Atherosclerosis: Difference between revisions

Unfortunately, these two atheroprotective endothelial functions can be impaired by several factors. The first factor is disturbed flow (low shear stress with rapid fluctuation), which is typically located at arterial branch points and bifurcations and can impair the protective functions. This is well illustrated by the difference in prevalence of atherosclerosis between branched arteries and bifurcated vessels. Bifurcation areas such as the common carotid and left coronary arteries are relatively more common deposition sites for atherosclerosis than arteries with few branches such as the internal mammary artery. Thus, many observations show that the distribution of atherosclerotic lesions is common in large vessels and they vary in location and frequency among different vascular beds. These findings encourage a belief that hemodynamic factors play an important role in atherogenesis. Furthermore, the fact that hypertension intensifies the severity of atherosclerotic lesions additionally supports this belief.<br />

Another major factor that can impair the atheroprotective endothelial function is chemical irritants such as cigarette smoking, abnormally high circulating lipid levels and high sugar levels (diabetes mellitus). They can contribute to endothelial dysfunction and are all well- known risk factors for atherosclerosis. Exposure to chemical irritants promotes endothelial dysfunction by increasing endothelial production of reactive oxygen species, which alter the metabolic and synthetic functions of endothelial cells. As a result, the endothelium is inclined to exhibit proinflammatory processes, such as secreting inflammatory cytokines.<br />

In conclusion, hemodynamic and chemical stressors contribute to disturbance of the endothelial homeostasis and promote endothelial dysfunction. This results in impairment of permeability barrier function, secretion of inflammatory cytokines, stimulation of adhesion molecules on the cell surface that promote leukocyte recruitment, and altered antithrombotic properties and release of vasoactive molecules (Figure 8). Consequently, these effects establish the groundwork for further advancement of atherosclerosis.<br />