Atherosclerosis Essay

Atherosclerosis (ath"er-o-skleh-RO'sis) comes from the Greek words athero (meaning gruel or paste) and sclerosis (hardness). It's the name of the process in which deposits of fatty substances, cholesterol, cellular waste products, calcium and other substances build up in the inner lining of an artery. This buildup is called plaque. It usually affects large and medium-sized arteries. Some

Atherosclerosis is narrowing of arteries caused by the accumulation of fatty deposits on the arterial walls.

Coronary Artery Disease, also known as CAD, is the most common form of heart disease. (Heart and Stroke Foundation, 2009) Coronary Artery Disease obstructs the blood flow in vessels that provides blood to the heart which is caused by the buildup of plaque on the artery walls. (Rogers, 2011, p.87) (Heart and Stroke Foundation, 2009) Plaque is a yellow substance that consists of fat substances, like cholesterol, and narrows or clogs the arteries which prevents blood flow. (Heart and Stroke Foundation, 2009) Plaque can build up in any artery but usually favors large and medium sized arteries. (Heart and Stroke Foundation, 2009)

Nitric oxide (NO) acts as a messenger molecule produced by the NO synthase (NOS) isoforms neuronal NOS (nNOS, or NOS1), inducible NOS (iNOS, or NOS2), and endothelial NOS (eNOS, or NOS3). NO has been involved in relaxing smooth muscle, inhibiting smooth muscle cell migration and proliferation, and decreasing platelet adherence and aggregation. NO also inhibits vascular inflammation [1].

Atherosclerosis is a disease affecting the innermost layer of large and medium sized such as aorta and coronary arteries. It is a slow developing disease, it is complex and often starts in childhood and progresses with increasing age (Miksch, Hunter, & Papailiou, 2005). It appears as focal thickenings called fibrofatty plaques in an artery wall, these plaques are

The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.

Atherosclerosis, the underlying cause of coronary heart disease which can affect any artery in the body, is essentially the narrowing of arteries due to excessive build up of cholesterol-rich lipids known as plaque (Insull 2009). Once the arteries become narrow, the flow of blood will be constricted, and the amount of blood, nutrients and oxygen that are able to reach the heart are reduced. As a consequence, the heart becomes increasingly hypoxic resulting in ineffective contraction. The aftermath of narrow arteries often poses serious consequences as it has a high probability of causing heart attack, angina, or even stroke (Marieb & Hoehn 2010; Insull 2009). Despite the fact that arteries will harden naturally as people age, the rate of plaque development is determined by the number of risk factors (Insull 2009). This essay will discuss and review the procedure in which the risk factors: hypertension, abnormal level of blood lipids, and smoking took to assist in the development of atherosclerosis.

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

Eagleton (2012) explains the pathological process inflammation has in weakening the arterial wall through the release of cellular and cytokine messengers which initiate various actions

With the increased consumption of fast-food and poor lifestyle choices, we have become an increasingly obese nation. For this reason, diseases such as cardiovascular disease have been on the rise. Cardiovascular disease is the combined term for a number of diseases concerning the heart and the blood vessels. Many of these life threatening diseases are related to a condition called atherosclerosis. The condition creates plaque build-up on the walls of the blood vessels. The plaque effects the flow of blood making it harder and can lead to blood clots which stops the flow of blood altogether. The two main effects to this are heart attacks and strokes however, other types of cardiovascular disease includes complete heart failure, arrhythmia

Coronary artery disease is the most common type of heart disease and the #1 cause of death for both men and women in the United States resulting in about 375,000 deaths a year. (National Heart, Lung, and Blood Institute, 2014). This disease refers to “any vascular disorder that arrows or occludes the coronary arteries leading to myocardial ischemia” (Huether & McCane, 2012). It occurs when the arteries that supply blood and oxygen to the heart becomes hardened and narrowed. Also, factors such as smoking, high levels of fat & cholesterol in the blood, hypertension, high levels of sugar in the blood, and blood vessel inflammation damage the inner layers of the coronary arteries. “This disease is prevalent in younger and elderly individuals. Coronary artery calcium is highly predicative of coronary heart disease event risk across all age groups” (Tota-Maharaj et al, 2014). Coronary artery disease is caused by the buildup of cholesterol and fatty deposits, or plaque, in the inner walls of the coronary arteries in a process called atherosclerosis. Normally, the coronary arteries are smooth and elastic, lined with a layer of cells called the endothelium. The endothelium acts as a physical barrier between the blood stream and the coronary artery walls.

Atherosclerosis is a disease in which fatty materials and plaque buildup on the inner lining of arteries. Arteries are blood vessels which carry rich blood to the heart and throughout the body. They’re lined by the endothelium, a thin layer of cells. The endothelium keeps blood flowing by keeping the inside of arteries smooth. However, when Atherosclerosis starts due to high blood pressure, smoking, or high cholesterol, it damages the endothelium. Atherosclerosis tends to happen throughout the body and arises when people grow older. This disease is mainly due to the deposition of fatty materials i.e., cholesterol, calcium and other substances found in the blood. The buildup of fat then hardens causing narrowing of the arteries. This

One source of great mortality and morbidity in Europe and North America is the cardiovascular disease, Atherosclerosis. It is recognized as a chronic inflammatory disease of the intermediate and large arteries characterized by the thickening of the arterial wall and is the primary cause of coronary and cerebrovascular heart disease (Wilson, 2005). It accounts for 4.35 million deaths in Europe and 35% death in the UK each year. Mortality rate are generally higher in men than pre-menopausal woman. Past the menopause, a woman’s risk is similar to a man’s (George and Johnston, 2010). Clinical trials have confirmed that lipid accumulation, endothelial dysfunction, cell proliferation, inflammation matrix alteration and foam cell formation are

784). The immune system attempts to attack the inflamed area in the artery with special white blood cells and “cells full of fatty nutrients, foam cells, begin to form there, too” (Sapolsky, 2004, p. 43). The white blood cells are unable to properly fight the affected area, and in turn, end up adding more substance to the build up. As this process continues, the affected area becomes inflamed and physically hardens. This produces a blockage in the artery and reduces blood flow, while also causing an increase in blood pressure. At this point of the atherosclerosis build up, many people, especially women, experience angina.

Many of the vaso-protective function of endothelium is provide by the Nitric Oxide(NO)20.Endothelium damaged by turbulent or non-laminar blood causes decreased production of NO.Such kind of blood flow also stimulates endothelial cells to produce adhesion molecules, which recruit and bind inflammatory cells. Hypercholesterolemia seems to inactivate the normal function of NO. The net effect is endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation of a local vascular inflammatory response. Lipids in the blood, particularly low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL), also bind to endothelial cells. 18Firstly LDL is transported across the healthy intima and become trapped in intima of a vessel wall.It undergoes oxidative modification and then oxidized LDL(OxLDL) is formed5.OxLDL is mighty inducer of inflammatory molecules.It adds up to the inflamotory signaling by endothelium that activates chemotactic substances, growth factors that attracts monocytes to vessel wall21Eventually OxLDL transforms monocytes into macrophages which makes the Forms cells, which are the hallmark of atherosclerosis. Oxidized LDL impair the signal transduction between endothelial cell surface receptors and NO production, inhibit NO synthase activity and inactivates NO realese from endothelial cells.22.Once the endothelium is impaired, oxidized LDL is stored in vascular endothelium and by the process of series of mechanism, foam cells are formed and then eventually fatty plaque that occludes the vessel along with the decreased amount of NO which decreases the ability of the vessel to dilate. As the plaque grows arterial wall narrowing and thickening occurs5. This plaque and narrowing of vessel results in decreased blood flow