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Atherosclerosis Essay

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Chapter 1
Introduction

History and background
Atherosclerosis:
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 …show more content…

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

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