Compliance mismatch may promote graft-artery intimal hyperplasia by altering suture-line stresses.

The role of graft-artery compliance mismatch in the development of distal anastomotic intimal hyperplasia (DAIH) is not yet resolved. Although DAIH develops at all surgically created anastomoses, increased compliance mismatch does not lead to greater hyperplasia formation in end-to-end anastomoses, but in end-to-side anastomoses, it leads to a profound increase in hyperplasia. The current study was undertaken to determine whether suture-induced anastomotic stresses could explain these findings. A large strain finite element analysis of vascular wall mechanics was performed to compare the influence of compliance mismatch on intramural stresses in end-to-end versus end-to-side anastomoses. A novel modelling approach was implemented which includes suture-induced stress concentrations. End-to-end and end-to-side graft-artery simulations were executed using (1) artery (compliance = C = 0.44% kPa(-1)), (2) vein (C = 0.33% kPa(-1)), and (3) Dacron (C = 0.14% kPa(-1)) grafts. Residual stresses due to axial tension were included and the anastomoses were statically inflated to 13.3 kPa (100 mmHg). Elevated intramural stresses were found to exist at both the end-to-end and end-to-side graft-artery junctions; however, in the end-to-end anastomosis, the maximum anastomotic stress was not a function of the graft compliance, whereas in the end-to-side anastomosis, the maximum stress was a strong function of graft compliance. For the 45 degree end-to-side geometry considered in this study, the maximum anastomotic stress concentration obtained using a stiff Dacron graft was more than 40% greater than that obtained using a compliant artery graft. In the end-to-end anastomosis, the Dacron graft led to a less than 5% increase in maximum stress over the artery graft. Therefore, increased compliance mismatch increases stresses and promotes DAIH in end-to-side junctions, but, it has little influence on either stresses or DAIH in end-to-end junctions. Thus, the proliferative influence of increased compliance mismatch on suture-line hyperplasia in end-to-side anastomoses can be explained by the resulting increase in intramural stresses. In addition, since high stresses were found in both geometries, elevated suture-line intramural stresses may be an important proliferative stimulus for intimal hyperplasia formation in all vascular reconstructions.

[1]  W. Sessa,et al.  Cyclic strain increases endothelial nitric oxide synthase activity. , 1994, Surgery.

[2]  W. Sessa,et al.  Cyclic strain upregulates nitric oxide synthase in cultured bovine aortic endothelial cells. , 1995, The Journal of clinical investigation.

[3]  R. T. Eppink,et al.  Pressure-induced mechanical stress in the carotid artery bifurcation: a possible correlation to atherosclerosis. , 1995, Journal of biomechanics.

[4]  R. Depalma,et al.  The protective effect of vein cuffed anastomoses is not mechanical in origin. , 1995, Journal of vascular surgery.

[5]  A. Moritz,et al.  Compliance and formation of distal anastomotic intimal hyperplasia in Dacron mesh tube constricted veins used as arterial bypass grafts. , 1994, ASAIO journal.

[6]  G. L’italien,et al.  Matched elastic properties and successful arterial grafting. , 1980, Archives of surgery.

[7]  B. Sumpio,et al.  Cyclic Strain Stimulates Endothelial Cell Proliferation: Characterization of Strain Requirements , 1994 .

[8]  J D Thomas,et al.  The effect of angle and flow rate upon hemodynamics in distal vascular graft anastomoses: a numerical model study. , 1991, Journal of biomechanical engineering.

[9]  W. Abbott,et al.  PULSATILE BLOOD-FLOW IN ARTERIAL GRAFTS , 1976, The Lancet.

[10]  W. Nichols McDonald's Blood Flow in Arteries , 1996 .

[11]  R D Kamm,et al.  Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. , 1992, Circulation research.

[12]  S Glagov,et al.  Anastomotic intimal hyperplasia: mechanical injury or flow induced. , 1992, Journal of vascular surgery.

