Key result
Simulated fibrotic venous valve lesions decrease orifice area while atrophic lesions cause incompetence and reflux.
Why the study?
The study aimed to understand the effect of venous valve lesions on the valve cycle.
Does abnormal elasticity variation (fibrosis/atrophy) affect venous valve cycle dynamics in a computational model?
Does abnormal elasticity variation (fibrosis/atrophy) affect venous valve cycle dynamics in a computational model?
Computational modeling demonstrates that venous valve fibrosis increases wall shear stress and flow velocity, while atrophy leads to venous incompetence and reflux.
Suggests stiffness modulates venous valve dynamics in models; hypothesis-generating for clinical valve incompetence.
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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Liu et al. (2019) studied Venous valve lesion. Venous valve lesions (fibrosis, atrophy) vs. Healthy valve was evaluated on Valve cycle dynamics (orifice area, transvalvular flow velocity, wall shear stress). Simulated fibrotic venous valve lesions decreased orifice area and increased wall shear stress, while atrophic lesions caused venous incompetence and reflux.
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