The aortic valve is located between the left ventricle and the aorta and ensures unidirectional blood flow between the left ventricle and the aorta by opening during systole (ventricle contraction) and closing during diastole (ventricle relaxation). The normal valve, known as the tricuspid aortic valve (TAV) consists of three leaflets. The bicuspid aortic valve (BAV) is the most common congenital valvular defect, in which two of the three leaflets fuse during the development. The most prevalent type-I morphology features two cusps of unequal size (resulting from the fusion of two of the three leaflets) and a fibrous raphe at the location of congenital fusion. While 71% of type-I BAVs result from the fusion between the right- and left-coronary leaflets (LR subtype), 15% feature right- and non-coronary cusp fusion (RN subtype) and 3% present with non- and left-coronary cusp fusion (NL subtype). While the BAV morphology may not intrinsically hamper valvular function, it is associated with a spectrum of secondary valvulopathy and aortopathy such as calcific aortic valve disease (CAVD) and aortic dilation. In addition, the particular leaflet fusion type affects the expression of dilation and thinning of the ascending aorta (AA) downstream of a BAV. While the LR cusp fusion is primarily associated with dilation of the aortic root and the AA convexity, dilation patterns downstream of RN-BAVs localize to the tubular AA and sometimes extend to the transverse aortic arch. While these BAV complications have been historically linked to the same genetic defect responsible for the BAV morphogenesis, recent in vivo, in vitro and computational studies have revealed the existence of abnormal hemodynamics in the BAV, which may contribute to the early and rapid development of CAVD and aortic dilation in BAV patients. However, the native fluid wall shear stress (WSS) environment in the BAV and BAV AA remain largely unknown, which hinders the assessment of this hemodynamic theory. Therefore, the objective of this dissertation was to computationally quantify the native mechanical environment on BAV leaflets and BAV aortas using fluid-structure interaction (FSI) modeling.In specific aim 1, arbitrary Lagrangian Eulerian (ALE) FSI models were designed to simulate the flow and leaflet dynamics in idealized TAV, type-0 and type-I BAV geometries subjected to physiologic transvalvular pressure. The regional leaflet mechanics was quantified in terms of temporal shear magnitude (TSM), oscillatory shear index (OSI), temporal shear gradient (TSG) and stretch. The simulations identified regions of WSS overloads and increased WSS oscillations in BAV leaflets relative to TAV leaflets. BAV leaflets also experienced larger radial deformations than TAV leaflets. Type-I BAV leaflets exhibited contrasted WSS environments marked by WSS overloads on the non-coronary leaflet and sub-physiologic WSS levels on the fused leaflet. This study demonstrated the existence of abnormal WSS on BAV leaflets, which may further our understanding of the role played by hemodynamic forces in BAV disease. In specific aim 2, an FSI model of the TAV with coronary arteries was developed to quantify the effect of coronary flow on leaflet WSS and assess the assumption of neglecting coronary arteries in specific aim 1. The study demonstrated that coronary flow increased WSS magnitude and decreased WSS oscillations on the tip and belly regions of the leaflet while the presence of coronary arteries had limited effect on the base of the leaflet fibrosa (i.e. region most prone to calcification). This study provided important insight into the effect of coronary flow on leaflet WSS and justified the assumption of neglecting coronary arteries in specific aim1 to predict WSS on leaflet regions most prone to calcification.In specific aim 3, 3D FSI models of unified valve-aorta geometries were designed to quantify hemodynamics and regional WSS in a non-dilated AA subjected to TAV and three type-I BAV morphotypes (LR, RN and NL) flows. This study revealed that BAVs generated eccentric and helical flow in the AA while flow was essentially axisymmetric in the TAV AA. BAVs also generated morphotype-dependent WSS abnormalities in terms of magnitude and directionality on the ascending aortic wall. The LR-BAV and NL-BAV generated WSS overloads on the proximal AA while the proximal segment of the RN-BAV AA was subjected to similar WSS to the TAV AA. In addition, all BAV models generated abnormal unidirectional WSS on the proximal segments as compared to the TAV. While the middle AAs of the TAV and the LR-BAV were subjected to bidirectional WSS, WSS on the RN-BAV and the NL-BAV AAs remained unidirectional on the middle segments. The results reported in this study indicated the existence of strong hemodynamic abnormalities in type-I BAV AAs, their dependence on BAV morphotype and their colocalization with sites vulnerable to dilation.In conclusion, this dissertation aimed at characterizing the key mechanical differences between TAV and BAV leaflets and aortas. The models demonstrated the existence of abnormal mechanical environment in BAVs and downstream AAs relative to the TAV. The results provided important insights into the mechanical characteristics of BAV leaflets and AAs, which may further our understanding of the role played by hemodynamic forces in BAV disease.