The Disease Process of Atherosclerosis
HTH SCI 2C06
Dr. Ruth Hannon
March 11, 2013
Atherosclerosis is the primary topic for this research paper. It is a disease process that can lead to many complications, one of which is called myocardial infarction; otherwise known as a heart attack. Atherosclerosis, or the hardening of the arteries, is defined as a disease characterized by abnormal thickening of the arteries due to fatty deposits (atheroma’s) of cholesterol on the arterial inner walls. (Merriam-Webster Dictionary, 2013). This paper will look at the pathogenesis of atherosclerosis and how its complication, myocardial infarction, is formed in correlation to atherogenesis. This paper will also explore various tests, common medications used in clinical application, and their significance and mechanisms of action on a cellular level. The disease process for atherosclerosis is vast and includes many specific biomarkers, inflammatory mediators and cells along its progression. The vast majority of the disease process begins within the endothelium of the vascular system. A healthy artery has healthy endothelial cells that regulate the tonicity of the vessels and help to apply antiplatelet, anticoagulation and fibrinolytic elements (Galkina & Ley, 2007). Without these components, platelets clump together and cause potential occlusions in the vessels, resulting in localized ischemia and possibly the formation of emboli or thrombi. The tonicity and shape of the endothelium are controlled by the release of several vasoconstrictor (endothelin and angiotensin II) and vasodilator (prostacyclin, bradykinin and nitric oxide) chemical mediators (Davignon & Ganz, 2004). Angiotensin II works to stimulate production of endothelin; these two work together to exert vasoconstricting properties and promote proliferation of the smooth muscle cells, which in turn contributes to atherosclerotic plaque formation. Nitric oxide (NO) and prostacyclin act in conjunction also as vasodilators to prevent platelet adherence and aggregation, while bradykinin works to stimulate the release of NO (NO being the most potent vasodilator in the endothelium). It works by preventing oxidation of low-density lipoproteins (LDL), which are considered a major mechanism in the commencement and progression of atherosclerosis (Divignon & Ganz, 2004). When an injury to the endothelium occurs or toxic cells disrupt homeostasis of the endothelium, this in turn upsets the balance between vasoconstrictors and vasodilators being released. As such, a series of dysfunctional developments begin (Arsenault, 2009). The result is the advancement of atherosclerosis; which includes increased permeability of the endothelium, platelet clumping, leukocyte adhesion and generation of cytokines (Divignon & Ganz, 2004). There are many factors that cause these dysfunctions, some of which are not reversible but many of which are (Hannon, Pooler, & Porth, 2010). Hypercholesterolemia, hypertension, smoking, diabetes, and family history of coronary artery disease are all indicated in numerous studies, and Divignon & Ganz (2004) have noted that these risk factors exhibit a strong connection between endothelial dysfunction and the presence of coronary risk factors; even in patients that have no clinical manifestations of coronary disease. Their study also revealed that regular exercise, a non-sedentary lifestyle, and a healthy, balanced diet have all shown positive effects in reducing the risks associated, help to maintain homeostasis within the endothelium and prevent the initiation, progression and complications of atherosclerosis. Vasoconstriction indicates that there is a reduction in NO and once this occurs, vascular smooth muscle cells will start to migrate from the tunica media into the tunica intima and proliferate. Hannon, et al. (2010) state that this process is a direct...
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