Peak wall stress predicts expansion rate in descending thoracic aortic aneurysms.

BACKGROUND: Aortic diseases, including aortic aneurysms, are the 12th leading cause of death in the United States. The incidence of descending thoracic aortic aneurysms is estimated at 10.4 per 100,000 patient-years. Growing evidence suggests that stress measurements derived from structural analysis of aortic geometries predict clinical outcomes better than diameter alone. METHODS: Twenty-five patients undergoing clinical and radiologic surveillance for thoracic aortic aneurysms were retrospectively identified. Custom MATLAB algorithms were employed to extract aortic wall and intraluminal thrombus geometry from computed tomography angiography scans. The resulting reconstructions were loaded with 120 mm Hg of pressure using finite element analysis. Relationships among peak wall stress, aneurysm growth, and clinical outcome were examined. RESULTS: The average patient age was 71.6 ± 10.0 years, and average follow-up time was 17.5 ± 9 months (range, 6 to 43). The mean initial aneurysm diameter was 47.8 ± 8.0 mm, and the final diameter was 52.1 ± 10.0 mm. Mean aneurysm growth rate was 2.9 ± 2.4 mm per year. A stronger correlation (r = 0.894) was found between peak wall stress and aneurysm growth rate than between maximal aortic diameter and growth rate (r = 0.531). Aneurysms undergoing surgical intervention had higher peak wall stresses than aneurysms undergoing continued surveillance (300 ± 75 kPa versus 229 ± 47 kPa, p = 0.01). CONCLUSIONS: Computational peak wall stress in thoracic aortic aneurysms was found to be strongly correlated with aneurysm expansion rate. Aneurysms requiring surgical intervention had significantly higher peak wall stresses. Peak wall stress may better predict clinical outcome than maximal aneurysmal diameter, and therefore may guide clinical decision-making.

Increased wall stress of saccular versus fusiform aneurysms of the descending thoracic aorta.

BACKGROUND: Repair of fusiform descending thoracic aortic aneurysms (DTAs) is indicated when aneurysmal diameter exceeds a certain threshold; however, diameter-related indications for repair of saccular DTA are less well established. METHODS: Human subjects with fusiform (n = 17) and saccular (n = 17) DTAs who underwent computed tomographic angiography were identified. Patients with aneurysms related to connective tissue disease were excluded. The thoracic aorta was segmented, reconstructed, and triangulated to create a mesh. Finite element analysis was performed using a pressure load of 120 mm Hg and a uniform aortic wall thickness of 3.2 mm to compare the pressure-induced wall stress of fusiform and saccular DTAs. RESULTS: The mean maximum diameter of the fusiform DTAs (6.0 ± 1.5 cm) was significantly greater (p = 0.006) than that of the saccular DTAs (4.4 ± 1.8 cm). However, mean peak wall stress of the fusiform DTAs (0.33 ± 0.15 MPa) was equivalent to that of the saccular DTAs (0.30 ± 0.14 MPa), as found by using an equivalence threshold of 0.15 MPa. The mean normalized wall stress (peak wall stress divided by maximum aneurysm radius) of the saccular DTAs was greater than that of the fusiform DTAs (0.16 ± 0.09 MPa/cm vs. 0.11 ± 0.03 MPa/cm, p = 0.035). CONCLUSIONS: The normalized wall stress for saccular DTA is greater than that for fusiform DTA, indicating that geometric factors such as aneurysm shape influence wall stress. These results suggest that saccular aneurysms may be more prone to rupture than fusiform aneurysms of similar diameter, provide a theoretical rationale for the repair of saccular DTAs at a smaller diameter, and suggest investigation of the role of biomechanical modeling in surgical decision making is warranted.

Increased ascending aortic wall stress in patients with bicuspid aortic valves.

