ABSTRACT
It is generally agreed that varicose veins afflict from 40 to 60% of women and 15 to 30% of men. Therefore, it is surprising that the etiology and development of this common problem remain obscure.
Actually, in Western populations the incidence of varicose veins varies with the definition applied. Most investigators favor the definition of Arnoldi,[1] who said that varicosities are “any dilated, elongated, or tortuous veins, irrespective of size.” Thus, some epidemiologic studies would include telangiectasias and reticular veins, while others would exclude these entities. The definition of Arnoldi is particularly useful because it presents a unifying concept for reticular varicosities, telangiectasias, and major varicose veins. Since all three are elongated, dilated, and have incompetent valves, they probably have a common origin and respond to the same physical forces and acquired influences. The dilation and elongation implies that these abnormal veins have been responsive to effects of pressure. The causes and results of venous valve dysfunction are more subtle. They might be explained simply by the dilation of a vein and valve annulus, which stretches beyond the capability of its leaflets to close together. However, such a simplistic view does not explain the disappearance, perforation, and splitting of valves noted by several authorities or the stunted valves observed angioscopically in refluxing vein segments.
