Abstract: Hyperplasia of atherosclerotic plaque can induce local hemodynamic abnormalities due to the resultant geometry of the blood vessels changed. This process can lead to serious complications such as stroke, ischemic eye disease, and acute renal failure, among others. The current lack of a deep understanding of early plaque dynamic evolution and its associated mechanisms involved in the inflammatory response and lipid metabolism pathways is still one of the major limitations of existing studies. Therefore, the establishment of a more detailed growth dynamics model is of great significance to enrich our research tools and capabilities. A set of novel fluid-structure coupling multi-physical field model integrating the early plaque growth dynamics was proposed in this work, which can simultaneously reflect the atherosclerotic plaque growth under the synergistic effect of lipoprotein concentration diffusion and plaque volume expansion, as well as the interactive coupling effect of subintimal deformation and hemodynamic response. In particular, the nonlinear mechanical properties of the atherosclerotic plaque were characterized using the neo-Hookean constitutive model. Additionally, the growth of the plaque was characterized by decomposing the total deformation gradient of the vessel wall into elastic and growth parts. Simultaneously, the dynamic coupling behavior between the blood flow and the intima through the displacement-stress boundary transfer mechanism was solved using the bidirectional iterative coupling algorithm. The numerical results showed that the early plaque growth morphology predicted by the model was highly consistent with the clinical experience curve. By defining the influence factor A (expansion/diffusion rate ratio), the regulation of lipoprotein diffusion-driven expansion deformation on plaque size was quantitatively revealed. Furthermore, it was confirmed by the numerical simulation results that the distribution of shear stress in the blood flow was altered by the plaque growth process through geometric deformation, thereby increasing the risk of thrombosis, and the critical plaque height for platelet activation was determined.