BACKGROUND: Patients with bicuspid aortic valves (BAV) are at increased risk of ascending aortic dilatation, dissection, and rupture. We hypothesized that ascending aortic wall stress may be increased in patients with BAV compared with patients with tricuspid aortic valves (TAV). METHODS: Twenty patients with BAV and 20 patients with TAV underwent electrocardiogram-gated computed tomographic angiography. Patients were matched for diameter. The thoracic aorta was segmented, reconstructed, and triangulated to create a mesh. Utilizing a uniform pressure load of 120 mm Hg, and isotropic, incompressible, and linear elastic shell elements, finite element analysis was performed to predict 99th percentile wall stress. RESULTS: For patients with BAV and TAV, aortic root diameter was 4.0 ± 0.6 cm and 4.0 ± 0.6 cm (p = 0.724), sinotubular junction diameter was 3.6 ± 0.8 cm and 3.6 ± 0.7 cm (p = 0.736), and maximum ascending aortic diameter was 4.0 ± 0.8 cm and 4.1 ± 0.9 cm (p = 0.849), respectively. The mean 99 th percentile wall stress in the BAV group was greater than in the TAV group (0.54 ± 0.06 MPa vs 0.50 ± 0.09 MPa), though this did not reach statistical significance (p = 0.090). When normalized by radius, the 99 th percentile wall stress was greater in the BAV group (0.31 ± 0.06 MPa/cm vs 0.27 ± 0.03 MPa/cm, p = 0.013). CONCLUSIONS: Patients with BAV, regardless of aortic diameter, have increased 99 th percentile wall stress in the ascending aorta. Ascending aortic three-dimensional geometry may account in part for the increased propensity to aortic dilatation, rupture, and dissection in patients with BAV.

Pathogenesis of acute aortic dissection: a finite element stress analysis.

BACKGROUND: Type A and type B aortic dissections typically result from intimal tears above the sinotubular junction and distal to the left subclavian artery (LSA) ostium, respectively. We hypothesized that this pathology results from elevated pressure-induced regional wall stress. METHODS: We identified 47 individuals with normal thoracic aortas by electrocardiogram-gated computed tomography angiography. The thoracic aorta was segmented, reconstructed, and triangulated to create a geometric mesh. Finite element analysis using a systolic pressure load of 120 mm Hg was performed to predict regional thoracic aortic wall stress. RESULTS: There were local maxima of wall stress above the sinotubular junction in the ascending aorta and distal to the ostia of the supraaortic vessels, including the LSA, in the aortic arch. No local maximum of wall stress was found in the descending thoracic aorta. Comparison of the mean peak wall stress above the sinotubular junction (0.43 ± 0.07 MPa), distal to the LSA (0.21 ± 0.07 MPa), and in the descending thoracic aorta (0.06 ± 0.01 MPa) showed a significant effect for wall stress by aortic region (p < 0.001). CONCLUSIONS: In the normal thoracic aorta, there are peaks in wall stress above the sinotubular junction and distal to the LSA ostium. This stress distribution may contribute to the pathogenesis of aortic dissections, given their colocalization. Future investigations to determine the utility of image-derived biomechanical calculations in predicting aortic dissection are warranted, and therapies designed to reduce the pressure load-induced wall stress in the thoracic aorta are rational.

Impact of design parameters on bileaflet mechanical heart valve flow dynamics.

BACKGROUND AND AIM OF THE STUDY: One significant problem encountered during surgery to implant mechanical heart valve prostheses is the propensity for thrombus formation near the valve leaflet and housing. This may be caused by the high shear stresses present in the leakage jet flows through small gaps between leaflets and the valve housing during the valve closure phase. METHODS: A two-dimensional (2D) study was undertaken to demonstrate that design changes in bileaflet mechanical valves result in notable changes in the flow-induced stresses and prediction of platelet activation. A Cartesian grid technique was used for the 2D simulation of blood flow through two models of bileaflet mechanical valves, and their flow patterns, closure characteristics and platelet activation potential were compared. A local mesh refinement algorithm allowed efficient and fast flow computations with mesh adaptation based on the gradients of the flow field in the gap between the leaflet and housing at the instant of valve closure. Leaflet motion was calculated dynamically, based on the fluid forces acting on it. Platelets were modeled and tracked as point particles by a Lagrangian particle tracking method which incorporated the hemodynamic forces on the particles. RESULTS: A comparison of results showed that the velocity, wall shear stress and simulated platelet activation parameter were lower in the valve model, with a smaller angle of leaflet traverse between the fully open to the fully closed position. The parameters were also affected to a lesser extent by local changes in the leaflet and housing geometry. CONCLUSION: Computational simulations can be used to examine local design changes to help minimize the fluid-induced stresses that may play a key role in thrombus initiation with the implanted mechanical valves.