Veins carry blood from tissues in the body back to the heart, to be pumped through the lungs, and to be replenished with oxygen and recirculated. When returning from the lower extremities, the veins have to work against gravity to move the blood to the heart. There are many mechanisms in place to assist in this task. Veins have elastic walls. They are also equipped with valves that open to allow blood to move toward the heart and close to prevent backflow.
There are several mechanisms that contribute to the development of varicose veins, including:
· Venous hypertension
· Venous valvular incompetence
· Changes in the vein walls
· Alterations in shear stress
Venous hypertension is high blood pressure in the veins. It is commonly caused by chronic venous reflux or the backflow of blood due to weak vein walls. Obstruction of venous outflow may also contribute to hypertension. In addition to elastic vein walls, and functioning valves, veins need calf muscle function to pump blood from the lower extremities back to the heart. The calf muscle, which is considered the second heart of the body, provides the force needed to push the blood up. Thus, calf muscle failure can also cause venous hypertension.
Venous valvular incompetence
Venous Valvular incompetence or the weakening of vein valves may cause several deleterious changes to vein valves such as deformation, tearing, thinning, and adhesion of the valve leaflets. Valvular incompetence can also cause venous hypertension.
Changes in the Vein Walls
Many changes can contribute to the breakdown of the strength and elasticity of vein walls:
· Overproduction of collagen type I
· Decreased synthesis of collagen type III
· Disrupted smooth muscle cell and elastin fiber arrangement
· Elastin fibers have been observed
· High levels of transforming growth factor β1 and fibroblast growth factor