According to the National Heart Lung and Blood Institute, Atherosclerosis is a disease in which plaque builds up mainly inside the medium to large elastic and muscular arteries that carry oxygenated blood to the heart and other areas of the body. Over time, plaque, made up of fat, cholesterol, calcium, and other substances, hardens and narrows the arteries limiting the flow of oxygen to organs and other parts of the body. This condition is the most significant underlying cause of heart failure, coronary artery disease, strokes and infarction resulting from ischaemia of the heart, brain or extremities. Atherosclerosis is a matter of the immune and vascular systems. Nitrogen Oxide release protects against atherogenesis by preventing smooth muscle cell proliferation and leukocyte adhesion. When a balance exists in the arteries between nitrogen oxide, a vasodilator, and endothelin-1, a vasoconstrictor, the endothelium is shielded from injury, inflammation, and thrombosis, leukocytes are unable to bind to endothelium, and platelet aggregation is minimized. Excessive NO release, however, may damage vascular wall cells especially in combination with other reactive oxygen intermediates (Matthys & Bult, 1997). When risk factors for atherosclerosis set in, this balance is disturbed and the immune system fails to counteract or destroy modified LDL, free radicals, infectious and other harmful agents detected by the system as foreign. Monocytes and t-lymphocytes fail to remove or destroy these foreign molecules resulting in the trigger of further immune response, which causes the artery to become inflamed (Boamponsem & Boemponsem, 1997).
The regulatory mechanisms of low-density lipoprotein (LDL) receptors function in such a way that the expression of these receptors by a cell is halted when it has taken up enough cholesterol for its metabolic needs. However, lipoprotein particles...