## 1 Introduction  
Worldwide, cardiovascular disease is the leading cause of death, accounting for approximately 30% of all deaths, which places a heavy burden on national economies [1; 2]. Coronary atherosclerosis is one of the most common causes of cardiovascular disease. Atherosclerosis plaque in coronary arteries can block blood, leading to insufficient blood supply to the downstream tissues and organs, which can contribute to cardiovascular problems, including coronary heart disease and myocardial infarction [3; 4]. Coronary atherosclerotic plaque formation is due to the activation of the immune system when the endothelial cells are damaged and inflammatory responses occur, due to disturbances in blood flow status or some other factors. At the site of the damage, cholesterol is oxidized and, then, continuously taken up by macrophages. At the same time, the smooth muscle cells divide, and the intima begins to thicken to form intimal hyperplasia. Macrophages and intimal hyperplasia, together, form atherosclerotic plaques in coronary arteries, which then protrude into the inner lumen and eventually block the blood flow.  
Clinically, it can be alleviated by medication, when the disease is mild. However, percutaneous coronary intervention (PCI) is required, when the disease is more severe. During PCI, surgeons rely on a coronary angiography and the fractional flow reserve (FFR) for treatment decisions. FFR is the gold standard for assessing the degree of stenosis and is defined as the pressure behind (or distal to) a stenosis relative to the pressure in front of the stenosis [5,6]. When the FFR value is 0.8, it means that a specific stenosis is causing a 20% drop in blood pressure. Usually, an FFR > 0.8 means that the stenosis is not severe, while an FFR < 0.8 means that the stenosis is more severe and requires further interventional treatment [2,7]. However, there is a clinical phenomenon in which patients with the same FFR (<0.8) value or the same degree of stenosis can show significant differences in the severity of their disease. This is suspected to be related to the circumferential distribution of the plaques. A coronary hemodynamic study was performed by a fluid-structure interaction (FSI) simulation in order to reveal the influence of the circumferential distribution of coronary atherosclerotic plaques on their continued development.  
Since in vivo experiments are very difficult and costly to perform, numerical simulations, at a fraction of the cost, are an effective alternative scheme. In the past, computational fluid dynamics (CFD) was often applied to the numerical simulation of blood flow, where mechanical parameters such as fluid velocity and pressure could be easily obtained. However, the interaction between the blood and the vessel wall cannot be solved by CFD, which limits its accuracy in coronary blood flow simulation. Now, the FSI method is popular in the numerical study of the coronary blood flow, and this method can effectively deal with the interaction between the fluid domain and the solid domain [8]. It has been shown that the FSI provides more satisfactory results than CFD in the analysis of coronary hemodynamics [9,10].  
In this study, a realistic 3D coronary artery model was created using a patient's coronary CT imaging data. In order to investigate the influence of the circumferential distribution of plaques, four models with the same shape of plaques with different circumferential positions were constructed. Realistic boundary conditions from in vivo measurements were applied, taking into account the pulsating effects of the blood flow. A patient-specific 3D coronary artery FSI study was conducted considering vascular compliance. The novelty of this work is its investigation of the effect of the plaque circumferential distribution at different stages on the blood flow within the same coronary artery. The time-averaged wall shear stress (TAWSS) and the oscillatory shear index (OSI) were used to evaluate the risk of further plaque development.