The pathological process begins very early with a fatty streak composed of lipid deposited in the intima of arteries. Modified macrophages known as foam cells accumulate in the plaque region. These lipoproteins and cholesterol esters induce collagen synthesis by subintimal fibroblasts . When the lesion becomes infiltrated with fibrous material it protrudes into the lumen of the artery. The lesion itself rarely occludes the artery but rather it is blood clots that form on top of the plaque that close off the channel.
Chronic lesions become calcified and the elasticity of the vessel is decreased.
This hardening of the arteries causes an increase in resistance to blood flow and therefore an increase in blood pressure . Any vessel in the body may theoretically be affected by atherosclerosis, but the aorta, coronary, carotid and iliac arteries are most frequently affected. Ischemia or infarction of specific regions causes specific symptoms and clinical outcomes. Atherosclerotic disease is a dynamic process and the progression of atheroma formation can be slowed if plasma lipoproteins are reduced. Several pharmacologic approaches are successful dependent on the underlying cause of hyperlipidemia.