ArticlePloS one2019
Effect of valve lesion on venous valve cycle: A modified immersed finite element modeling.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Three-dimensional fluid-structure interaction modelling of the venous valve using immersed boundary/finite element method.Computers in biology and medicine · 2025Article
- Platelet accumulation in an endothelium-coated elastic vein valve model of deep vein thrombosis is mediated by GPIbFrontiers in cardiovascular medicine · 2023Article
- Effect of intermittent pneumatic compression on preventing deep vein thrombosis using microfluidic vein chip.Frontiers in bioengineering and biotechnology · 2023Article
- Effects of non-Newtonian viscosity on arterial and venous flow and transport.Scientific reports · 2022Article
- Fluid-structure interaction of blood flow around a vein valve.BioImpacts : BI · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to understand the effect of venous valve lesion on the valve cycle. A modified immersed finite element method was used to model the blood-tissue interactions in the pathological vein. The contact process between leaflets or between leaflet and sinus was evaluated using an adhesive contact method. The venous valve modeling was validated by comparing the results of the healthy valve with those of experiments and other simulations. Four valve lesions induced by the abnormal elasticity variation were considered for the unhealthy valve: fibrosis, atrophy, incomplete fibrosis, and incomplete atrophy. The opening orifice area was inversely proportional to the structural stiffness of the valve, while the transvalvular flow velocity was proportional to the structural stiffness of the valve. The stiffening of the fibrotic leaflet led to a decrease in the orifice area and a stronger jet. The leaflet and blood wall shear stress (WSS) in fibrosis was the highest. The softening of the atrophic leaflet resulted in overly soft behavior. The venous incompetence and reflux were observed in atrophy. Also, the atrophic leaflet in incomplete atrophy exhibited weak resistance to the hemodynamic action, and the valve was reluctant to be closed owing to the large rotation of the healthy leaflet. Low blood WSS and maximum leaflet WSS existed in all the cases. A less biologically favorable condition was found especially in the fibrotic leaflet, involving a higher mechanical cost. This study provided an insight into the venous valve lesion, which might help understand the valve mechanism of the diseased vein. These findings will be more useful when the biology is also understood. Thus, more biological studies are needed.
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