Impact of the bicuspid aortic valve on aortic root haemodynamics: three-dimensional computed fluid dynamics simulation.

OBJECTIVES: The aim was to evaluate the impact of a bicuspid aortic valve (BAV) on local shear stress and on the pressure profile on the elements of the aortic root (AoR). METHODS: The experiment setup included a BAV with aortic valve stenosis (n = 5 pigs, 67 ± 3.5 kg) and insufficiency (n = 5 pigs, 66.7 ± 4.4 kg). By implanting 6 high-fidelity microsonometric crystals in each AoR, we determined the 3-dimensional (3D) geometry of the AoR. Experimental and geometric data were used to create a 3D time- and pressure-dependent computed fluid dynamic model of the AoR with the BAV. RESULTS: 3D AoR geometry was determined by AoR tilt (α) and rotation angle (ß). Both values were maximal at the end of diastole: 24.41 ± 1.70° (α) and 20.90 ± 2.11° (ß) for BAV with stenosis and 31.92 ± 11.51° (α) and 20.84 ± 9.80° (ß) for BAV with insufficiency and minimal at peak ejection 23.42 ± 1.65° (α), 20.38 ± 1.61° (ß) for stenosis and 26.62 ± 7.86° (α), 19.79 ± 8.45° (ß) for insufficiency. In insufficiency, low shear stress of 0-0.08 Pa and moderate pressure (60-80 mmHg) were present. In BAV with stenosis, low shear stress of 0-0.5 Pa and moderate pressure (0-20 mmHg) were present at diastole; at peak ejection high shear stress >2 Pa and elevated pressure of >80 mmHg were present. CONCLUSIONS: In a BAV with aortic valve stenosis, the haemodynamics are less favourable. The elevated pressure with elevated shear stress may over the long term promote degenerative processes in the leaflets and consequently valve function failure.

Aortic Valve Pathology as a Predictive Factor for Acute Aortic Dissection.

BACKGROUND: In this study, the effect of aortic valve (AV) pathology on local hemodynamic conditions was evaluated as a potential trigger for the onset of acute type A and B aortic dissection. METHODS: A time- and pressure-related four-dimensional (4-D) computed fluid dynamic model of the aorta was established. In an experimental setup, AV stenosis and AV insufficiency were created. 4-D pressure-related geometry of the aortic root (AR) with valve insufficiency and valve stenosis were determined by high-fidelity (200 Hz) microsonometric crystals. Flow and pressure were obtained at the left ventricle, ascending aorta, and aortic arch. RESULTS: Expansion of the AR in AV insufficiency was higher with expansion in AV stenosis, at peak ejection, and at the end of systole. In AV insufficiency, there was low shear stress (0 to 0.6 Pa), turbulent flow, and high pressure (80 to 95 mm Hg) at the anterior wall of the ascending aorta, at the proximal aortic arch, and at the aortic isthmus. In stenosis, high shear stress (>2 Pa) and high pressure (>95 mm Hg) were found at the ascending aorta and at the bifurcation of the brachiocephalic trunk. CONCLUSIONS: In AV insufficiency, low shear stresses and turbulent flow regions were documented at the traditional levels of entry tears for acute type A and B dissection. In AV stenosis, high shear stress with elevated pressure at the ascending aorta may be a trigger element for vessel dilatation, aneurysm formation, and intimal tear, which is typical for type A aortic dissection.

Numerical analysis of the 3-dimensional aortic root morphology during the cardiac cycle.

OBJECTIVES: The aim was to define the 3-dimensional (3D) geometrical changes of the aortic root and to determine the local shear stress profile of aortic root elements during the cardiac cycle. METHODS: Six sonomicrometric crystals (200 Hz) were implanted into the aortic root of five pigs at the commissures and at the aortic root base (AoB). 3D aortic root deformation including volume, torsion and tilt angle were determined. Geometrical data with measured local flow and pressure conditions was used for computed fluid dynamics modelling of the aortic root. RESULTS: Compared with end-diastole, the sinotubular junction and AoB have maximal expansion at peak ejection: 16.42 ± 6.36 and 7.60 ± 2.52%, and minimal at isovolaemic relaxation: 2.87 ± 1.62 and 1.85 ± 1.79%. Aortic root tilt and rotation angle were maximal at the end of diastole: 17.7 ± 8.8 and 21.2 ± 2.09°, and decreased to 15.24 ± 8.14 and 18.3 ± 0.1.94° at peak ejection. High shear stress >20 Pa was registered at peak ejection at coaptations, and during diastole at the superior two-thirds of the leaflets and intervalvular triangles (IVTs). The leaflet body, inferior one-third of the IVTs and valve nadir were exposed to moderate shear stress (8-16 Pa) during the cardiac cycle. CONCLUSIONS: Aortic root geometry demonstrates precise 3D changes of tilt and rotation angle. Reduction of angles during ejection results in a straight cylinder with low shear stress that facilitates the ejection; the increase during diastole results in a tilted frustum with elevated shear stress. Findings can be used for comparative analysis of native and synthetic structures with individual compliance.

Fluid dynamics simulation of right ventricular outflow tract oversizing.

