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Updated: Jan 5, 2026

Occlusion of the Great and Small Saphenous Vein Using Copolymeric Glue Based on N-Butyl Cyanoacrylate and Methacryloxy Sulfolane
Published on: December 9, 2022
[Venous wall weackness pathogenesis in varicose vein disease]
V V Studennikova1, L O Severgina1, G V Sinyavin1
1Sechenov First Moscow State Medical University, Ministry of Health of the Russia, Moscow, Russia.
Abstract:
Varicose veins of lower extremities, varicocele and varicose dilation of pelvic veins including ovaricovaricocele are the most common non-inflammatory diseases of venous system. The same mechanisms determined varicose dilatation regardless localization of the vein. First of all, these are wall weakness and valvular insufficiency combined with hereditary collagen fiber defectiveness in case of undifferentiated connective tissue syndrome. Imbalance between different types of collagen in vascular wall (especially types I and III) also results wall weakness. Other important mechanisms are smooth muscle cells dysfunction followed by excessive intracellular synthesis and intramuscular fibrosis and imbalance of protease system due to overproduction of metalloproteinases. We consider that different forms of varicose veins (varicose veins of lower extremities, varicocele, ovaricovaricocele) may be unified within one pathology (varicose vein disease).
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