The formation of arterial plaques begins with endothelial dysfunction. Factors such as high blood pressure, smoking, and high cholesterol levels can damage the endothelial layer of the artery. This damage allows low-density lipoprotein (LDL) cholesterol to enter the arterial wall, where it becomes oxidized. The oxidized LDL triggers an inflammatory response, attracting monocytes that differentiate into macrophages. These macrophages ingest the oxidized LDL, turning into foam cells and contributing to the formation of a fatty streak.
