Genetic Biomarkers in Chronic Venous Disease

Abstract

Chronic venous disease (CVD) is a very common clinical syndrome affecting up to 80% of the western world. CVD involves primarily peripheral vein circulation of lower limbs with the onset of venous reflux. In healthy subjects, in the erect position, the blood column in the lower limbs shows a venous pressure of 90-100 mmHg at the ankle, and the lower limbs veins are endowed with means to deal with this hydrostatic pressure in order to avoid blood pooling in the legs. Therefore, bicuspid valves are located along the superficial and profound veins, to enable a unidirectional blood flow toward the heart and prevent blood return down to the lower limb segments. In particular, the valves work in harmony with venous muscle pumps, mainly in the calf as well in the foot and thigh, to permit blood return to the heart against gravity. Venous reflux is seen when valves damage or impairment occurs determining venous hemodynamic dysfunction. Valvular reflux leads to an elevation in ambulatory venous pressure and a number of clinical pathologic events such as varicose veins, lower limbs edema, pain, itching, skin changes and venous ulceration (VU). Varicose veins are the main clinical manifestation of CVD happening in a quarter to a third of the Western adult population Several studies have proposed a familiar transmission in the cause of varicose veins that can be due also to genetic factors [14,16-21].

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