Objective/background: Mechanochemical endovenous ablation (MOCA) has been developed as a tumescentless technique to ablate saphenous veins and to avoid heat induced complications and post-procedural pain. The mechanism of action of MOCA is poorly understood. The present experiments were conducted to determine the effect of MOCA on vein wall injury and sclerosis in an animal model.

Methods: A total of 36 lateral saphenous veins (LSVs) were treated in 18 goats according to the human protocol. Veins from nine goats were evaluated 45 min after the procedure, while in the remaining nine, the treated veins were evaluated 6 weeks later. All treated veins were divided equally over three treatment groups: (i) MOCA, (ii) mechanical ablation without the sclerosant, and (iii) liquid sclerotherapy alone. The histological effects of treatment on the vein wall were systematically evaluated.

Results: The average diameter of the LSV was 4.0 ± 0.5 mm. Technical success was achieved in all but one LSV (35/36; 97%), with a median procedure time of 14 min (range 9-22 min). In the acute group, histological examination showed that mechanical ablation (alone or MOCA) induced severe injury to the endothelium in 82% but no damage to other layers of the vein wall. Mechanical ablation led to vasoconstriction. After 6 weeks follow-up, four of six MOCA treated veins were occluded. The occluded segments consisted mainly of fibrotic lesions probably evolved from organised thrombus. No occlusions were observed after sclerotherapy or mechanical treatment alone. No major complications occurred during procedures or follow-up.

Conclusion: MOCA is associated with an increased occlusion rate compared with its separated components of mechanical ablation or sclerotherapy. The occlusion consists of cellular fibrotic material likely to be evolved from organised thrombus with fibrotic alterations to the surrounding media and adventitia. This study underlines the hypothesis that the additive use of MOCA increases the effectiveness of sclerosants alone by inducing endothelial damage and probably vasoconstriction.

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http://dx.doi.org/10.1016/j.ejvs.2016.11.024DOI Listing

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