Changes in the extracellular matrix of the vein wall - The cause of primary varicosis?

Citation
D. Kirsch et al., Changes in the extracellular matrix of the vein wall - The cause of primary varicosis?, VASA, 29(3), 2000, pp. 173-177
Citations number
19
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
VASA-JOURNAL OF VASCULAR DISEASES
ISSN journal
03011526 → ACNP
Volume
29
Issue
3
Year of publication
2000
Pages
173 - 177
Database
ISI
SICI code
0301-1526(200007)29:3<173:CITEMO>2.0.ZU;2-W
Abstract
Background: Conflicting theories on the development of primary varicosis ha ve led to the molecular biological investigation of the vein wall or, more accurately, of the extracellular matrix. It was the aim of this study to qu antify matrix expression and to compare pathological changes in the vein wa ll with valve-orientated staging of varicosis, in order to determine indica tors of the primary cause of varicosis. Materials and methods: Three hundred seventy-two tissue specimens of greate r saphenous veins were obtained from 17 patients with varicosities and cate gorised according to Hach stage and procurement site. The specimens were co mpared with 36 specimens collected from six patients without varicosities, incubated with fluorescence-stained antibodies for collagen 4, laminin, fib ronectin and tenascin prior to being assessed with confocal laser scan micr oscopy. In addition, 22 vein specimens (16 varicose, 6 normal veins) servin g as negative controls were investigated. Results: Image analysis and statistical evaluation showed that compared wit h normal veins, varicose veins are associated with a significant increase i n matrix protein expression for collagen 4, laminin and tenascin. A trend t owards an increase in matrix expression was further observed for fibronecti n. There was, however, no difference between varicose veins and clinically healthy vein segments inferior to a varicose segment. Conclusion: If the findings of the present investigation can be confirmed b y other studies, alterations in the vein wall may be regarded as the primar y cause of varicosis and valvular insufficiency as the result of these chan ges.