Explain The Pathophysiology Of Atherosclerosis

     Atherosclerosis is one of a group of health problems that define coronary artery disease, oftentimes referred to as heart disease. Atherosclerosis is the leading cause of heart disease in the United States. The following is the definition provided by the American Heart Association:

Coronary artery disease remains number one killer of the western civilization despite 40 years of aggressive drug and surgical interventions (Esselstyn). Usually, pharmaceutical drugs, such as statin, are given to try to slow the progression, but may provide uncomfortable side effects. In fact, the majority of patients discontinue statins within 1 year of treatment initiation (Maningat). Furthermore, surgery is performed to circumvent clogged arteries and literally bypass the symptoms. In the last year, 500,000 coronary bypass procedures were performed (Swaminathan et al). However, these surgeries can have significant risks, including the potential to cause further heart damage, stroke, and brain dysfunction. Thus, it is evident that these way of treatments may not be enough on its own, and that getting to the

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

One of the patient’s secondary diagnoses is atherosclerotic heart disease of native coronary artery without angina pectoris. He had a heart valve replacement in 2011. Atherosclerosis is a disease in which plaque made of fat, cholesterol, calcium, and other substances builds up inside the arteries. This is an issue because the plaque hardens over time and narrows the arteries, which then limits the flow of oxygenated blood to vital tissues. This condition can lead to heart attacks, strokes, and death. Coronary artery atherosclerosis is the single largest killer of both men and women in the United States (Boudi, 2016). The patient’s atherosclerosis is located in the coronary artery. This artery is one of two main blood vessels that branch off

Atherosclerosis means "hardening of the arteries"; this is caused by a build up of cholesterol and other fatty substance within the walls of the arteries. In atherosclerosis, fatty deposits called plaque, build up on the inner wall of the coronary arteries. These fatty deposits usually develop over

What is Atherosclerosis Disease?Well Atherosclerosis is a disease in which plaque builds up inside your arteries.Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body.The Atherosclerosis Disease is caused by high blood pressure,smoking,or high cholesterol.Did you know that about 360,000 people will die from the Atherosclerosis disease each year. Nikolai N. Anichkov was the one who discovered the Atherosclerosis disease.Atherosclerosis was discovered in 1964 by Anichkov.

Its function is to maintain smooth and toned arteries so blood can easily flow through them. Atherosclerosis creates damage to the endothelium through various factors, such as smoking, high cholesterol, and high blood pressure. Smoking increases the growth of the condition in coronary arteries, aorta, and arteries in the legs. Cholesterol and other cellular substances can build up into plaque in the arteries and make them narrow and cut down the blood and oxygen supply. The plaque forms a bump in the wall of the artery and can continue to develop into a blockage in the artery as it grows with the progressing condition. Pain can develop and the blockages can rupture, which will make the blood clot in the area of the rupture. However, there are cases where plaque builds up but doesn’t cut off blood supply, showing no symptoms of the

Atherosclerosis is a reduction of the arteries triggered by a buildup of plaque. It is also called arteriosclerosis or hardening of the arteries. Arteries are the blood vessels that transport oxygen and nutrients from the heart to the rest of the body. As the body gets older, fat and cholesterol can collect in the arteries and form plaque. The buildup of plaque makes it difficult for blood to flow through the arteries. This buildup may transpire in any artery in the body and can result in a shortage of blood and oxygen in various tissues of the body. Pieces of plaque can also break off, causing a blood clot. If left untreated, atherosclerosis can lead to heart attack, stroke, and heart failure. Atherosclerosis is a fairly common problem associated with aging. According to the University of Maryland

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.

Atherosclerosis begins with damage to the inner wall of an artery. Substances in the body such as cholesterol, fats and cellular waste products accumulate inside the damaged area. Chemical reactions occurring within the build-up of these waste products cause cholesterol molecules to oxidize. This initiates an inflammatory response within the body in which the endothelial cells release chemicals. These chemicals are toxic to the body, signaling a call for help. In response to this chemical reaction, monoxides from the bloodstream travel to the affected site. Stimulation from the oxidized cholesterol turns the monoxides into macrophages. As a result, the macrophages change into foam cells, which accumulate over time to form plaque. As the plaque

Since atherosclerosis has been identified as an inflammatory disorder, there has been much interest in the effect of n-3 fatty acids on inflammation. Dietary supplementation with ALA significantly decreased inflammatory markers in a study in middle aged men. Hypotensive Effects: Although ALA is a precursor of EPA and DHA, it may have inde-pendent effects on blood pressure and blood

This paper indicates a mechanism to target disease sites in diseases such as atherosclerosis and cancer, which are sources of TNFa. If a cell is engineered to seek TNFa sources like those in cancer and atherosclerosis, they could be utilized as a targeted therapy. In order to accomplish this a system of engineered proteins was utilized TNFa chimeric receptor (namedTNFR1chi), a previously engineered Ca2+-activated RhoA (named CaRQ), vesicular stomatitis virus glycoprotein G (VSVG), and thymidine kinase (Qudrat at al., 2017).. When bound by TNFa, TNFR1chi generates a Ca^2+ signal that activates CaRQ-mediated-non-apoptotic blebs that allow migration towards the TNFa source. The VSVG causes membrane fission of the engineered cell and TNFa

Currently, cardiovascular disease is “the number one killer in the United States and the developed world” (Sapolsky, 2004, p. 41). Coronary heart disease (CHD) is the most common form of cardiovascular disease, which is killing more than 7 million individuals on an annual basis.