Stranger in a strange land: The pathogenesis of saphenous vein graft stenosis with emphasis on structural and functional differences between veins and arteries

Cox, Jafna L.; Chiasson, David A.; Gotlieb, Avrum I.

doi:10.1016/0033-0620(91)90019-i

Cited by 310 publications

(231 citation statements)

References 169 publications

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“…During the late period (more than 12 months), atherosclerosis becomes the major reason for graft stenosis and occlusion. As in native coronary arteries, vein graft atheromas can rupture and cause thrombotic occlusion of the graft (1). Vein graft atheromas are more diffuse and concentric, less calcified and have poorly developed or absent fibrous caps (2).…”

Section: Pathogenesis and Models Of Vein Graft Diseasementioning

confidence: 99%

Coronary vein graft disease: Pathogenesis and prevention

Parang

Arora

2009

Canadian Journal of Cardiology

152

109

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Section: Pathogenesis and Models Of Vein Graft Diseasementioning

confidence: 99%

Coronary vein graft disease: Pathogenesis and prevention

Parang

Arora

2009

Canadian Journal of Cardiology

152

109

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“…Lumenal narrowing and superimposition of atheroma on the thickened intima promote thrombotic occlusion and hence account for the poor patency rates observed. [3][4][5] The matrix metalloproteinases (MMPs) have the ability to degrade all components of the basement membrane and the interstitial matrix. 6 Increased proteolysis by MMPs has been associated with cancer cell invasion, rheumatoid arthritis and more recently with the neointima formation that characterises vascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Gene transfer of tissue inhibitor of metalloproteinase-2 inhibits metalloproteinase activity and neointima formation in human saphenous veins

et al. 1998

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Metalloproteinases (MMPs) are implicated in neointima for-21.8 ± 2.9 ng/mg wet weight/day (P Ͻ 0.05, n = 3). In situ mation and hence vein graft failure. Gene transfer to elevzymography revealed a marked inhibition of gelatinolytic ate local levels of tissue inhibitor of metalloproteinases activity by TIMP-2 gene transfer throughout the vein seg-(TIMPs) is therefore a potential treatment. In this study, we ments. Neointima formation and neointimal cell numbers have used lumenal application of a replication-defective were reduced 79% and 71%, respectively (P Ͻ 0.05; recombinant adenovirus to overexpress TIMP-2 and n = 8). TIMP-2 overexpression had no effect on smooth observe the effects on neointimal thickening in a well muscle cell proliferation, secretion of pro-MMP-2 or -9 and characterised human saphenous vein organ culture model.did not inhibit the processing of pro-MMP-2 to its active Increased TIMP-2 expression was localised to lumenal form. Our data indicate that TIMP-2 overexpression surface cells but nevertheless increased total functional reduces neointimal thickening, primarily by inhibiting MMP TIMP-2 secretion after 14 days culture from 4.0 ± 2.0 to activity and hence smooth muscle cell migration.

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“…However, the process of AVF maturation is complex and remains poorly understood despite numerous studies looking into the pathophysiology of the process and biomechanical factors associated with maturation. Intimal hyperplasia (IH) has been identified as the main reason behind non-maturation in the newly formed arteriovenous conduit, it is the process of cellular proliferation within the inner most layer of the vessel resulting in remodelling of both the arterial and venous ends of the new fistula [35][36][37]; however factors influencing this process are yet to be fully elucidated.…”

Section: Discussionmentioning

confidence: 99%