Atherosclerosis, which is a chronic inflammatory disease amongst the arteries of the human body, remains the principal cause of cardiovascular related disease (Gets, 2011). Atherosclerosis results from a complicated relationship between different factors such as lipid metabolism, blood coagulation elements, cytokines, hemodynamic stress, and behavioral risk factors. (Singla et al., 2011) The pathogenesis of atherosclerosis involves oxidative stress, endothelial dysfunction and chronic inflammation, which are initiated in response to high plasma lipid levels, especially Low Density Lipoproteins. (Yu et al., Getz., 2011) Atherosclerosis is a benefactor to the pathogenesis of myocardial and cerebral infarctions, gangrene and loss of function in the limbs, which results from an inconsistent inflammatory-fibro proliferative reactions to destruction of the endothelium and smooth muscle of the arterial walls (Morenoa et al., 1992). Researches have found that free radicals and reactive oxygen species have been suggested to be part of this pathophysiology (Calderon et al., 2008).
As atherosclerosis progresses over the decades, there seems to be lesion growth that are mostly facilitated by cellular adhesion molecules, which are expressed on the vascular endothelium and on circulating leukocytes in reaction to inflammatory stimuli; this is largely due to the recruitment of inflammatory cells from the circulation and their trans-endothelial movements. (Blankenberga et al., 2003) furthermore, there is now an agreement that atherosclerosis characterizes a state of heightened oxidative stress characterized by lipid and protein in the vascular wall (Singla et al., 2011). Over several decades Atherosclerotic plaque matures and is known to involve inflammatory cell infiltration, accumulation of extracellular matrix, smooth muscle cell proliferation, fibrous cap formation, and angiogenesis. (Genis et al., 2000). In addition, coronary calcification has long been known to appear as part of the atherosclerotic process, which is known to over time resemble bone formation within the vessel wall. (Nikolaos et al., 2009)
Atherosclerotic research has recently concentrated on inflammatory cytokines involved in vascular inflammation and how they stimulate the production of endothelial adhesion molecules, which could enter circulation in soluble form, and have the cytokines stimulate the production of messenger cytokine interleukin-6, which incites the liver production of acute-phase reactants such as C-reactive protein to increase. (Packard et al., 2007) In short, cytokines released into the bloodstream have a tendency to bring about an inflammatory response. Researchers have also found that that treatment with lipid-reducing agents is correlated with reduced morbidity and mortality from coronary heart disease and it seems to work near the atherosclerotic lesion, causing stabilization, slowed progression and, in some cases, regression of lesions....