Protection from atherosclerosis in vein grafts by a rigid external support.

Batellier, J; Wassef, Michel; R, Merval; Duriez, Micheline; Tedgui, Alain

doi:10.1161/01.atv.13.3.379

Cited by 52 publications

(30 citation statements)

References 21 publications

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“…Wall motion and stress are to some extent interrelated, and reduction in wall motion probably indicates reduction in cyclic wall stress. External wrapping of vein grafts 17,18 has been studied in detail, but the reduction in the normal wall proliferative response to an arterialized vein due to the external wrap cannot be correlated with the study of arteries and atherogenesis in the presence of hypertension. In addition, wall motion was not measured in these studies.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Aortic Wall Motion Inhibits Hypertension-Mediated Experimental Atherosclerosis

Tropea

Schwarzacher

Chang

et al. 2000

ATVB

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Abstract-Hypertension is a well-known risk factor for coronary artery disease and carotid and lower extremity occlusive disease. Surgically induced hypertension in hypercholesterolemic animals results in increased aortic wall motion and increased plaque formation. We tested the hypothesis that reduction in aortic wall motion, despite continued hypertension, could reduce plaque formation. New Zealand White rabbits (nϭ26) underwent thoracic aortic banding to induce hypertension and were fed an atherogenic diet for 3 weeks. In 13 rabbits, a segment of aorta proximal to an aortic band was externally wrapped to reduce wall motion. All animals were fed an atherogenic diet for 3 weeks. Four groups were studied: 1, coarctation control (no wrap, nϭ7); 2, coarctation with loose wrap (nϭ6); 3, coarctation with firm wrap (nϭ7); and 4, control (noncoarcted, nϭ6). Wall motion, blood pressure, and pulse pressure were measured at standard reference sites proximal and distal to the coarctation by use of intravascular ultrasound. Quantitative morphometry was used to measure intimal plaque. Mean arterial pressure and cyclic aortic wall motion were equally increased proximal to the aortic coarctation in all 3 coarcted rabbit groups compared with the control group (PϽ0.001). Wall motion in the segment of aorta under the loose and firm wraps was no different from the control value. The external wrap significantly reduced intimal thickening in the 4 groups by the following amounts: group 1, 0.30Ϯ0.03 mm 2 ; group 2, 0.06Ϯ0.02 mm 2 ; group 3, 0.04Ϯ0.02 mm 2 ; and group 4, 0.01Ϯ0.01 mm 2 (PϽ0.001). Localized inhibition of aortic wall motion in the lesion-prone hypertensive aorta resulted in significant reduction in intimal plaque formation. These data suggest that arterial wall cyclic motion may stimulate cellular proliferation and lipid uptake in experimental atherosclerosis. Key Words: wall motion Ⅲ hypertension Ⅲ atherosclerosis Ⅲ pulse pressure H ypertension is an independent risk factor for coronary artery disease 1,2 and for carotid 3,4 and lower extremity 5,6 occlusive disease. Other multivariate clinical studies have shown that pulse pressure is also an independent risk factor for atherosclerosis. 7,8 Previous experimental studies in our laboratory 9,10 and in others 11,12 have demonstrated that surgically created aortic coarctations increase blood pressure proximal to the coarctation and increase the rate of plaque deposition in hypercholesterolemic rabbits and monkeys.On the other hand, the aorta distal to a severe coarctation experiences reduced wall motion and is largely protected from plaque formation despite hypercholesterolemia in animals. 13 In a separate study, rigid external casts of lesion-prone arteries in normotensive hypercholesterolemic rabbits inhibited plaque formation, perhaps because of reduced wall motion. 14 In the present experiment, we reduced aortic wall motion in the hypertensive atherosclerosis-prone aorta proximal to a coarctation by externally wrapping a segment of aorta and studied the effect on plaq...

