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Atherosclerosis

 

Table Of Contents


<p> </p><p>

Chapter ONE

</p><p>1.0 &nbsp; &nbsp; Introduction</p><p>1.1 &nbsp; &nbsp; Atherosclerosis</p><p>1.2 &nbsp; &nbsp; Pathogenesis</p><p>1.2.1 Atherogenesis</p><p>1.2.1.1 Initiation</p><p>1.2.1.2 Progression</p><p>

Chapter TWO

</p><p>2.0 &nbsp; &nbsp; Biochemical basis</p><p>2.1 &nbsp; &nbsp; Types of &nbsp;plaque</p><p>2.1.1 Features plaques</p><p>2.1.1.1 Lipid-rich core</p><p>2.1.1.2 Cell death</p><p>2.1.1.3 Calcification</p><p>2.1.1.4 &nbsp; Neovascularization and intraplaque hemorrhage</p><p>2.1.1.5 &nbsp; Vascular remodeling and luminal stenosis</p><p>2.1.1.6 Plaque rupture</p><p>2.1.1.7 Nonfatal thrombosis</p><p>2.1.1.8 &nbsp; Fatal thrombosis</p><p>2.1.1.9 Fibrin and platelets</p><p>2.1.1.10 Contribution of bone marrow-derived cells</p><p>2.1.2 Immunohistochemistry in plaque</p><p>

Chapter THREE

</p><p>3.0 &nbsp; &nbsp; Inflammation in</p><p>3.1 &nbsp; &nbsp; Inflammation and the initiation</p><p>3.2 &nbsp; &nbsp; Inflammation causes various forms of plaque disruption</p><p>3.3 &nbsp; &nbsp; Inflammation as a therapeutic target in</p><p>3.4 &nbsp; &nbsp; Inflammatory markers as gauges risk</p><p>3.5 &nbsp; &nbsp; Itherosclerosis and cardiovascular disease</p><p>

Chapter FOUR

</p><p>4.0 &nbsp; &nbsp; Physical activity in prevention</p><p>

Chapter FIVE

</p><p>5.0 &nbsp; &nbsp; Conclusion and recommendation</p><p>5.1 &nbsp; &nbsp; Conclusion</p><p>5.2 &nbsp; &nbsp; Recommendation</p> <br><p></p>

Project Abstract

Abstract
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, immune cells, and fibrous elements in the walls of arteries. This condition is a major cause of cardiovascular disease, including heart attacks and strokes, which are leading causes of death worldwide. The development of atherosclerosis involves a complex interplay of various cellular and molecular mechanisms, including endothelial dysfunction, lipid accumulation, inflammation, smooth muscle cell proliferation, and plaque formation. Risk factors for atherosclerosis include high cholesterol, hypertension, smoking, diabetes, obesity, and a sedentary lifestyle. These factors can lead to damage and dysfunction of the endothelium, which lines the inner surface of blood vessels, and promote the accumulation of low-density lipoprotein (LDL) cholesterol in the arterial wall. This initiates an inflammatory response, attracting immune cells such as macrophages to the site of injury. The macrophages engulf the LDL particles and become foam cells, which contribute to the formation of fatty streaks in the arterial wall. Over time, the fatty streaks can progress to more advanced lesions, characterized by the formation of a fibrous cap over a lipid-rich core. These advanced lesions are prone to rupture, leading to the formation of a blood clot that can block blood flow to vital organs. This process can result in acute cardiovascular events such as heart attacks or strokes. Diagnosis of atherosclerosis typically involves a combination of imaging studies (such as ultrasound, computed tomography, or magnetic resonance imaging) and blood tests to assess cholesterol levels and other risk factors. Treatment strategies for atherosclerosis aim to reduce the risk of cardiovascular events by controlling risk factors, such as lowering cholesterol levels, managing blood pressure, quitting smoking, improving diet and exercise habits, and taking medications such as statins, antiplatelet agents, and anticoagulants. In conclusion, atherosclerosis is a complex disease process involving multiple factors that contribute to the development of arterial plaques and cardiovascular events. Understanding the pathophysiology of atherosclerosis and addressing modifiable risk factors are essential for the prevention and management of this condition. Further research is needed to develop new treatment strategies and improve outcomes for patients with atherosclerosis.

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