipid-laden foam cells, which cluster into the earliest visible lesion, the fatty streak.
This stage can be present silently for years, even in young adults, without symptoms.
Plaque maturation and rupture risk
Over time, smooth muscle cells migrate and lay down a fibrous cap over a growing core of lipid and cellular debris, forming a fibrous plaque. Plaques can narrow the vessel and limit flow, but the more dangerous event is rupture: a thin-capped, inflamed plaque can tear, exposing its core and triggering a clot that may abruptly block the artery, causing a heart attack or stroke.
Plaque stability often matters more than size for acute risk. This is general educational information about disease mechanisms, not medical advice; cardiovascular risk and treatment should be assessed by a qualified clinician.