The research group, led by Xiaolong Du of the Affiliated Hospital of Nanjing University of Chinese Medicine and Kai Ren of Nanjing Forestry University, retrospectively analyzed eight patients treated with fenestrated PMEGs at Nanjing Drum Tower Hospital. Six carried primary abdominal aortic aneurysms, while two had previously undergone thoracic endovascular repair with untreated distal segments. From preoperative and postoperative computed tomography angiography scans, the team reconstructed paired three-dimensional models of each patient’s aortic lumen before and after the procedure, then ran pulsatile computational fluid dynamics simulations under deliberately matched inlet and outlet conditions. The matched loading was the methodological heart of the study: by applying an identical time-varying inlet waveform with a 0.952 second cardiac period and identical three-element Windkessel outlet parameters within each paired comparison, the investigators isolated the hemodynamic consequences of the PMEG-induced geometric remodeling itself, rather than confounding them with patient-specific physiological variability.

The modeling pipeline was technically demanding. CTA data with a 512 by 512 matrix and 1 millimeter slice thickness were segmented in Mimics, with contours corrected by roughly one pixel, or 0.4 millimeters, where adjacent structures obscured the aortic boundary. Surface defects were repaired and smoothed in Geomagic Wrap, and inlets and outlets were extended to reduce backflow-related numerical instability. Mesh sensitivity testing on a representative case showed that area-averaged aneurysm TAWSS changed by only 1.6 percent between a 3.54 million element mesh and a 5.46 million element fine mesh, supporting the use of comparable mid-range configurations, between 3.35 and 5.46 million elements, for the remaining models. Five prism layers were retained at the wall to resolve the steep near-wall velocity gradients that dominate shear stress calculations. Blood was treated as an incompressible Newtonian fluid with a density of 1,060 kilograms per cubic meter and a dynamic viscosity of 3.5 times ten to the minus three Pascal-seconds, with laminar flow assumed throughout. Transient simulations ran in ANSYS Fluent for roughly ten cycles to reach cycle-to-cycle convergence, and the subsequent ten cycles were used to compute time-averaged indices.

The results tell a coherent physical story. Before PMEG, the expanded aneurysm lumen produced slow flow, separation, and recirculating vortices, particularly near the aneurysm neck, exactly as continuity and momentum balance predict for sudden expansion and tight curvature. After repair, flow was directed through a smaller and generally smoother conduit, so an increase in velocity under the fixed inlet waveform was expected from first principles. Across the cohort, mean velocity rose from approximately 0.8 meters per second before PMEG to 1.5 meters per second after, a statistically significant increase with a P value of 0.0021. The spread was wide: Case 4 showed the largest velocity jump at 0.993 meters per second, while Case 8 changed by only 0.017 meters per second because its preoperative flow was already fast and its geometric alteration modest. These outliers demonstrate that the cohort-average direction cannot be assumed to represent every reconstructed anatomy, a caution the authors emphasize throughout.

Pressure loss told a similar story with an important reversal. The pressure drop between the aortic root and the aneurysm analysis region decreased significantly across the cohort, with a P value of 0.0183, consistent with reduced geometry-related viscous energy loss in the smoother postoperative conduit. The largest reduction occurred in Case 4, whereas Case 6 changed little and Case 8 showed a small increase. The authors flag the Case 8 result as clinically relevant: despite technically successful aneurysm exclusion, the reconstructed path did not reduce pressure loss under standardized loading. Such model-derived flags, they suggest, could motivate closer imaging review or comparison of alternative virtual configurations, although this proposed use requires prospective validation before it can inform surveillance decisions.

The study’s most biologically resonant findings concern the wall itself. Wall shear stress is the tangential traction blood exerts on the endothelium; persistently low shear indicates poor near-wall washout and has been linked to atherogenic endothelial signaling, while very high shear may reflect localized jets or impingement. The team quantified time-averaged wall shear stress, or TAWSS, which summarizes cumulative shear exposure over one cardiac cycle, along with the relative residence time, or RRT, which combines shear magnitude and directional oscillation to estimate how persistently blood-borne particles linger near the wall, and the endothelial cell activation potential, or ECAP, the ratio of oscillatory shear index to TAWSS proposed by Di Achille and colleagues as a spatial marker of a pro-thrombotic endothelial environment. Before PMEG, extensive low-shear regions occupied the aneurysm sac and inner curvatures, and high RRT and ECAP values dominated much of the sac. After exclusion, low-TAWSS regions became less extensive, the shear field along the patent lumen became more continuous, and both RRT and ECAP decreased significantly, with P values of 0.0008 and 0.0063 respectively. Mean TAWSS and WSS increased after PMEG with P values below 0.0001 and 0.0002.

