Current Mechanism And Concepts Of Pathogenesis Of Atherosclerosis

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

6. Atherosclerosis, pp.1157. is a form of arteriosclerosis in which thickening and hardening of the vessel are caused by the accumulation of lipid-laden macrophages w/I the arterial wall, which leads to the formation of a lesion called a plaque. It is not a single disease but rather a pathologic process that can affect vascular syustemns throughtout the body, resulting in ischemic syndromes that can vary widely in their severity and clinical manisfestations. It is the leading contributor to coronary artery and cerebrocascular disease. Athrosclerosis is an inflammatory disease, the lesions progress from endothelial injury and dysfunction

To begin with, cells create atherosclerotic deposits, and these deposits arise on vessel walls. This is formed when LDL deposits tend to become stuck in the matrix, and they undergo oxidation and glycation. Macrophages then feast on LDL’s, becoming fueled with fatty droplets. If there is an inflammatory disease, this can cause more growth of plaque, and a fibrous cap or the lipid core is established. Then, foam cells weaken the caps by digesting matrix molecules, which then leads to the damage of smooth muscle, resulting in the inability to repair the cap. If a clot is big enough, the flow of blood will be interrupted resulting

A sufficient coronary artery blood flow is essential to supply oxygen for normal cardiac activities (Craft, 2014, p. 599). Atherosclerosis is a common form of CHD. It is an inflammation disease when plasma cholesterol is high. Risk factors such as hypertension, high cholesterol, smoking and diabetes increase the risk of endothelium injuries, contributing to the increase in oxidated lipid-lipoprotein (LDL). Foam cell is produced by the increase in the number of macrophages signalled by oxidated LDL. Next, the accumulation of foam cells will cause the formation of fatty streak lesions on arteries walls. Over time, fatty streak lesions migrate to the site and form fibrous plaque due to the increase in smooth muscles and collagen. The thickening and hardening initiated by an accumulation in calcified fibrous plaque caused the blood vessels to narrow. As a result, a decrease in tissue perfusion contributing to the development of myocardial ischemia (Craft, 2014, p. 599; McCance & Huether, 2014, pp. 1145-1147).

Artery coronariasLa artery disease coronary (EAC) affects more than 15 million Americans, being both the most common type of cardiovascular disease. The EAC and its complications, such as arrhythmia, angina pectoris and heart attack, are the main causes of death in the United States. The most frequent cause of EAC is a disease known as 'atherosclerosis' that occurs when forms a waxy substance within the arteries that irrigate the heart. This substance, called «plate», is composed of cholesterol, fatty, calcium and a coagulant substance called «fibrin». Identified two types of plate: plate hard and soft plate.

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.

Coronary artery disease is the most common cause of a myocardial infarction (MI). As a result of CAD, plaque builds up in the arteries, thus narrowing the coronary arteries and preventing adequate blood flow to the heart. This condition is called atherosclerosis. In 2012, Huether, S., & McCance, K. defines Atherosclerosis when it begins to occur when there has been an injury to the coronary vessel wall. When injury occurs on the vessels endothelial layer it triggers a clotting mechanism. That mechanism sends chemotaxsis signals through the body for monocytes/macrophages to come clean the open vessel wall that is leaking LDL into the blood. The macrophages attempt to digest the fatty substance but have a hard time doing so. When the cells cannot digest the LDL, cell proliferation happens and they become static. Static macrophages turn into foam cells that then begin to cover the open vessel wall. Stasis of these foam cells occurs and forms a fatty streak, beginning to slowly occlude the artery. Then with time, build up of collagen occurs on top of the

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 develops over the course of 50 years, beginning in the early teenage years. The causes of this process appear to be lipid retention, oxidation, and modification, which provoke chronic inflammation at susceptible sites in the walls of all major conduit arteries. Initial fatty streaks evolve into fibrous plaques, some of which develop into forms that are vulnerable to rupture, causing thrombosis or stenosis. Erosion of the surfaces of some plaques and rupture of a plaque's calcific nodule into the artery lumen also may trigger thrombosis. The process of plaque development is the same regardless of race/ethnicity, sex, or geographic location, apparently worldwide. However, the rate of development is faster in patients with risk

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

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

Atherosclerosis is the underlying cause of coronary heart disease which can affect any artery in the body. Atherosclerosis 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, resulting in the reduction of the nutrients and oxygen that are able to reach the heart. As a consequence, the heart becomes increasingly hypoxic resulting in ineffective contractions. 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 blood lipids, and smoking took to assist in the development of atherosclerosis.

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

The current epidemic of coronary heart diseases continues to increase as “cardiovascular disease (CVD) is the leading cause of death globally resulting in about 30% of deaths annually” (Jaleta, Gudina, & Getinet, 2014) and with Atherosclerosis being one of the top diseases among African Americans and obese children. Atherosclerosis is described as the disease of clogged arteries from buildup of plaque, causing arteries to become narrow, thick, and stiff which makes blood flow very difficult to pass. As many factors do contribute to the growth of this disease, this literature review will discuss the factors of the African American race as well as children being affected by Atherosclerosis. The substances of the plaque is usually composed of cholesterol, fat, and calcium which sticks together to harden over time in the walls of the arteries. As a result of such action, narrowed arteries can cause blood clots which can overtime lead to a heart attack. Although it is a treatable condition, lots of preventable methods are required to see improvements such as nutrition and exercise.

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