Varicose veins are caused by a combination of genetic and environmental factors that ultimately lead to venous dysfunction. Normally, healthy veins return blood to the heart with the help of skeletal muscle pumps (which are activated during muscle contraction) and one-way valves (which prevent blood from flowing backward).[1]
In people with varicose veins, these mechanisms do not work properly, often due to high blood pressure, insufficient one-way valve function, or structural/functional changes to the walls of the veins. Consequently, blood begins to flow backwards (venous reflux), increasing venous blood pressure. Over time, this leads to weaker blood vessel walls, dilated (stretched) blood vessels, and dysfunctional one-way valves. The result is the appearance of large, discolored, and twisting veins in the lower extremities.
High blood pressure and altered blood flow patterns in the veins also elevate levels of inflammatory cytokines, lymphocytes, neutrophils, monocytes, macrophages, and other growth factors, which further contribute to venous remodeling and structural damage.[2] All of these processes are enhanced in the presence of risk factors, such as obesity, pregnancy, tall height, a family history of varicose veins, age, smoking, and occupations that require prolonged standing or sitting.[2]
References
- ^Chwała M, Szczeklik W, Szczeklik M, Aleksiejew-Kleszczyński T, Jagielska-Chwała MVaricose veins of lower extremities, hemodynamics and treatment methods.Adv Clin Exp Med.(2015)
- ^Gregory PiazzaVaricose veinsCirculation.(2014 Aug 12)