Mechanochemical ablation causes endothelial and medial damage to the vein wall resulting in deeper penetration of sclerosant compared with sclerotherapy alone in extrafascial great saphenous vein using an ex vivo model

2017 
Abstract Background Nonthermal, tumescentless devices are the next generation of minimally invasive devices to treat varicose veins. We aimed to investigate the effects of mechanochemical ablation (MOCA) using ClariVein (Vascular Insights, Quincy, Mass) on ex vivo great saphenous vein with histology and immunofluorescent staining. Methods Extrafascial great saphenous veins were harvested during surgery for varicose veins and were treated ex vivo for 10 to 11 minutes with either liquid sclerotherapy or the use of ClariVein, with and without 3% sodium tetradecyl sulfate. Veins were sectioned and subjected to hematoxylin and eosin staining and immunofluorescent staining for endothelial and smooth muscle cell markers (CD31 and α-actin) to assess overall damage and cell death in the vein wall compared with control sections. Results Histologic observations confirmed intimal damage from ClariVein, as has been previously shown; however, medial damage was also evident, which was not observed in control or liquid sclerotherapy sections. Immunofluorescent staining in the three sections studied showed a 42% decrease in CD31 staining and 27% mean reduction in α-actin staining up to a depth of 300 μm with liquid sclerotherapy. This cytotoxic effect was significantly enhanced by MOCA with a reduction in CD31 staining just above 60% and a 46% mean decrease in α-actin staining noted up to a depth of 300 μm. Far greater reductions in staining compared with sclerotherapy were observed up to a depth of 600 μm. Conclusions MOCA using 3% sodium tetradecyl sulfate increases the penetration of the sclerosant and its effect into the vein wall and shows superior rates of tissue destruction compared with liquid sclerotherapy alone. In this model, it appears not solely to damage the endothelium but also to shear the medial layer, creating small lesions into which sclerosant can flow and exert its cytotoxic effect.
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