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ATHEROSCLEROSIS

CHAPTER ONE

INTRODUCTION

1.1 Background of the Study

Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, inflammatory cells, and fibrous elements in the arterial walls, leading to the formation of plaques that can obstruct blood flow (Libby et al., 2019). This condition is a significant precursor to various cardiovascular diseases, including coronary artery disease, stroke, and peripheral artery disease, which collectively contribute to high morbidity and mortality rates worldwide (Bachmann et al., 2021). The pathogenesis of atherosclerosis is complex and multifactorial, involving a combination of genetic, environmental, and lifestyle factors that can disrupt normal endothelial function and promote inflammatory processes (Matsuzawa et al., 2019).

The initial stage of atherosclerosis involves endothelial injury, which may be caused by factors such as hypertension, hyperlipidemia, diabetes, and smoking (Böhm et al., 2020). This injury leads to the activation of endothelial cells, which become more permeable to lipoproteins, particularly low-density lipoprotein (LDL) cholesterol. The retention of LDL within the arterial intima triggers an inflammatory response, attracting monocytes that differentiate into macrophages and engulf oxidized LDL, forming foam cells (Friedman et al., 2022). These foam cells accumulate and contribute to the development of fatty streaks, the earliest visible lesions of atherosclerosis (Hansson et al., 2018).

As the disease progresses, the plaques evolve through a series of stages characterized by changes in composition and stability. Early plaques are primarily lipid-rich and may be relatively stable, but as inflammation persists, they become fibrotic, with smooth muscle cell proliferation and collagen deposition (Gisterå & Hansson, 2017). The balance between pro-inflammatory and anti-inflammatory processes is crucial in determining plaque stability. Unstable plaques are prone to rupture, leading to thrombosis and acute cardiovascular events, highlighting the importance of understanding the mechanisms that drive atherosclerosis progression (Sokolis et al., 2020).

Lifestyle factors play a significant role in the development of atherosclerosis. Diets high in saturated fats, trans fats, and cholesterol can exacerbate lipid accumulation and promote inflammation (Cheng et al., 2021). Conversely, diets rich in fruits, vegetables, whole grains, and healthy fats have been associated with a reduced risk of atherosclerosis (Esposito et al., 2020). Physical inactivity is another critical risk factor, as regular exercise has been shown to improve endothelial function, reduce inflammation, and promote healthy lipid profiles (Mora et al., 2020).

Diabetes mellitus is a significant risk factor for atherosclerosis, as it contributes to endothelial dysfunction, increases oxidative stress, and promotes inflammatory pathways (Khan et al., 2021). Individuals with diabetes often have elevated levels of advanced glycation end products (AGEs), which can further damage endothelial cells and enhance plaque formation (Liu et al., 2022). Moreover, hypertension accelerates the process of atherosclerosis by inducing mechanical stress on the arterial walls, leading to endothelial injury and remodeling (Safar et al., 2021).

Genetic predisposition also plays a critical role in atherosclerosis susceptibility. Familial hypercholesterolemia, a genetic disorder characterized by high cholesterol levels, significantly increases the risk of early-onset atherosclerosis (Khera et al., 2018). Genetic variations affecting lipid metabolism, inflammation, and vascular function can contribute to individual differences in atherosclerosis risk (Zhang et al., 2021).

Recent advances in imaging techniques, such as computed tomography (CT) and magnetic resonance imaging (MRI), have enhanced the ability to detect early atherosclerotic changes and assess plaque characteristics (Stojanovic et al., 2020). These technologies allow for the identification of

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