scholarly journals Computational Simulation of the Adaptive Capacity of Vein Grafts in Response to Increased Pressure

2015 ◽  
Vol 137 (3) ◽  
Author(s):  
Abhay B. Ramachandra ◽  
Sethuraman Sankaran ◽  
Jay D. Humphrey ◽  
Alison L. Marsden

Vein maladaptation, leading to poor long-term patency, is a serious clinical problem in patients receiving coronary artery bypass grafts (CABGs) or undergoing related clinical procedures that subject veins to elevated blood flow and pressure. We propose a computational model of venous adaptation to altered pressure based on a constrained mixture theory of growth and remodeling (G&R). We identify constitutive parameters that optimally match biaxial data from a mouse vena cava, then numerically subject the vein to altered pressure conditions and quantify the extent of adaptation for a biologically reasonable set of bounds for G&R parameters. We identify conditions under which a vein graft can adapt optimally and explore physiological constraints that lead to maladaptation. Finally, we test the hypothesis that a gradual, rather than a step, change in pressure will reduce maladaptation. Optimization is used to accelerate parameter identification and numerically evaluate hypotheses of vein remodeling.

2018 ◽  
Vol 140 (2) ◽  
Author(s):  
Keith J. Gooch ◽  
Michael S. Firstenberg ◽  
Brittany S. Shrefler ◽  
Benjamin W. Scandling

Within several weeks of use as coronary artery bypass grafts (CABG), saphenous veins (SV) exhibit significant intimal hyperplasia (IH). IH predisposes vessels to thrombosis and atherosclerosis, the two major modes of vein graft failure. The fact that SV do not develop significant IH in their native venous environment coupled with the rapidity with which they develop IH following grafting into the arterial circulation suggests that factors associated with the isolation and preparation of SV and/or differences between the venous and arterial environments contribute to disease progression. There is strong evidence suggesting that mechanical trauma associated with traditional techniques of SV preparation can significantly damage the vessel and might potentially reduce graft patency though modern surgical techniques reduces these injuries. In contrast, it seems possible that modern surgical technique, specifically endoscopic vein harvest, might introduce other mechanical trauma that could subtly injure the vein and perhaps contribute to the reduced patency observed in veins harvested using endoscopic techniques. Aspects of the arterial mechanical environment influence remodeling of SV grafted into the arterial circulation. Increased pressure likely leads to thickening of the medial wall but its role in IH is less clear. Changes in fluid flow, including increased average wall shear stress, may reduce IH while disturbed flow likely increase IH. Nonmechanical stimuli, such as exposure to arterial levels of oxygen, may also have a significant but not widely recognized role in IH. Several potentially promising approaches to alter the mechanical environment to improve graft patency are including extravascular supports or altered graft geometries are covered.


2010 ◽  
Vol 10 (04) ◽  
pp. 593-609 ◽  
Author(s):  
FOAD KABINEJADIAN ◽  
LEOK POH CHUA ◽  
DHANJOO N. GHISTA ◽  
YONG SENG TAN

Venous valves and sinuses are frequently observed in vein grafts in the coronary artery bypass grafts (CABG). However, from the biomedical engineering viewpoint, vein grafts are always assumed as smooth tubes in the existing simulations, and no effort has been made to investigate the effects of jaggedness of the graft inner wall due to the valve cusps remnants and valve sinus (in case of valve-stripped saphenous vein (SV) grafts) on the blood flow patterns and hemodynamic parameters (HPs). In this paper, the effects of the inner surface irregularities of a vein graft on the blood flow is investigated in the graft as well as in the distal anastomotic region, with a more realistic geometry of valve-stripped SV, by means of numerical simulation of pulsatile, Newtonian blood flow. The simulation results demonstrate that the valve remnants and sinuses cause disturbances in the flow field within the graft (due to vortices formation within the valve sinuses) and undesirable distribution of HPs, which can result in early atherosclerotic lesion development in the graft.


