The Pathophysiology Of Atherosclerosis: Arterial Tree

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 the leading cause of coronary heart disease, the number one killer of Americans (). The inflammatory process is known to lead to a myriad of other cardiovascular complications including, coronary heart disease, stroke and myocardial infarctions. It is important

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 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

Narrowing and hardening of the artery walls causing buildup of fatty tissues (plaque), cholesterol and other substances, which may restrict blood flow is referred to as atherosclerosis. Having restriction of blood flow develops damage to a patients’ organs and also increases the risk of heart attacks, blood clots, and strokes overtime (WebMD, 2015). It is said to be the most common form of arteriosclerosis that forms small patches and arterial spasms. The plaque also known as atheroma, builds up and may cause the blood clots to burst. Atherosclerosis is considered to be a heart condition, but may also affect arteries in any part of the body and could be prevented and treated (Mayo Clinic, 2015).

The frequent consumption of fast food disturbs the levels of cholesterol and fat that the body cannot process and results in atherosclerosis or clotting of the blood. The accumulation of fat and cholesterol in the body not only results in atherosclerosis but also increases the risk of blood clotting (Miller). Blood clotting is also a primary cause of cardiovascular diseases apart from atherosclerosis because it escalates the resistance of blood flowing through the veins and arteries. Fast food consumption is not only one of the leading causes of obesity and cardiovascular diseases but also leads to several other health disorders, including diabetes and hypertension.

The pathogenesis of arthrosclerosis is a progressive disease of the vascular system, it starts while we are young and progresses throughout our lives. The progression of arthrosclerosis, starts with an injury to the endothelial lining of the arteries, from such diseases as, hypertension, high cholesterol, diabetes and smoking. The damage to the endothelial cells causes dysfunction and the area with endothelial cell inflammation draws leukocytes, cholesterol, vascular smooth muscle cells and other debris, the buildup creates atherosclerotic plaque deposits in areas on an artery wall causing an inflammatory process (Hoffman, 2007).

Normally, the plasma from the lumen is able to leak out to the tunica layers and supply nutrients to the cells within. In large vessels, vasa vasorum, a network of small blood vessels, is another source of nutrients that supplies large, thick arteries & veins. In the pathophysiology of atherosclerosis, the process starts by damage in the tunica intima. When the endothelial cell is damaged. It releases a chemical called von willebrand

Atherosclerosis is a type of arteriosclerosis. Arteriosclerosis is a general term for the thickening and hardening of arteries. Atherosclerosis, or hardening of the arteries, is a pathological situation in which plaque builds up inside the arteries. Plaque is usually made of cholesterol, fatty substances, cellular products, calcium and fibrin (a clotting material in the blood). Atherosclerosis is the leading cause of mortality and morbidity from cardiovascular disease (CVD) around the world. The magnitude of this problem is so high that atherosclerosis claims more lives than all types of cancer combined and the financial burden are considerable1. It a complex, chronic pathological

This vascular condition affects the entire vascular tree and is also the cause of cerebrovascular and peripheral vascular disease (PAD), as well as the reason for major clinical complications such as restenosis and vein graft arterialisation. The development of atherosclerotic vascular disease involves a complex interplay of genetic, metabolic, cellular, and immunological factors, and understanding these factors is the first step in targeting heart disease.

Atherosclerosis is a disease dealing with the heart. This disease causes hardening and narrowing (or even blockage) of the arteries, which makes the arteries thicken. Accumulations of fat, calcium and plaque build up are all components of having this disease known as atherosclerosis. The accumulations of calcium, fat, and plaque build up quietly and slowly block the arteries, putting blood flow at an extremely high risk. Atherosclerosis is typically the source of heart attacks, strokes, and peripheral vascular disease— what with each other are called cardiovascular disease (“Atherosclerosis: Causes, Symptoms, Tests, and Treatment - WebMD,” n.d.).

Atherosclerosis is a complex process involving entrance, modification and accumulation of plasma low density lipoproteins (LDLs); recruitment and proliferation of the cells in the arterial wall. The process advances through a series of stages that begins with the formation of foam cells and tends towards the formation of the complex atherosclerotic plaque, which consists of a lipid core covered by a fibrous cap and areas that are rich in inflammatory cells. Free radical mediated oxidation of LDL plays a key role in atherogenesis. The oxidation of LDL is a process during which both the proteins and lipids undergo oxidative changes to form the oxidized–LDL.

Atherosclerosis is classified as a chronic, progressive, and multifactorial disease of moderate and large sized arteries categorised by intimal lesions called atheroma plaques that pushes into the vessel lumens. Atherosclerosis leading to coronary artery is the main cause of coronary artery disease (CAD). It is vital to appreciate the central mechanisms of atherogenesis in order to understand the adverse clinical results of Coronary Artery Disease and their ensuing management. The progression of atheroma consist of several cellular and molecular events with endothelial dysfunction, leucocyte recruitment and dispedesis, LDL transcytosis, LDL oxidation, recruitment and proliferation of smooth muscle cells, synthesis of extracellular matrix proteins, build-up of foamy macrophages as well as interplay of different cytokines. (Bisht et al, 2012).