ArticleFrontiers in bioengineering and biotechnology2026
Investigating the impact of collateral circulation pathways on hemodynamics in iliac vein compression syndrome.
Article in Frontiers in bioengineering and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study aims to investigate the hemodynamic effects of collateral circulation in Iliac Vein Compression Syndrome (IVCS) using computational fluid dynamics (CFD). Two patient-specific three-dimensional models were reconstructed from Computed Tomography Angiography (CTA) data: one with a well-developed collateral circulation system (collateral model) and the other without significant collateral development (non-collateral model). A porous medium model was applied to simulate venous spur-like obstruction within the compressed iliac vein segment. The Shear Stress Transport (SST) k-ω model was employed to simulate blood flow under physiological boundary conditions, incorporating the influence of gravity. Key hemodynamic parameters including blood reflux, pressure distribution, flow velocity, and wall shear stress (WSS), were systematically analyzed and compared between the two models. The results demonstrate that the presence of collateral circulation significantly altered and stabilized the hemodynamic environment. In the collateral model, minimal blood reflux was observed due to flow redistribution, resulting in a notably lower pressure gradient across the stenotic region (peak pressure difference: 619 Pa) and reduced WSS (peak WSS: 10 Pa). In contrast, the non-collateral model exhibited extensive reflux and large-scale vortex formation, an extreme pressure gradient (peak pressure difference: 20,190 Pa, approximately 32.6 times higher than that of the collateral model (619 Pa), and significantly elevated WSS (peak WSS: 56 Pa). Furthermore, the total venous outflow to the inferior vena cava in the collateral model was 39.38% higher than that in the non-collateral model, indicating enhanced venous return. These findings suggest that collateral circulation may play important compensatory hemodynamic role in IVCS by redistributing venous flow and reducing pressure burden, wall shear stress, and the extent of disturbed-flow structures in the compressed region. The present results should be interpreted as mechanistic and hypothesis-generating rather than as direct evidence of thrombotic risk or clinical treatment effect. Assessment of collateral pathways may nevertheless provide useful mechanistic insight into venous return in patient-specific IVCS anatomy.
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