Atheromatous Lesion Research Paper

Atherosclerosis is the process in which substances known as plaques, which are made up of cholesterol and platelets, adhere to tears in the walls of arteries. Over time these plaques build up to the point where they occlude blood flow in the arteries. When this happens in the coronary arteries, either directly, as the result of buildup in the arteries themselves, indirectly in the form a clot from another part of the body breaking loose and becoming lodged in the coronary arteries, the usual result is a heart attack.3

Coronary heart disease occurs when some of the arteries that carry blood to the heart muscle become narrowed with fatty deposits. In this condition fatty deposits called plaque, composed of cholesterol (see later) and fats, build up on the inner wall of the coronary arteries. When arteries are narrowed, the heart is not fully supplied with the

When LDL or the cholesterol crossed the endothelium, which is already damaged, it will force the cholesterol to move through the artery wall. This will force the white blood cells in the body to stream, and because of that, it would digest the LDL. When this process goes on for a very long time, it would constitute a plaque to the artery wall.

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

The plaque restricts blood flow to the heart and deprive the heart of oxygen it needs to function properly. CAD can be chronic, which is narrowing of the coronary artery and limitation of the blood supply to part of the muscle, or it can be acute, which results from a sudden plaque that ruptures. According to Warnica (2013), rupturing of the plaque “exposes collagen and other thrombogenic material, which activates platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.” The major risk factors that can lead to atherosclerosis and coronary artery disease are hypertension, dyslipidemia, tobacco smoking, diabetes mellitus, obesity, sedentary lifestyle, and genetic predisposition. The risk factors present in M.T.’s life are history of angina pectoris, history of uncontrolled hypertension due to non-compliance with treatment, obesity, and stress. M.T. is overweight with 289 pounds. M.T.’s cholesterol level is high at 280mg/dl. M.T.’s stress is related to experiencing the death of his best friend and business partner from cancer. Having three teenage children who are constantly in trouble at school and a wife who recently lost her job can be a stress factor in M.T.’s

Sometimes atherosclerosis occurs in the carotid arteries, especially at the bifurcation or the point where the common carotid divides into the internal and external carotids. Atherosclerosis means that a potentially dangerous plaque has formed on the artery wall. Plaque is a sticky material made of fat and calcium which hardens the arteries and can block the flow of blood. This narrowing is sometimes called a carotid artery stenosis, meaning that the carotid artery has narrowed significantly.

Some people who are injured in falls or motor vehicle crashes develop thoracic aortic aneurysms.

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

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

Atherosclerosis disturbs the flow of blood and damages vessel endothelium causing an increase in platelet adherence. There is also an increased sensitivity by platelets to factors that cause adhesiveness and aggregation.

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

These cells are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which activate endothelial cells, proliferation of smooth muscle cells, lesion progression, and the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Many of these molecules involved can be measured systemically and has been shown that elevated concentrations in the circulation are associated with future cardiovascular

Macrophage which is now foam-like accumulates on the blood vessel to form visible fatty streak which then undergoes apoptosis. The plaque continues to grow and hardens narrowing the arteries. This ruptures and causes a blood clot which limits the flow of oxygen-rich blood to the body causing a heart attack, stroke or even death. Factors that are known to predispose to atherosclerosis are physical inactivity, diabetes mellitus, hyperlipidemia, cigarette smoking and hypertension which increase the chances by two-fold by damaging the vascular endothelium. Experimental studies have just shown that excess blood levels of iron can lead to atherosclerosis (Guyton and Hall, 2011).

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).

Plaque build-up in the arteries is known as atherosclerosis. “Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood.” (National Institutes of Health, 2016). After a while, plaque solidifies and constricts the arteries. This reduces the movement of oxygen rich blood to the heart. When plaque accumulates in the coronary arteries it is called Coronary Artery Disease. “When a plaque in a heart artery breaks, a blood clot forms around the plaque. This blood clot can block the blood flow through the heart muscle.” (American Heart Association, Inc., 2016).