Transcatheter aortic valve implantation (TAVI) can treat symptomatic patients with calcific aortic stenosis. However, the severity and distribution of the calcification of valve leaflets can impair the TAVI efficacy. Here we tackle this issue from a biomechanical standpoint, by finite element simulation of a widely adopted balloon-expandable TAVI in three models representing the aortic root with different scenarios of calcific aortic stenosis. We developed a modeling approach realistically accounting for aortic root pressurization and complex anatomy, detailed calcification patterns, and for the actual stent deployment through balloon-expansion. Numerical results highlighted the dependency on the specific calcification pattern of the "dog-boning" of the stent. Also, local stent distortions were associated with leaflet calcifications, and led to localized gaps between the TAVI stent and the aortic tissues, with potential implications in terms of paravalvular leakage. High stresses were found on calcium deposits, which may be a risk factor for stroke; their magnitude and the extent of the affected regions substantially increased for the case of an "arc-shaped" calcification, running from commissure to commissure. Moreover, high stresses due to the interaction between the aortic wall and the leaflet calcifications were computed in the annular region, suggesting an increased risk for annular damage. Our analyses suggest a relation between the alteration of the stresses in the native anatomical components and prosthetic implant with the presence and distribution of relevant calcifications. This alteration is dependent on the patient-specific features of the calcific aortic stenosis and may be a relevant indicator of suboptimal TAVI results.

Numerical modeling can provide detailed and quantitative information on aortic root (AR) biomechanics, improving the understanding of AR complex pathophysiology and supporting the development of more effective clinical treatments. From this standpoint, fluid-structure interaction (FSI) models are currently the most exhaustive and potentially realistic computational tools. However, AR FSI modeling is extremely challenging and computationally expensive, due to the explicit simulation of coupled AR fluid dynamics and structural response, while accounting for complex morphological and mechanical features. We developed a novel FSI model of the physiological AR simulating its function throughout the entire cardiac cycle. The model includes an asymmetric MRI-based geometry, the description of aortic valve (AV) non-linear and anisotropic mechanical properties, and time-dependent blood pressures. By comparison to an equivalent finite element structural model, we quantified the balance between the extra information and the extra computational cost associated with the FSI approach. Tissue strains and stresses computed through the two approaches did not differ significantly. The FSI approach better captured the fast AV opening and closure, and its interplay with blood fluid dynamics within the Valsalva sinuses. It also reproduced the main features of in vivo AR fluid dynamics. However, the FSI simulation was ten times more computationally demanding than its structural counterpart. Hence, the FSI approach may be worth the extra computational cost when the tackled scenarios are strongly dependent on AV transient dynamics, Valsalva sinuses fluid dynamics in relation to coronary perfusion (e.g. sparing techniques), or AR fluid dynamic alterations (e.g. bicuspid AV).

Bicuspid aortic valve (BAV) is the most common congenital cardiac disease and is a foremost risk factor for aortopathies. Despite the genetic basis of BAV and of the associated aortopathies, BAV-related alterations in aortic fluid-dynamics, and particularly in wall shear stresses (WSSs), likely play a role in the progression of aortopathy, and may contribute to its pathogenesis. To test whether WSS may trigger aortopathy, in this study we used 4D Flow sequences of phase-contrast cardiac magnetic resonance imaging (CMR) to quantitatively compare the in vivo fluid dynamics in the thoracic aorta of two groups of subjects: i) five prospectively enrolled young patients with normo-functional BAV and with no aortic dilation and ii) ten age-matched healthy volunteers. Through the semi-automated processing of 4D Flow data, the aortic bulk flow at peak systole was quantified, and WSSs acting on the endothelium of the ascending aorta were characterized throughout the systolic phase in terms of magnitude and time-dependency through a method recently developed by our group. Variables computed for each BAV patient were compared vs. the corresponding distribution of values obtained for healthy controls. In BAV patients, ascending aorta diameter was measured on cine-CMR images at baseline and at three-year follow-up. As compared to controls, normo-functional BAV patients were characterized by minor bulk flow disturbances at peak systole. However, they were characterized by evident alterations of WSS distribution and peak values in the ascending aorta. In particular, in four BAV patients, who were characterized by right-left leaflet fusion, WSS peak values exceeded by 27-46% the 90th percentile of the distribution obtained for healthy volunteers. Only in the BAV patient with right-non-coronary leaflet fusion the same threshold was exceeded by 132%. Also, evident alterations in the time-dependency of WSS magnitude and direction were observed. Despite these fluid-dynamic alterations, no clinically relevant anatomical remodeling was observed in the BAV patients at three-year follow-up. In light of previous evidence from the literature, our results suggest that WSS alterations may precede the onset of aortopathy and may contribute to its triggering, but WSS-driven anatomical remodeling, if any, is a very slow process.