OBJECTIVES: Repair of the right ventricular outflow tract (RVOT) in paediatric cardiac surgery remains challenging due to the high reoperation rate. Intimal hyperplasia and consequent arteriosclerosis is one of the most important limitation factors for graft durability. Since local shear stress and pressure are predictive elements for intimal hyperplasia and wall degeneration, we sought to determine in an oversized 12-mm RVOT model, with computed fluid dynamics simulation, the local haemodynamical factors that may explain intimal hyperplasia. This was done with the aim of identifying the optimal degree of oversizing for a 12-mm native RVOT. METHODS: Twenty domestic pigs, with a weight of 24.6 ± 0.89 kg and a native RVOT diameter of 12 ± 1.7 mm, had valve conduits of 12, 16, 18 and 20 mm implanted. Pressure and flow were measured at 75, 100 and 125% of normal flow at RVOT at the pulmonary artery, pulmonary artery bifurcation and at the left and right pulmonary arteries. Three-dimensional computed fluid dynamics (CFD) simulation in all four geometries in all flow modalities was performed. Local shear stress and pressure conditions were investigated. RESULTS: Corresponding to 75, 100 and 125% of steady-state flow, three inlet velocity profiles were obtained, 0.2, 0.29 and 0.36 m/s, respectively. At inflow velocity profiles, low shear stress areas, ranged from 0 to 2 Pa, combined with high-pressure areas ranging from 11.5 to 12.1 mmHg that were found at distal anastomosis, at bifurcation and at the ostia of the left and right pulmonary arteries in all geometries. CONCLUSIONS: In all three oversized geometries, the local reparation of shear stress and pressure in the 16-mm model showed a similar local profile as in the native 12 mm RVOT. According to these findings, we suggest oversizing the natural 12-mm RVOT by not more than 4 mm. The elements responsible for wall degeneration and intimal hyperplasia remain very similar to the conditions present in native RVOT.

Analysis of flow dynamics in right ventricular outflow tract.

BACKGROUND: The mechanism behind early graft failure after right ventricular outflow tract (RVOT) reconstruction is not fully understood. Our aim was to establish a three-dimensional computational fluid dynamics (CFD) model of RVOT to investigate the hemodynamic conditions that may trigger the development of intimal hyperplasia and arteriosclerosis. METHODS: Pressure, flow, and diameter at the RVOT, pulmonary artery (PA), bifurcation of the PA, and left and right PAs were measured in 10 normal pigs with a mean weight of 24.8 ± 0.78 kg. Data obtained from the experimental scenario were used for CFD simulation of pressure, flow, and shear stress profile from the RVOT to the left and right PAs. RESULTS: Using experimental data, a CFD model was obtained for 2.0 and 2.5-L/min pulsatile inflow profiles. In both velocity profiles, time and space averaged in the low-shear stress profile range from 0-6.0 Pa at the pulmonary trunk, its bifurcation, and at the openings of both PAs. These low-shear stress areas were accompanied to high-pressure regions 14.0-20.0 mm Hg (1866.2-2666 Pa). Flow analysis revealed a turbulent flow at the PA bifurcation and ostia of both PAs. CONCLUSIONS: Identified local low-shear stress, high pressure, and turbulent flow correspond to a well-defined trigger pattern for the development of intimal hyperplasia and arteriosclerosis. As such, this real-time three-dimensional CFD model may in the future serve as a tool for the planning of RVOT reconstruction, its analysis, and prediction of outcome.

Computational fluid dynamics of the right ventricular outflow tract and of the pulmonary artery: a bench model of flow dynamics.

OBJECTIVES: The reconstruction of the right ventricular outflow tract (RVOT) with valved conduits remains a challenge. The reoperation rate at 5 years can be as high as 25% and depends on age, type of conduit, conduit diameter and principal heart malformation. The aim of this study is to provide a bench model with computer fluid dynamics to analyse the haemodynamics of the RVOT, pulmonary artery, its bifurcation, and left and right pulmonary arteries that in the future may serve as a tool for analysis and prediction of outcome following RVOT reconstruction. METHODS: Pressure, flow and diameter at the RVOT, pulmonary artery, bifurcation of the pulmonary artery, and left and right pulmonary arteries were measured in five normal pigs with a mean weight of 24.6 ± 0.89 kg. Data obtained were used for a 3D computer fluid-dynamics simulation of flow conditions, focusing on the pressure, flow and shear stress profile of the pulmonary trunk to the level of the left and right pulmonary arteries. RESULTS: Three inlet steady flow profiles were obtained at 0.2, 0.29 and 0.36 m/s that correspond to the flow rates of 1.5, 2.0 and 2.5 l/min flow at the RVOT. The flow velocity profile was constant at the RVOT down to the bifurcation and decreased at the left and right pulmonary arteries. In all three inlet velocity profiles, low sheer stress and low-velocity areas were detected along the left wall of the pulmonary artery, at the pulmonary artery bifurcation and at the ostia of both pulmonary arteries. CONCLUSIONS: This computed fluid real-time model provides us with a realistic picture of fluid dynamics in the pulmonary tract area. Deep shear stress areas correspond to a turbulent flow profile that is a predictive factor for the development of vessel wall arteriosclerosis. We believe that this bench model may be a useful tool for further evaluation of RVOT pathology following surgical reconstructions.