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Section: Discussionmentioning

confidence: 99%

Reduction of Aortic Wall Motion Inhibits Hypertension-Mediated Experimental Atherosclerosis

Tropea

Schwarzacher

Chang

et al. 2000

ATVB

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“…[55][56][57][58][59][60] Previous studies showed that relief from increased tensile stress in the vein graft wall by use of a rigid, external support could partially prevent intimal hyperplasia and medial thickening, indicating a role for tensile stress in the regulation of vein graft remodeling. 56 -60 Several recent studies further showed that increased tensile stress induced SMC actin filament degradation and SMC death, 24 influenced the orientation of newly generated SMCs, and might contribute to medial and adventitial hypertrophy in experimental vein grafts.…”

Section: Influence Of Eddy Blood Flow On At 1 Receptor Expressionmentioning

confidence: 99%

Focal Expression of Angiotensin II Type 1 Receptor and Smooth Muscle Cell Proliferation in the Neointima of Experimental Vein Grafts

Liu

1999

ATVB

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Abstract-Eddy flow has been shown to promote focal smooth muscle cell (SMC) proliferation and neointimal formation in experimental vein grafts. This study focuses on whether the angiotensin II type 1 (AT 1 ) receptor mediates these events. Experimental vein grafts with and without eddy flow were created in the rat. Losartan was used to assess the influence of the AT 1 receptor on SMC proliferation. In vein grafts with eddy flow, apparent focal expression of AT 1 mRNA and protein was found in the leading region of the proximal focal neointima, where eddy flow occurred, but not in the trailing region, where eddy flow diminished, at days 5, 10, 20, and 30. These studies have demonstrated that atherosclerotic lesions in human and animal arteries develop mainly in curved and bifurcation regions where eddy or secondary blood flow occurs. [1][2][3][4] The coincidence of eddy blood flow with atheroma suggests that eddy blood flow may play a role in the initiation and development of vascular atherosclerosis.Vein grafts, which are commonly used to replace malfunctioned arteries, are subject to eddy blood flow. Experimental studies have demonstrated that the location and pattern of eddy blood flow vary in different vein graft models, depending on the vessel geometry for a given blood flow rate and blood viscosity. [5][6][7][8] In an end-to-end anastomosed vein graft model, eddy blood flow occurs in the proximal region due to graft-host diameter mismatch, whereas in an end-to-side or side-to-side anastomosed vein graft, eddy blood flow occurs in the distal toe and heel regions due to geometric distortions and curvatures. It has been known that eddy blood flow in these regions is often associated with focal intimal hyperplasia, a pathological event causing vein graft restenosis. [5][6][7][8] Thus, these vein graft models have been used to study the influence of blood flow on vascular remodeling. Recently, the author demonstrated, by using an end-to-end anastomosed vein graft model, that focal intimal hyperplasia and smooth muscle cell (SMC) proliferation were initiated in the proximal region where eddy flow was found. When eddy flow was eliminated by matching the graft-host diameters by using a biomechanical engineering approach, focal intimal hyperplasia and SMC proliferation were significantly prevented. 7 These results further support the role of eddy blood flow in the regulation of intimal hyperplasia and SMC proliferation. However, the mechanisms that link fluid dynamics to focal SMC proliferation remain unclear.Studies using molecular and cellular approaches have demonstrated that growth-related factors regulate cell proliferation. In blood vessels, endothelial cells and SMCs are able to produce and release a number of growth-related factors,

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“…While the neointimal hyperplasia that occurs in all vein grafts helps to achieve mechanical stability in these otherwise thin-walled conduits, it is believed that this neointima serves as the substrate for the development of atherosclerotic disease. In fact, strikingly better long-term patency rates have been achieved when arterial graft conduits devoid of significant neointima are used in bypass surgery (6 (22)(23)(24). Our "arterialized" grafts not only displayed a structural, biochemical, and mechanical similarity to native arteries but also proved resistant to this accelerated vein graft atherosclerosis.…”

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confidence: 99%