blood cells) have a constant interaction, but this interaction increases with elevated cholesterol levels. As the cholesterol levels increase, the monocytes begin to attach onto the endothelium, where they are transformed into macrophages. These macrophages begin to oxidize the LDL and they become toxic to the endothelium which leads to platelet adhesion and aggregation and fibrin deposition. The macrophages begin to ingest the oxidized LDLs transforming them into foam cells, which begins the formation of the lipid core of unstable plaques. Damage to the vessel wall causes macrophages, lipids and cholesterol to form a plaque leading to the last level of atherosclerosis, complicated lesions which includes hemorrhage, ulcerations and scar tissue