[13]  Y. Fung,et al.  The development of mechanical strength of surgically anastomosed arteries sutured with Dexon. , 1985, Journal of biomechanics.

[14]  R. Depalma,et al.  Vein Cuff Interposition Prevents Juxta‐Anastomotic Neointimal Hyperplasia , 1988, Annals of surgery.

[15]  M. Ojha Wall shear stress temporal gradient and anastomotic intimal hyperplasia. , 1994, Circulation research.

[16]  M Ojha,et al.  Spatial and temporal variations of wall shear stress within an end-to-side arterial anastomosis model. , 1993, Journal of biomechanics.

[17]  R S Cobbold,et al.  Influence of angle on wall shear stress distribution for an end-to-side anastomosis. , 1994, Journal of vascular surgery.

[18]  D. Ku,et al.  Collapse of diseased arteries with eccentric cross section. , 1993, Journal of biomechanics.

[19]  B. Sumpio,et al.  Cyclic strain causes heterogeneous induction of transcription factors, AP-1, CRE binding protein and NF-kB, in endothelial cells: species and vascular bed diversity. , 1995, Journal of biomechanics.

[20]  D. Steinman,et al.  Simulation of non-Newtonian blood flow in an end-to-side anastomosis. , 1994, Biorheology.

[21]  G L'Italien,et al.  Effect of compliance mismatch on vascular graft patency. , 1987, Journal of vascular surgery.

[22]  C. R. Ethier,et al.  Steady and pulsatile flow fields in an end-to-side arterial anastomosis model. , 1990, Journal of vascular surgery.

[23]  A. Galloway,et al.  Mammary artery versus saphenous vein grafts: assessment of basic fibroblast growth factor receptors. , 1994, The Annals of thoracic surgery.

[24]  L V McIntire,et al.  Cyclical strain effects on production of vasoactive materials in cultured endothelial cells , 1992, Journal of cellular physiology.

[25]  L. Sauvage,et al.  The direct effect of graft compliance mismatch per se on development of host arterial intimal hyperplasia at the anastomotic interface , 1993, Annals of vascular surgery.

[26]  D. Steinman,et al.  A numerical simulation of flow in a two-dimensional end-to-side anastomosis model. , 1993, Journal of biomechanical engineering.

[27]  R. Schwartz,et al.  Does the end-to-end venous anastomosis offer a functional advantage over the end-to-side venous anastomosis in high-output arteriovenous grafts? , 1990, Journal of vascular surgery.

[28]  Bradley Rd NECROSIS OF THE ANTERIOR PITUITARY AND ZONA GLOMERULOSA OF THE ADRENAL. , 1964 .

[29]  B. Sumpio,et al.  Stimulation of adenylate cyclase activity in cultured endothelial cells subjected to cyclic stretch. , 1990, The Journal of cardiovascular surgery.

[30]  R. T. Eppink,et al.  Study of stress concentration in the walls of the bovine coronary arterial branch. , 1990, Journal of biomechanics.

[31]  G. L’italien,et al.  Abnormal wall strain at distal end-to-side anastomoses , 1993, Annals of vascular surgery.

[32]  D. Lyman,et al.  Effect of elasticity of prosthetic wall on patency of small-diameter arterial prostheses. , 1979, Surgical forum.

[33]  Y. Fung,et al.  Pseudoelasticity of arteries and the choice of its mathematical expression. , 1979, The American journal of physiology.

[34]  V. Sottiurai,et al.  Distal anastomotic intimal hyperplasia: histopathologic character and biogenesis. , 1989, Annals of vascular surgery.

[35]  L. Ferrell,et al.  Does compliance mismatch alone cause neointimal hyperplasia? , 1989, Journal of vascular surgery.

[36]  K. Morinaga,et al.  Effect of wall shear stress on intimal thickening of arterially transplanted autogenous veins in dogs. , 1985, Journal of vascular surgery.