ABSTRACT
This chapter discusses the pathogenesis and pathophysiology of varicose vein formation and the molecular regulation of inflammatory damage to the lower extremity dermis caused by persistent ambulatory venous hypertension. Venous reflux is observed when valvular destruction or dysfunction occurs in association with varicose vein formation. Vein wall remodeling has been consistently observed in histologic varicose vein specimens. Chronic venous insufficiency (CVI) is the seventh leading cause of chronic debilitating disease in the United States. The chronicity of CVI and lack of effective treatment modalities place a heavy burden on the healthcare system, underscoring the need for more extensive CVI-related research. Numerous investigations have attempted to evaluate the microcirculation of patients with CVI. Patients with eczematous skin changes may have an autoimmune component to their CVI, whereas patients with dermal fibrosis may reflect changes that are consistent with chronic inflammation and altered tissue remodeling.