One representative case, Case 7, underwent exploratory fluid-structure interaction analysis, coupling the pulsatile flow to a deformable wall modeled as homogeneous, isotropic, and linearly elastic with a Young’s modulus of six million Pascals and a Poisson’s ratio of 0.45. Because CTA could not provide a reliable spatial map of wall thickness, a uniform nominal 2.0 millimeter wall was generated from the lumen surface, and intraluminal thrombus and calcified plaque were not modeled as separate material domains. Within those constraints, the coupled analysis showed that computed wall deformation was concentrated in the mid-aneurysm region before PMEG and was substantially lower in the reconstructed wall after repair under the same imposed loading. The deformation followed the cardiac cycle, beginning in the mid-aneurysm wall during early systolic acceleration, reaching its maximum at peak systole, decreasing during deceleration, and approaching the initial configuration in diastole. The FSI wall shear contours showed the same phase-dependent migration, with high shear near high-velocity jets and pronounced curvature while the expanded mid-sac remained dominated by low shear.

The clinical follow-up provides complementary support. At one year, all branch stents remained patent without occlusion or displacement, no endoleaks of any type were observed across the eight cases, and no adverse events such as chest pain, abdominal pain, or spinal cord ischemia were reported. The computational findings also align with an independent paired CTA-CFD study that reported restored visceral flow, higher postoperative abdominal-aortic TAWSS, and significantly lower RRT and ECAP after PMEG, as well as with long-term results from a prospective physician-sponsored PMEG trial in juxtarenal aneurysms demonstrating durable treatment with low long-term morbidity and mortality.

The authors are careful about what these surrogate markers can and cannot claim. Hemodynamics is one contributor within a multifactorial process that also includes intraluminal thrombus, wall inflammation, tissue properties, and systemic risk factors, and longitudinal studies have reported inconsistent or even spatially discordant relationships between low shear, thrombus accumulation, aneurysm growth, and rupture. Intraluminal thrombus itself may reduce local wall stress while simultaneously promoting hypoxia, inflammation, and proteolytic weakening. TAWSS, RRT, and ECAP should therefore be regarded as mechanistic surrogate markers rather than direct causal predictors of aneurysm progression or rupture, and no threshold in this study has been validated to predict thrombosis or rupture. The statistical analysis treated pre- and post-PMEG measurements as paired observations, applied exact P values with significance at 0.05, and deliberately avoided pseudo-replication by analyzing patient-level values rather than surface nodes or time steps, though no multiplicity correction was applied given the small exploratory cohort.

What the framework ultimately offers is a noninvasive window onto quantities that routine postoperative imaging cannot see. CTA can confirm graft position, branch patency, sac exclusion, and endoleak, but it does not provide spatial distributions of wall shear stress, relative residence time, endothelial activation potential, or aneurysm-wall deformation, and patient-specific outlet waveforms are rarely available for every branch. Computational fluid dynamics and fluid-structure interaction fill that gap, generating surveillance hypotheses by indicating where slow washout or unfavorable shear persists despite technically successful aneurysm exclusion. The study remains retrospective, includes eight patients with no matched conventional-EVAR group, uses standardized rather than measured patient-specific loading, assumes rigid walls in the cohort analysis, and performs fluid-structure interaction in a single case with uniform thickness and homogeneous material properties. Larger prospective comparative studies with measured boundary conditions, spatially resolved wall and thrombus properties, matched comparators, and longer event-based follow-up are still required to quantify the extent to which these surrogate improvements translate into fewer clinical thrombotic or rupture events. Physically, the observed effects are governed by the PMEG-induced redistribution of flow area and vascular geometry, which alters local velocity, pressure loss, near-wall shear, flow stasis, and wall loading in ways that diameter reduction alone cannot capture.

Subject of Research: Patient-specific hemodynamic evaluation of fenestrated physician-modified endografts in complex abdominal aortic aneurysms

Article Title: Patient-specific hemodynamic evaluation of fenestrated physician-modified endografts in complex abdominal aortic aneurysms

Article References: Du, X., Jiang, S., Zhang, H., Yu, H., Zhang, L., Ren, K., & Ran, F. (2026). Patient-specific hemodynamic evaluation of fenestrated physician-modified endografts in complex abdominal aortic aneurysms. Frontiers in Physics, 14, Article 1970930. https://doi.org/10.3389/fphy.2026.1970930

Image Credits: AI Generated

DOI: 10.3389/fphy.2026.1970930

Keywords: Patient-specific, hemodynamic, evaluation, fenestrated, physician-modified, endografts, complex, abdominal, aortic, aneurysms, scientific research