A framework for studying oxygen and nitric oxide transport in unstable flow through a patient-based abdominal aortic aneurysm model

Robert A. Peattie, Sudharsan Madhavan, Brian Fix, Robert J. Fisher, Simone Melchionna and Erica Cherry Kemmerling

Computer Methods in Biomechanics and Biomedical Engineering, 2025, vol. 28, issue 9, 1500-1519

Abstract: Abdominal Aortic Aneurysm (AAA) is a potentially life-threatening permanent, localized dilation in the abdominal aorta wall. Previous studies have suggested that the presence of a layer of intraluminal thrombus (ILT), which is found adhering to the wall inner surface in 80–90% of all AAAs, is associated with a significant decrease in the oxygen (O2) level within the wall. However, although turbulence normally has a major influence on solute transport, its effect on this decrease has not yet been investigated. In the present study, a computational technique for evaluating wall O2 and NO concentration distributions in a patient-based model with separate lumen, thrombus, and wall layers is developed. Flow in this model was evaluated by Direct Numerical Simulation, using pathophysiologically realistic flow and transport conditions accounting for instability and turbulence development. Concentration distributions were determined by solution of advection-diffusion-reaction equations appropriate to each layer. Normalized O2 concentration at the wall inner surface decreased as ILT thickness increased up to 0.4 cm but then plateaued at ∼0.7 (normalized). Contrary to expectations, turbulence had minimal impact on transport, which was consistent with calculation of an effective Damkohler number for the AAA, indicating that solute levels were governed by reaction-limited rather than transport-limited dynamics. Since NO production was driven by shear stress at the lumen-wall interface, NO was absent in ILT-covered regions, creating spatial disparities in wall NO concentration between thrombus-covered and clear regions of the wall surface. The results suggest that ILT induces wall hypoxia and impairs NO-mediated vascular homeostasis.

Date: 2025
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DOI: 10.1080/10255842.2025.2510363

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