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The great saphenous vein (GSV) is the longest superficial vein in the human body, extending from the foot to the groin [8, 10]. Its primary biological function is to return deoxygenated blood from the lower limbs to the deep venous system via the femoral vein, a process supported by one-way valves that prevent retrograde flow [10, 12]. Pathologically, the GSV is the most common site for the development of varicose veins and chronic venous insufficiency, typically resulting from valvular incompetence and venous reflux [1, 12]. While the GSV is an anatomical structure rather than a molecular target, it is the primary focus of surgical and endovascular interventions such as stripping, laser ablation, and sclerotherapy [10, 13, 14]. Pharmacological treatments targeting GSV-related conditions include venoactive drugs like micronized purified flavonoid fraction (MPFF) and sulodexide, which improve venous tone and reduce inflammation [2, 3, 5]. Additionally, the GSV is frequently harvested as a vascular conduit for coronary artery bypass grafting (CABG) and peripheral revascularization [1, 11, 13].
Sclerosing agents and medical adhesives induce endothelial damage or physical occlusion to close the vein lumen; venoactive drugs enhance venous tone and reduce capillary permeability and inflammation.
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