Monocytes enter damaged epithelium and become macrophages. Oxidative changes probably via the action of free radicals take place on the LDL which damages it and makes it a target for phagocytosis. Note that this oxidation of the LDL may cause it to damage the receptor it normally interacts with during its clearance. Macrophages and smooth muscle of the damaged vessel take up cholesterol from LDL and TG from VLDL to form atheroma. Fibrosis begins, plaque grows and begins to obstruct blood flow.
Platelets attach to the atheroma.
Hypertrophy of smooth muscle and the atheroma enlarges. Thrombosis, embolism Reasons for thrombosis 1. The rough surface of the atheroma can promote the formation of fibrin. The hard atheroma can fracture and this can stimulate coagulation of blood. The thrombus can block the blood vessel where it is formed or break off and form an embolus which will travel and block a narrower or smaller blood vessel.