How Atherosclerosis Is Associated With The Major Killer Ailments

Many of the risk factors for cardiovascular disease cause problems because they lead to atherosclerosis. Atherosclerosis is the narrowing and thickening of arteries and develops for years without causing symptoms. It can happen in any part of the body. Around the heart, it is known as coronary artery disease, in the legs it is known as peripheral arterial disease. The narrowing and thickening of the arteries is due to the deposition of fatty material, cholesterol and other substances in the walls of blood vessels. The deposits are known as plaques. The rupture of a plaque can lead to stroke or a heart attack. (World Heart Federation).

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

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

Cholesterol and fatty deposits build up in the heart's arteries, causing less blood to reach the heart muscle. The muscle becomes damaged and the remaining heart tissue has to work harder.

Nevertheless, there is an understandable and noticeable link between circulatory related diseases and lifestyle diseases, such as Coronary Heart Disease. Coronary heart disease can occur when fatty acids, such as cholesterol in an inadequate diet, build up in the walls of the coronary artery. These fatty deposits collect minerals and harden to become a plaque. Eventually, this plaque grows and can swells up, forming an aneurism. In some cases, this aneurism may burst leading to instant death. As it continues to grow and swell up, it finally blocks the artery completely and forms blood clots. This is known as coronary thrombosis. A myocardial infarction, or in other words as heart attack, occurs when no oxygen is able to reach the coronary artery and thus it is unable to fulfil its role in providing the heart muscle with a sufficient supply of blood. Heart attacks are very common in the society nowadays, especially occurring in smokers or obesity related diseases (Millar, June 2014)

LDL carries plaque which attaches to the walls of arteries and beings to build up. The plaque is a combination of cholesterol, fat, calcium and other substances. As it builds up over time, it hardens and the arteries become narrow, a condition called atherosclerosis. The blood cannot flow as freely and oxygen cannot get throughout the body as it should. If the plaque ruptures or breaks open, a blood clot can form. If the clot becomes large enough, blood flow is impaired or blocked completely. You may experience extreme pressure or pain in the chest called angina or possible pain in the shoulders, jaw, arms, back, or the discomfort associated with indigestion. This is a heart attack. Heart damage or even death may result if blood flow is not quickly restored. However, arteries leading to other parts of the body can have plaque buildup resulting in strokes, carotid artery disease, and peripheral artery disease. On the other hand, if the HDL is higher, the risk for heart disease is lower.

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

Coronary illness is the development of plaque (fat store on the inward dividers of the veins) in the coronary conduits that supply O2 rich blood to the heart muscle, the development of plaque is called atherosclerosis. After some time passes plaques may solidify therefore limiting blood stream or totally obstructing the corridor. The development of plaque is straightforwardly identified with a people way of life, normal danger elements incorporate stoutness, high blood cholesterol and diabetes. At the point when the endothelium is harmed by blood stream, the cholesterol and fats in the blood get stuck shaping plaques. This outcomes in hypertension due the heart endeavoring to supply obliged levels of blood to the body. In the event that the blood stream to the heart muscles is limited or blocked it may

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 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

LDL deposits cholesterol in the arteries which cause plaque that restrict blood flow and increase the risk of a heart attack. (Timberlake, 2014, pg. 535)

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

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).

Coronary artery disease (CAD) is caused by fatty buildup in the arteries of the heart. Your arteries are made to carry oxygen infused blood to your heart and other parts of your body if it is filled up with plaque, which is the fatty substance that clogs and blocks up the arteries. If it gets clogged enough to where your heart is not receiving fresh oxygen, you could have a heart attack that could cause very serious damage to your body and could even kill you. When you are younger, you can begin to grow plaque in your blood vessels from not eating right and not exercising regularly. When your arteries are being filled up with plaque they become more narrow and harder for blood to get through as easily as it is supposed to be. When you have

Many of the vaso-protective function of endothelium is provide by the Nitric Oxide(NO)20.Endothelium damaged by turbulent or non-laminar blood causes decreased production of NO.Such kind of blood flow also stimulates endothelial cells to produce adhesion molecules, which recruit and bind inflammatory cells. Hypercholesterolemia seems to inactivate the normal function of NO. The net effect is endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation of a local vascular inflammatory response. Lipids in the blood, particularly low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL), also bind to endothelial cells. 18Firstly LDL is transported across the healthy intima and become trapped in intima of a vessel wall.It undergoes oxidative modification and then oxidized LDL(OxLDL) is formed5.OxLDL is mighty inducer of inflammatory molecules.It adds up to the inflamotory signaling by endothelium that activates chemotactic substances, growth factors that attracts monocytes to vessel wall21Eventually OxLDL transforms monocytes into macrophages which makes the Forms cells, which are the hallmark of atherosclerosis. Oxidized LDL impair the signal transduction between endothelial cell surface receptors and NO production, inhibit NO synthase activity and inactivates NO realese from endothelial cells.22.Once the endothelium is impaired, oxidized LDL is stored in vascular endothelium and by the process of series of mechanism, foam cells are formed and then eventually fatty plaque that occludes the vessel along with the decreased amount of NO which decreases the ability of the vessel to dilate. As the plaque grows arterial wall narrowing and thickening occurs5. This plaque and narrowing of vessel results in decreased blood flow