## 1 Introduction  
Atherosclerosis stands as a formidable adversary in cardiovascular medicine, characterized by the insidious accumulation of plaques within the arterial walls. This complex process, which heralds the onset of numerous cardiovascular diseases, often initiates with the formation of fatty streaks (FS) in the aorta. These early lesions, predominantly manifesting in the aortic arch and abdominal aorta, mark a critical juncture in the cascade of events that may escalate to more advanced stages of atherosclerosis, including the development of fibrous plaques and culminating in cardiovascular disease. The progression from benign fatty streaks to obstructive atherosclerotic plaques involves a multifaceted interplay of inflammatory cells and extracellular lipid accumulation, laying the groundwork for significant arterial blockage and compromised cardiovascular health [1]. Historically, the exploration of FS and their contribution to atherosclerosis has been approached through a molecular and biochemical lens, focusing on the cellular activities and chemical mediators within the FS regions. This perspective has underscored the role of damage-associated molecular patterns (DAMPs), which are released following cellular distress or death, and cytokines, which are pivotal in activating the endothelial lining of the arteries [2]. Furthermore, the activated cells within the evolving plaque secrete matrix proteases, enzymes capable of degrading the extracellular matrix and facilitating the penetration and accumulation of inflammatory cells and lipids [3]. This biochemical narrative, while foundational, provides only a partial view of the complex mechanisms at play in atherosclerosis development. The mechanical forces acting upon the arterial walls, particularly endothelial shear stress (ESS), have emerged as critical factors influencing the initiation and progression of atherosclerosis. ESS, the frictional force exerted by blood flow on the endothelial layer, varies significantly across different vascular regions, influenced by factors such as blood velocity, vessel geometry, and the presence of vascular lesions like FS. Understanding how FS alters the distribution of ESS and, by extension, affects endothelial function and plaque progression requires sophisticated analytical tools capable of simulating these complex biomechanical interactions. In response to this challenge, the present study leverages a hybrid approach that combines the precision of computational fluid dynamics (CFD) simulations with the versatility of numerical analysis. CFD simulations have revolutionized our ability to visualize and quantify the fluid dynamics within cardiovascular systems, offering a window into the intricate patterns of blood flow and shear forces that traditional experimental models cannot provide. This computational method allows for a detailed examination of how variations in blood flow dynamics, induced by the presence of FS, impact ESS distribution and contribute to the pathological landscape of atherosclerosis. By integrating CFD with numerical analysis performed through MATLAB, this study aims to bridge the gap between mechanical forces and biochemical processes in atherosclerotic progression, offering novel insights into the mechanical underpinnings of plaque development. This approach is not without precedence; numerous studies have underscored the utility of CFD in elucidating the relationship between blood flow dynamics and vascular pathology. For instance, research utilizing ANSYS CFX for CFD simulations has illuminated the significant correlation between simulated arterial characteristics and actual measurements of arterial lumen area, wall area, and plaque burden, reinforcing the hypothesis that regions subjected to low ESS are hotspots for plaque accumulation and growth. In contrast, innovative mathematical and agent-based modeling techniques have offered alternative perspectives on cardiovascular dynamics, enriching our understanding of the systemic nature of atherosclerosis [4; 5; 6].