Varicose veins were identified in early history, and a treatment was recorded about 400 A.D.1 The cause of varicose veins has been discussed for years. They are known to be common (about 30% of people will have them at some point during their lives), but it has been said that they have “no specific cause.”2 In a study published in 2004, Carpentier et al3 stated that the “number one risk factor for the development of varicosities is a first-degree relative with the disease.” However, newer research has shed light on the possible mechanisms causing varicose veins, suggesting there may be multiple factors contributing to their development.4,5
Varicose veins are defined as segments of the superficial venous system of the lower extremities that are “ectatic and tortuous.”5 Interestingly, varicose veins are not one long vein of damaged tissue; there are areas where the vessel is tortuous and diseased while other segments appear normal. The problem is that the valves in the veins become non-functional, allowing venous reflux and venous hypertension in the extremity. This predisposes the patient to develop superficial venous thrombosis, venous thromboembolic disease, edema, lymphedema, and venous ulcers.6 The question that begs answering is whether the venous hypertension is due to damaged venous valves and subsequent venous reflux or does vein wall damage cause venous dilatation and subsequent insufficient valves? Interestingly, there is evidence for both problems.
The literature does show patients with varicosities actually have fewer venous valves than patients without varicosities.7 It has been found that there may be a defect in the area of the valve attachment to the vein wall, which allows the vein wall distal to the valve itself to dilate. This pulls the leaflets apart, resulting in valve insufficiency.5 There are also specific gene defects that predispose to venous valve development and valve failure causing reflux.8,9
Vein wall problems have long been considered the primary problem causing varicose vein formation. There are numerous problems occurring in the vein wall due to a chronic inflammatory reaction. In varicosities there are abnormalities in collagen and elastin content and metabolism. These vessels have decreased extracellular matrix and disruption and abnormalities of the smooth muscle cell layers. Endothelial cell dysfunction, excess protease production in the vessel wall, increased inflammatory cytokine levels in the vessel wall, and an accumulation of inflammatory cells in the vessel wall all contribute to damage to the vessel wall.4,5 This microvascular damage could be the main underlying cause of the development of varicose veins. If it is not the main cause, it is a major contributing factor.
Varicose veins and the complications they cause are a major health problem. It is promising to see researchers and clinicians trying to understand the underlying etiology. Hopefully, this will lead to treatments that can result in prevention of these abnormal vessels—then no longer will anyone have to wonder how they got those “very close veins.”