1989 ◽  
Vol 28 (06) ◽  
pp. 234-242 ◽  
Author(s):  
U. Sechtem ◽  
Sabine Langkamp ◽  
M. Jungehülsing ◽  
H. H. Hilger ◽  
H. Schicha ◽  
...  

Fortyfour patients with recent cardiac catheterization because of recurrent chest pain after coronary artery bypass surgery were studied by magnetic resonance imaging to evaluate graft patency. To assess the efficacy of this non-invasive method 92 coronary artery bypass grafts were examined by the spin-echo technique. ECG-gated transversal sections were acquired between the diaphragm and the aortic arch. The specificity of magnetic resonance imaging was 83% (48/58) for patent grafts. However, the sensitivity in the detection of occluded bypasses was only 56% (19/34). Despite the good specificity, clinical applications of this method are limited because of its low sensitivity.


2020 ◽  
Vol 26 (2) ◽  
pp. 52
Author(s):  
V. V. Bazylev ◽  
E. V. Rosseĭkin ◽  
D. A. Radzhabov ◽  
A. I. Mikuliak

Circulation ◽  
1996 ◽  
Vol 93 (4) ◽  
pp. 660-666 ◽  
Author(s):  
Michel A. Galjee ◽  
Albert C. van Rossum ◽  
Teddo Doesburg ◽  
Machiel J. van Eenige ◽  
Cees A. Visser

Vascular ◽  
2021 ◽  
pp. 170853812199985
Author(s):  
Yuanyuan Guo ◽  
Fan Zhu ◽  
Xiong Zhang ◽  
Guangmin Wu ◽  
Pinting Fu ◽  
...  

Objectives Vein graft adaptation (VGA) is a process that vein as a vascular graft conduits in arterial reconstructive surgery; VGA can lead to postoperative vein graft stenosis (VGS) and complications after coronary artery bypass graft and other peripheral artery bypass surgeries. VGA is characterized by vein graft loss the venous features without exhibiting arterial features; furthermore, the activation of ERK inhibited the maintenance of venous properties of the vein graft. We hypothesized that ERK inhibition can affect vein VGS through regulating the expression of EphB4. Methods Rat vein transplantation model was established using wild-type and EphB4+/− Sprague-Dawley rats. Hematoxylin-eosin, Masson, Verhoeff, actin staining, and immunohistochemistry were applied to observe the structure of the vein grafts. Vascular smooth muscle cells (VSMCs) were isolated from the vein and vein grafts. Western blotting was used to determine the expression of p-ERK1/2 and EphB4, and immunofluorescence was applied to detect the expression and location of EphB4. Cell wound scratch assay and CCK8 assay were used to determine the migration and proliferation of VSMCs. Real-time polymerase chain reaction was used to determine the mRNA expression of EphB4. Results Western blotting in vein sample and vein graft sample detected p-ERK1/2 and ERK1/2 expression in both EphB4+/+ and EphB4+/− rats. The expression of p-ERK was increased in vein graft compared to vein. Immunofluorescence in VSMCs form EphB4+/+ and EphB4+/− rats detected EphB4 expression in both cells, and the expression of EphB4 was increased in VSMCs form EphB4+/+ rats. SCH772984 reduces the proliferation and migration of VSMCs. Inhibition of ERK suppressed the increase of vein graft wall thickness, and the expression of collagen fibers, elastic fibers, and α-actin was decreased. Vein graft from EphB4+/− rats reduces the expression of EphB4, and SCH772984 suppressed the decrease of EphB4 in vivo. Vein graft from EphB4+/− rats increased the expression of EphB4, and SCH772984 suppressed the increase of EphB4 in vivo. Conclusions The inhibition of ERK1/2 suppressed the process of VGS by decreasing the proliferation of VSMCs. The ERK-inhibitor SCH772984 suppressed the level of VGS by extending the time of EphB4 expression during the process of VGA, thus maintaining the venousization of vein graft. The mechanism may be that the inhibitor SCH772984 suppresses the level of VGS by extending the time of EphB4 expression during the process of VGA. Therefore, our research provides a new target of VGS treatment by inhibiting the expression of ERK1/2 through the process of VGA.


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