Distal anastomotic intimal hyperplasia: Biogenesis and etiology

Sottiurai, Vikrom S.; Sue, Shirley Lim; Feinberg, Edgar L.; Bringaze, Walter L.; Tran, Anthony T.; Batson, Robert C.

doi:10.1016/s0950-821x(88)80034-3

Cited by 63 publications

(22 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This sharp switch in the direction of the shear stress may induce endothelial deformation or injury and explain the rapid development of fibrous intimal hyperplasia in 2 to 4 months on the bed of various canine iliac anastomoses reported elsewhere.7-10 Further support of the proposed shear-induced endothelial injury or deformation mechanism is gained from the similarity of the fibrous tissue composition between hyperplasia on the bed and that around the suture line, where surgical injury compounded by compliance mismatch are the initiating factors. [7][8][9] Rapidly decreasing positive shear stress can also lead to large negative gradients. …”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Wall shear stress temporal gradient and anastomotic intimal hyperplasia.

Ojha

1994

Circulation Research

144

View full text Add to dashboard Cite

Unusual wall shear stress patterns on the bed of end-to-side arterial anastomoses appear to be the primary factor in the development of intimal hyperplasia that often leads to arterial bypass graft failure. In this in vitro study using the photochromic tracer technique, the shear stress variation on the bed of a 30°anastomosis was examined before and after the development of hyperplasia. With the disease-free model, a rapid downstream shift in the stagnation point was seen on the bed during the systolic phase of the flow cycle, which led to sharp temporal changes in the shear stress from positive to negative values, ie, rapid changes in the direction of the shearing force. The resulting negative temporal gradients were roughly eight times larger than those seen in a straight tube, and it is suggested that this may lead to endothelial deformation or injury and eventually to intimal thickening. With the diseased model, the simulated tissue overgrowth on the bed appeared to act as a flow divider that restricted the motion of the stagnation point, and this drastically reduced the rapid changes in the direction of the shearing forces. Thus, it seems that the development of bed anastomotic intimal hyperplasia may be a response designed to reduce shear-induced endothelial deformation or injury. (Circ Res. 1994;74:1227-1231 Key Words * shear stress * bypass graft occlusion fibrous intimal hyperplasia * hemodynamics T issue responses induced by shearing forces appear to contribute to homeostasis of the arteries and to various arterial disorders.1-3 Three examples of arterial disorders that are probably induced by wall shear stress are focal atherosclerotic lesions,34 poststenotic dilatation,56 and anastomotic intimal hyperplasia.7-10 In the present study, the potential role of wall shear stress in the development of anastomotic intimal hyperplasia is examined.Anastomotic intimal hyperplasia is a common cause for postoperative failure of arterial bypass grafts, particularly at the outflow end.1" With end-to-side configuration (see Fig 1), hyperplasia develops at the heel and toe around the suture line and on the bed of the native artery. Around the suture line, it seems that hyperplasia initiated by surgical injury is promoted by low wall shear stress and also by compliance mismatch between the graft material and native artery.7-10 On the bed, however, hyperplasia seems to be induced simply by adverse wall shear stress created by the end-to-side geometry.7-10 In the present study, a disease-free and a diseased model were investigated in an attempt to understand the initiation of intimal thickening and to determine whether or not its development represents an adaptive response to the adverse wall shear stress on the bed.Previous attempts to determine the shear stress on the bed using conventional flow measurement techniques such as hot-wire anemometry,12 dye injection,13 Doppler ultrasound,14 and particle tracking10 have yielded limited results because of the complexity of the underlying velocity field. The presen...

show abstract

Section: Methodsmentioning

confidence: 99%

“…[7][8][9][10] In the present study, the potential role of wall shear stress in the development of anastomotic intimal hyperplasia is examined.…”

mentioning

confidence: 99%

Wall shear stress temporal gradient and anastomotic intimal hyperplasia.

Ojha

1994

Circulation Research

144

View full text Add to dashboard Cite

show abstract

“…Contributing events include compliance mismatch, turbulent flow, and altered wall shear stress leading to endothelial injury, platelet activation, cellular proliferation, and the deposition of extracellular matrix. 14,[95][96][97] A number of models are available for the study of IH and restenosis after arterial insult, although these often use nonsurgical methods to generate localized endothelial and mural injury, most commonly by inflating and withdrawing a Fogarty balloon catheter. These methods have been used to experimentally produce complex lesions, similar to those seen in humans, in nonhuman primates and pigs.…”

Section: Large-animal Models For the Assessment Of Novel Vascular Conmentioning

confidence: 99%

Animal models for the assessment of novel vascular conduits

Byrom

Bannon

White

et al. 2010

Journal of Vascular Surgery

158

132

View full text Add to dashboard Cite

The development of an ideal small-diameter conduit for use in vascular bypass surgery has yet to be achieved. The ongoing innovation in biomaterial design generates novel conduits that require preclinical assessment in vivo, and a number of animal models have been used for this purpose. This article examines the rationale behind animal models used in the assessment of small-diameter vascular conduits encompassing the commonly used species: baboons, sheep, pigs, dogs, rabbits, and rodents. Studies on the comparative hematology for these species relative to humans are summarized, and the hydrodynamic values for common implant locations are also compared. The large- and small-animal models are then explored, highlighting the characteristics of each that determine their relative utility in the assessment of vascular conduits. Where possible, the performance of expanded polytetrafluoroethylene is given in each animal and in each location to allow direct comparisons between species. New challenges in animal modeling are outlined for the assessment of tissue-engineered graft designs. Finally, recommendations are given for the selection of animal models for the assessment of future vascular conduits.

show abstract

“…(2) Cyclic stretching has a positive influence on replication of vascular smooth muscle (SMC) and production of extracellular matrix (ECM) [56,57]. It has been demonstrated that SMCs produce ECM and replicate when they are subjected to high levels of distension [58] and tangential stress [59].…”

Section: Anastomotic Compliance Mismatchmentioning

confidence: 99%

The Mechanical Behavior of Vascular Grafts: A Review

Goldner²,

et al. 2001

View full text Add to dashboard Cite

The development of intimal hyperplasia (IH) near the anastomosis of a vascular graft to artery is directly related to changes in the wall shear rate distribution. Mismatch in compliance and diameter at the end-to-end anastomosis of a compliant artery and rigid graft cause shear rate disturbances that may induce intimal hyperplasia and ultimately graft failure. The principal strategy being developed to prevent IH is based on the design and fabrication of compliant synthetic or innovative tissue-engineered grafts with viscoelastic properties that mirror those of the human artery. The goal of this review is to discuss how mechanical properties including compliance mismatch, diameter mismatch, Young's modulus and impedance phase angle affect graft failure due to intimal hyperplasia.

show abstract

Distal anastomotic intimal hyperplasia: Biogenesis and etiology

Cited by 63 publications

References 10 publications

Wall shear stress temporal gradient and anastomotic intimal hyperplasia.

Wall shear stress temporal gradient and anastomotic intimal hyperplasia.

Animal models for the assessment of novel vascular conduits

The Mechanical Behavior of Vascular Grafts: A Review

Contact Info

Product

Resources

About