Impact of a New Maneuver on Foam Sclerotherapy for the Treatment of Large Varices With a One-step Approach in Combined EVLA/UGFS Techniques

degradation, monocyte infiltration, disruption of redox balance with elevated reactive oxygen and nitrogen species, leading to skin changes and venous ulcers.The expression of proinflammatory cytokines, enzymes, proteinases, and adhesion molecules are upregulated during these processes.Upstream to the reactions within the vein wall, epigenetics plays a large role in the development of CVD.Thus, we performed a scoping review to provide information on the genetic underpinnings of CVD.Methods: We performed a comprehensive search of the English literature in PUBMED, MEDLINE, and Web of Science on genetic studies and reviews in humans on CEAP 2-6 (excluded VTE, DVT, PE) diseases including GWAS, linkage, gene expression, Mendelian genetics, pathway analysis, candidate gene approach studies, micro RNA, metabolic profiling, non-coding RNA, and population/epidemiologic studies (Fig 1).The literature reviewed was extracted for data on study methods, materials, topic category, findings, and genes of interest and divided this by topic, ensuring a thorough and reliable research process.Results: Of the 247 identified studies, a diverse range of results covering various aspects related to CVD was identified (Table ).This included target genes that may connect with pathology or findings associated with disease process/vascular biology.Other areas included agnostic genetic findings, collagen/skeletal biology, congenital diseases, epigenetic modulation, predisposing risk factors, aging, congenital disease, and venous leg ulcers.Conclusions: There is a wide range of findings regarding CVD-associated genes, SNPs, metabolic and molecular expressions, and pathways.Having performed a comprehensive and inclusive review, our findings demonstrated a diversity in the results among studies and highlight the underlying pathology of CVD as a complex interplay of genetics and epigenetics.