Essay on Role of Inflammation in Atherosclerosis

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

Atherosclerosis can be a serious condition; it is when the arteries become clogged by fatty substances such as plaques or atheroma. This causes arteries to become narrow and harden which can restrict blood flow preventing organs from functioning properly (Williams 2000).

2(529) Atherosclerosis is the main pathologic process responsible for the progression of this disease. Initiation of atherosclerosis begins with injury to the endothelial lining of the arterial wall. Platelets adhere to the injury site causing aggregation and growth factors to be released (PDGF). 4(110) An inflammatory response is then activated promoting further adhesion of platelets. Next, blood cells pick up low-density lipoprotein (LDL) turning them into non-functioning cells, or plaque. The build of plaque causes intimal hyperplasia, forming a fibrous cap, which slowly occludes the lumen of the artery. 5

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

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

Atherosclerosis can be associate with atheromata’formation, which are raised, fibroadipose plaques that develop within the intimal layer of the artery or within the innermost layers of the tunica media. Some atheromata undergo calcification or ulceration, and mural thrombi can form over complicated and uncomplicated atheromata. As a result, can block or diminished the blood flow in the artery, turning tissue and organs oxygen deprived.

The inflammatory process is a pathological feature that contributes to the stages of atherosclerosis. It is initiated by attracting white blood cells such as monocytes and T lymphocytes to the injury site. The injury site can be caused by risk factors that can contribute to the disease such as; non-modifiable risk factors that include advanced age, men or women post menopause, family history or modifiable risk factors that include hypertension, smoking, diabetes and insulin resistance, obesity, hyperlipidemia and a sedentary lifestyle (Huether & McCance, 2008, p. 622). The monocytes mature in macrophages and Low-Density Lipoproteins (LDL) begin oxidisation. Once these LDL’s have been oxidised they penetrate the damaged endothelial lining and gather between the tunica intima and tunica media (two layers of an artery wall), where the macrophages then engulf the LDL’s forming foam cells that accumulate to form lesions called fatty streaks. With damage to the

Atherosclerosis, which leads to the formation of atheromas, is the foundation of cardiovascular disease (CVD). Though much is already known about the benefits of statins, their disease-modifying properties, in regards to inducing the regression of atheroma is still to be elucidated. Previous research has explored atheroma regression in specific diseases, but there is a need for a holistic literature review to come to a definitive conclusion as to whether atheroma reversal can occur.

Atherosclerosis is a type of cardiovascular disease that affects the arteries. I chose this disease because a few years ago my dad was having the beginning symptoms of a heart attack. We didn’t know what was wrong with him, but we thought he had acid reflux. Fortunately, we got him to go to the emergency room before anything bad happened. My dad had atherosclerosis in several of his arteries for his heart. Our insurance only covers the arteries that have so much blockage, so this is not solved forever. Thus, I chose this disease to inform and learn more about it.

Cardiovascular diseases are the leading cause of death in the United States with more than 610,00 people who die every year because of the complications attached to these diseases. Not only that, more than 735,000 people have heart attacks of different intensities ranging from slight to dangerous and life-threatening. The main heart disease that is diagnosed among patients is known as atherosclerosis.

The cardiovascular system is the network of blood vessels with the major role in transportation of oxygen and nutrition to the tissues and the waste products from organs and tissues. The diseases of the cardiovascular system, either acquired or congenital, may result in ischemia or undersupply of major organs, which would be a threat to the overall health of an individual. Events caused by cardiovascular diseases are the leading cause of morbidity and mortality worldwide. Despite improvements in the treatment and the preventive strategies of cardiovascular diseases, the social and economic burdens due to these diseases continue to grow. Further efforts, therefore,

Cardiovascular disease is the most common cause of mortality and morbidity and is accounted for almost 1 out of 5 deaths in the world. Atherosclerosis is a chronic heart disease that causes most of the vascular deaths. The fat deposition in arterial walls progressively develop into atheroma leading to restriction in blood circulation thus increasing risk of local thrombosis. Local thrombosis often forms the base that leads to partial or total obstruction of the artery. At the time of birth, the probability of a cardiovascular disease is 47%. The impact of Atherosclerosis on morbidity and mortality and its economic implications created a necessity for new treatments and prevention strategies. It

Integrin Signaling in Endothelial Cell Activation. In quiescent vessels, the endothelial layer regulates vascular tone, provides an anti-thrombotic surface, and forms a tight barrier to restrict the passage of blood components into surrounding tissue [39]. Activation of the endothelial cell layer during inflammatory responses involves a phenotypic transition that increases vascular permeability and enhances the expression of leukocyte counter-receptors (e.g. ICAM-1, VCAM-1), proinflammatory cytokines (tumor necrosis factor α (TNFα), interleukin-1B (IL-1β)), and pro-coagulant molecules (tissue factor (TF)) [39]. Molecularly, endothelial activation represents the first discernable sign of local atherosclerotic susceptibility and is maintained during subsequent stages of atherosclerotic progression [40]. Several stimuli promote endothelial activation, including mechanical stress, oxidized LDL (oxLDL), proinflammatory cytokines (e.g. TNFα, IL-1β), and the bacterial endotoxin LPS [39]. Much of the reprogramming in endothelial gene expression can be attributed to the proinflammatory transcription factor nuclear factor-κB (NF-κB) [41, 42]. The NF-B family of homodimeric and heterodimeric transcription factors is maintained in an inactive state in the cytoplasm but translocates to the nucleus upon activation in response to a variety of endothelial cell activators

Coronary Heart Disease initially is an area of athermanous plaque formation due to lipid accumulation under the lining of the coronary artery. The lipid infiltrate which is a foreign substance, prompts white blood cells (macrophages) to engulf the lipids generating a foam cell discharge thereof smooth muscle penetrate and enlarge the area. It is until plaque obstructs more that 50% of the diameter of the coronary artery lumen, that the flow of blood is decreased. However when the subject heart requires more oxygen example during