## 1 Introduction  
Worldwide, cardiovascular diseases (CVDs) constitute the major cause of mortality and morbidity. Ischemic heart disease and stroke were the world's top fatalities for the last 15 years, according to WHO data, with a total 15.2 million fatalities in 2016 [1]. Atherosclerosis, the leading cause of cardiovascular disease, can express itself in a variety of ways, including myocardial ischemia, hemorrhagic stroke, and peripheral arterial disease [2]. It is a chronic inflammatory disorder involving multiple cells such as endothelial cells (ECs), monocytes, and VSMC (vascular smooth muscle cells), monocyte-derived macrophages, dendritic cells, and regulatory T cells (TREG). Biomedically, it is defined as the existence of \"cholesterol-enggorged\" (fat) macrophages in arterial atherosclerotic plaques [3]. Endothelial cells could be activated and in turn release adhesive molecules; ICAM-1 (Inter-Cellular Adhesion Molecule-1) and VCAM-1 (Vascular Cell Adhesion Molecule-1), under the influence of several factors namely: disturbed blood flow, greater plasma low density lipoprotein (LDL) compositions, pathogens from bacterial antigens, cigarette smoke (VCAM-1) and high blood pressure (HBP). This leads to thrombus formation in large and medium-sized arteries such as a coronary artery [4; 5; 6]. Atherosclerotic lesions tend to deposit at multiple locations within the coronary artery, and this then results in hemodynamic disturbances that restrict the flow of blood to the tissues [7] creating a situation of flow impediment. Disturbed blood flow patterns generate signatures of altered hemodynamic wall loading that essentially forces the patient to face higher health risks. Employing computational fluid dynamics (CFD) together with medical imaging techniques, such as, magnetic resonance imaging (MRI), computed tomography (CT), and echocardiography has become an efficient tool in the recent past, to investigate the hemodynamics within multiple stenosed coronary arteries [8]. Moreover, earlier studies claimed that blood flow, especially in stenosed arteries, cannot be considered a single-phase homogeneous viscous fluid [7; 9; 10] and instead employs a multiphase model. The more realistic multiphase model provides more information, such as, RBC volume fraction (VF), RBC velocity, viscosity of RBC and plasma [11]. Fewer studies incorporating a multiphase model while considering a real geometry model from an 8-year-old female patient with a moderate coarctation of aorta (CoA) [12], idealized geometric arteries [13; 14; 15] and pulsatile blood flow in coronary arteries [11; 16] have been reported. Additionally, the mechanism of atherogenic disease progression is somewhat complex, so the hemodynamic indicators arising from multiphase modelling serve as bio markers for healthcare providers [17]. Researchers have reported for ideal as well as patient-specific models that the regional wall shear stress (WSS) and oscillatory shear index (OSI) play a critical and fundamental role in the progression of atherosclerosis [14; 18; 19]. These indicators are significantly linked to the prediction or development of atherosclerosis in arteries as they tend to alter, the structure of endothelial cell layer in the surrounding tissues, and the relationship between biomechanical stresses or deformation [20; 21]. In a flexible artery, exhibiting single and double stenoses [22], showed that laminar flow occurs for a 70% stenosis while, the flow becomes turbulent for 80% occlusion. Additionally, dilation in the arterial walls in double stenoses was found to be more common than in single stenosis. This in turn, caused a suppression in the maximum mean WSS value in a double stenosis, compared to single stenosis. More details of CFD fluid-solid interaction (FSI) studies are available in the literature [19; 20; 21; 23; 24; 25; 26], respectively. Furthermore, an atherosclerotic condition develops near bifurcations as well as areas of highest curvature in the arteries, as they result in blockage of blood supply in the myocardium [23; 27].