Home / Human Nutrition and Dietetics / Atherosclerosis

Atherosclerosis

 

Table Of Contents


Chapter ONE

1.0     Introduction

1.1     Atherosclerosis

1.2     Pathogenesis

1.2.1 Atherogenesis

1.2.1.1 Initiation

1.2.1.2 Progression

Chapter TWO

2.0     Biochemical basis

2.1     Types of  plaque

2.1.1 Features plaques

2.1.1.1 Lipid-rich core

2.1.1.2 Cell death

2.1.1.3 Calcification

2.1.1.4   Neovascularization and intraplaque hemorrhage

2.1.1.5   Vascular remodeling and luminal stenosis

2.1.1.6 Plaque rupture

2.1.1.7 Nonfatal thrombosis

2.1.1.8   Fatal thrombosis

2.1.1.9 Fibrin and platelets

2.1.1.10 Contribution of bone marrow-derived cells

2.1.2 Immunohistochemistry in plaque

Chapter THREE

3.0     Inflammation in

3.1     Inflammation and the initiation

3.2     Inflammation causes various forms of plaque disruption

3.3     Inflammation as a therapeutic target in

3.4     Inflammatory markers as gauges risk

3.5     Itherosclerosis and cardiovascular disease

Chapter FOUR

4.0     Physical activity in prevention

Chapter FIVE

5.0     Conclusion and recommendation

5.1     Conclusion

5.2     Recommendation


Thesis Abstract

Abstract
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, inflammatory cells, and fibrous elements in the arterial walls. This condition leads to the formation of plaques that can obstruct blood flow and increase the risk of cardiovascular events such as heart attacks and strokes. The pathogenesis of atherosclerosis involves a complex interplay of various factors, including endothelial dysfunction, lipid deposition, inflammation, and smooth muscle cell proliferation. Risk factors for atherosclerosis include hypertension, hyperlipidemia, diabetes, smoking, and a sedentary lifestyle. Current research focuses on understanding the molecular mechanisms underlying the development and progression of atherosclerosis. Endothelial dysfunction, characterized by impaired nitric oxide production and increased expression of adhesion molecules, plays a crucial role in the initiation of atherosclerotic lesions. Dyslipidemia, particularly elevated levels of low-density lipoprotein cholesterol, promotes the accumulation of cholesterol in the arterial walls, leading to the formation of foam cells and fatty streaks. Inflammation is a key driver of atherosclerosis, with immune cells such as macrophages and T lymphocytes infiltrating the arterial walls and contributing to plaque formation and destabilization. Advanced imaging techniques, such as intravascular ultrasound and optical coherence tomography, allow for the visualization and characterization of atherosclerotic plaques in vivo, aiding in risk stratification and treatment decision-making. Pharmacological interventions targeting lipid lowering, blood pressure control, and antiplatelet therapy have been shown to reduce the risk of cardiovascular events in patients with atherosclerosis. Additionally, lifestyle modifications, including a healthy diet, regular exercise, smoking cessation, and weight management, play a crucial role in the prevention and management of atherosclerosis. Novel therapeutic approaches are being explored to target specific pathways involved in atherosclerosis, such as the use of monoclonal antibodies against pro-inflammatory cytokines or inhibitors of cholesterol absorption. Gene therapy and nanotechnology-based drug delivery systems hold promise for the future treatment of atherosclerosis. Overall, a multidisciplinary approach combining basic science research, clinical trials, and preventive strategies is essential for addressing the burden of atherosclerotic cardiovascular disease and improving patient outcomes.

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