Veränderungen der extrazellulären Matrix in der varikösen Venenwand

Kirsch, D.; Schreiber, Jenny; Dienes, Hans‐Peter; Böttger, Th.; Junginger, T

doi:10.1024/0301-1526.28.2.95

Cited by 11 publications

(5 citation statements)

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“…Indirect biochemical studies have demonstrated a decrease in the elastin content of the affected vein wall [8, 9, 17, 18, 19, 20, 21]. Recently Kirsch et al [22], who examined the structure and arrangement of elastic fibers in the varicose condition, found an increase in these during the initial stages of disease. However, as disease progressed, a reduction and fragmentation of fibers was observed, thus explaining the rigidity of the varicose vein wall compared to the walls of healthy veins.…”

Section: Discussionmentioning

confidence: 99%

Expression of Elastic Components in Healthy and Varicose Veins

et al. 2003

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This study evaluates possible changes in the synthesis/degradation of elastic components of the vein wall in an attempt to explain the development of varicosis. Healthy and varicose saphenous veins were subjected to immunohistochemical analysis using anti-elastin, anti-fibrillin-1, anti-elastase, anti-transforming growth factor (TGF)-beta and anti-latent TGFbeta binding protein (LTBP)-2 monoclonal antibodies. In situ hybridization was performed using specific probes for tropoelastin and fibrillin-1. In healthy veins, elastin and fibrillin-1 showed even, overlapping distribution patterns indicating their particular abundance in the adventitia and at the intima/media interface. The expression of tropoelastin and fibrillin-1 was high in smooth muscle cells bordering the elastic laminae. Elastin, fibrillin-1, and cells expressing fibrillin-1 and tropoelastin mRNA showed a patchy disorganized pattern, particularly in the proximal varicose segments of patients under 50 years of age. Enhanced elastase activity was noted in both control and varicose specimens from elderly subjects. Varicose veins specimens showed greater LTBP-2 and TGF expression. Both molecules were detected in the subendothelium and the media, particularly in areas of marked injury. Our findings suggest that the development of the varicose condition involves a restructuring of the elastic component of the vein wall, perhaps as a consequence of changes in the transcription mechanisms of muscle layer cells.

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Section: Discussionmentioning

confidence: 99%

Expression of Elastic Components in Healthy and Varicose Veins

et al. 2003

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“…The abnormal wall structure of varicose veins, with increased fiber propagation parallel to the enlargement of the vessel wall, decreased mechanical properties, and variations in lumen diameter, can lead to hemodynamic disturbance, turbulence, aneurysm development, and increased long-term risk of thrombosis, embolization, and rupture when exposed to arterial pressure. 16,17 Even long-term functioning normal vein grafts have been found to be at significant risk of aneurysmal degeneration. 18,19…”

Section: Discussionmentioning

confidence: 99%

Reinforced Long Saphenous Vein Bypass Graft for Infrainguinal Reconstruction Procedures: Case Series and Literature Review

et al. 2006

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Poor rehabilitation rates and the high-cost of managing postamputation patients justify an aggressive revascularization policy in critical lower limb ischemia. Endovascular therapy is our first choice for limb salvage in these patients. However there are patients for whom endovascular therapy is not feasible. When bypass is necessary, autologous vein is a superior conduit to synthetic material. However, varicosities usually contraindicate autologous vein bypass because of the risk of aneurysm formation, rupture and increased intimal hyperplasia compared with nonvaricose venous grafts. We report the use of varicosed long saphenous vein (LSV) with external Dacron support in infrainguinal bypass procedures for limb salvage, where endovascular therapy was not feasible. The external Dacron tube was not brought close to the distal anastomotic area itself. With a mean follow-up of 18 months, duplex ultrasonography and computed tomography angiography showed no evidence of stenosis of the reinforced vein segments or aneurysmal degeneration of the residual vein. External reinforcement with Dacron prosthesis allows the use of autogenous greater saphenous veins with varicose dilatation without compromising graft patency and limb salvage.

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“…Furthermore, collagen fibrils enter the area between the muscle fibers in the media layer, thereby disturbing the circular order of muscles (19,20). There is a decrease in the elastin fibers (10,18,21) and a fragmentation in the internal elastic lamina (13,18,20). However, there is an increase in other matrix proteins fibronectin, laminin and tenascin (18).…”

Section: Introductionmentioning

confidence: 98%

“…Although there are findings that show a decreased amount of collagen (7,8), the amount of collagen generally increases (9)(10)(11)(12)(13)(14)(15) and this situation is even observed in cellular cultures (15)(16)(17). The increase in collagen occurs both in the intima (13) and in the media (12,18). Furthermore, collagen fibrils enter the area between the muscle fibers in the media layer, thereby disturbing the circular order of muscles (19,20).…”

Section: Introductionmentioning

confidence: 99%

“…There is a decrease in the elastin fibers (10,18,21) and a fragmentation in the internal elastic lamina (13,18,20). However, there is an increase in other matrix proteins fibronectin, laminin and tenascin (18). The changes in the mentioned matrix proteins were examined as per the Hach stages; however, no statistical difference could be identified (22).…”

Section: Introductionmentioning

confidence: 99%

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Does extracellular matrix of the varicose vein wall change according to clinical stage?

Demirkıran¹,

Köksoy

Heper

et al. 2014

UCD

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Objective:The etiology and pathophysiology of chronic venous disease is not fully understood. This study aimed to determine the variation of the extracellular matrix proteins in varicose vein wall according to clinical stage. Material and Methods:Forty varicose and 10 control veins were sampled from the saphenofemoral junction. The Clinical Etiologic Anatomic Pathophysiologic (CEAP) classification was used in patients with varicose veins. Samples were stained with hematoxylin-eosin, Masson's trichrome, EVG (Elastica-van Gieson) stain and with laminin, fibronectin, tenascin antibodies. Stained samples were examined immuno-histochemically. Changes in extracellular matrix were determined semi-quantitatively using light microscopy. Results:It was observed that in the early stages (C2-C3) of chronic venous disease, fibrosis is increased in the intima and media layers, with fragmentation in lamina elastica interna, and increased tenascin expression in the intima layer. In advanced stages (C4-C6), the accumulation of tenascin in the intima continued along with fibrosis in the media layer, the thickness of the media layer increased and fibronectin deposition was observed. Conclusion:This study showed that changes first occur in the intima during the early stages of the disease with addition of alterations in the media layer at later stages.

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Veränderungen der extrazellulären Matrix in der varikösen Venenwand

Cited by 11 publications

References 0 publications

Expression of Elastic Components in Healthy and Varicose Veins

Expression of Elastic Components in Healthy and Varicose Veins

Reinforced Long Saphenous Vein Bypass Graft for Infrainguinal Reconstruction Procedures: Case Series and Literature Review

Does extracellular matrix of the varicose vein wall change according to clinical stage?

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