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Transcatheter mitral valve replacement (TMVR) has been used for “off-label” treatment when annuloplasty band ring for mitral repair fails. However, the complex anatomy and function of the mitral valve may lead to fatal complications as a result of the left ventricular outflow tract (LVOT) obstruction in TMVR. We report the structural and hemodynamic response of LVOT obstruction resulting from TMVR with the Edwards SAPIEN 3 Ultra (S3) device. We modified the original Living Heart Human Model (LHHM) to account for a failed mitral valve with an annuloplasty band ring and simulated the cardiac beating condition in the setting of S3 device implantation. Findings demonstrated a high dynamic behavior of the newly formed LVOT (neoLVOT) as confined by the displaced mitral valve and the interventricular septum. During the cardiac beat, the neoLVOT area oscillated from a maximum of 472.1 mm2 at early systole to the minimum of 183 mm2 at end-systole. The profile of both anchoring force and contact pressure revealed that the band ring serves as the anchoring zone while mitral valve is primally displaced by the deployed device. At early systole, computational flow dynamics highlighted hemodynamic disturbances associated with the LVOT obstruction, with a skewed flow towards the septum and a pressured drop of 4.5 mmHg between the left ventricular apex and the neoLVOT region. This study can lead to a more accurate assessment of the risk induced by the LVOT obstruction when stratifying patient anatomic suitability for TMVR.

Quantifying local aortic stiffness properties in vivo is acknowledged as essential to assess the severity of an ascending thoracic aortic aneurysm (ATAA). Recently, the LESI (local extensional stiffness identification) methodology has been established to quantify non-invasively local stiffness properties of ATAAs using electrocardiographic-gated computed tomography (ECG-gated CT) scans. The aim of the current study was to determine the most sensitive markers of local ATAA stiffness estimation with the hypothesis that direct measures of local ATAA stiffness could better detect the high-risk patients. A cohort of 30 patients (12 BAV and 18 TAV) referred for aortic size evaluation by ECG-gated CT were recruited. For each patient, the extensional stiffness Q was evaluated by the LESI methodology whilst computational flow analyses were also performed to derive hemodynamics markers such as the wall shear stress (WSS). A strong positive correlation was found between the extensional stiffness and the aortic pulse pressure (R = 0.644 and p < 0.001). Interestingly, a significant positive correlation was also found between the extensional stiffness and patients age for BAV ATAAs (R = 0.619 and p = 0.032), but not for TAV ATAAs (R = −0.117 and p = 0.645). No significant correlation was found between the extensional stiffness and WSS evaluated locally. There was no significant difference either in the extensional stiffness between BAV ATAAs and TAV ATAAs (Q = 3.6 ± 2.5 MPa.mm for BAV ATAAs vs Q = 5.3 ± 3.1 MPa.mm for TAV ATAAs, p = 0.094). Future work will focus on relating the extensional stiffness to the patient-specific rupture risk of ATAAs on larger cohorts to confirm the promising interest of the LESI methodology.

Hemodynamic alterations occur when the elephant trunk (ET) technique is adopted to treat extensive aortic aneurysms. In planning the 2nd stage operation to complete ET repair, surgeons must weigh an adequate recovery time after initial surgery against the risk of postoperative ET-related complications. The purpose of this study was to understand the mechanistic link between the flow alteration caused by the ET graft and the development of premature aortic rupture before the 2nd stage operation. Specifically, fluid-structure interaction (FSI) analysis was performed using the CT imaging data of aorta at different stages of ET repair, and then computational variables were compared to those observed in patients who underwent a prophylactic 2nd stage operation to complete aortic repair. Results show that intramural stress exerted near the distal ET anastomosis (IMS=37.5 kPa) at the time of urgent intervention was comparable to that of the extensive aortic aneurysm (IMS=47.4 kPa) at initial in-hospital admission, but was considerably higher than that occurring after the 1st stage procedure (IMS=3.5 kPa). Pressure index suggested higher peri-graft pressurization than aortic lumen pressure during diastole, imparting an apparent risk of aortic dilatation. These critical hemodynamic and structural parameters are related to the impending rupture of descending aorta observed clinically and can thus guide prophylactic intervention and optimal timing for the 2nd stage operation of a ET technique.

The aortic dissection (AoD) of an ascending thoracic aortic aneurysm (ATAA) initiates when the hemodynamic loads exerted on the aneurysmal wall overcome the adhesive forces holding the elastic layers together. Parallel coupled, two-way fluid–structure interaction (FSI) analyses were performed on patient-specific ATAAs obtained from patients with either bicuspid aortic valve (BAV) or tricuspid aortic valve (TAV) to evaluate hemodynamic predictors and wall stresses imparting aneurysm enlargement and AoD. Results showed a left-handed circumferential flow with slower-moving helical pattern in the aneurysm's center for BAV ATAAs whereas a slight deviation of the blood flow toward the anterolateral region of the ascending aorta was observed for TAV ATAAs. Blood pressure and wall shear stress were found key hemodynamic predictors of aneurysm dilatation, and their dissimilarities are likely associated to the morphological anatomy of the aortic valve. We also observed discontinues, wall stresses on aneurysmal aorta, which was modeled as a composite with two elastic layers (i.e., inhomogeneity of vessel structural organization). This stress distribution was caused by differences on elastic material properties of aortic layers. Wall stress distribution suggests AoD just above sinotubular junction. Moreover, abnormal flow and lower elastic material properties that are likely intrinsic in BAV individuals render the aneurysm susceptible to the initiation of AoD.