Pathogenesis of varicose veins and implications for clinical management

Varicose veins (VVs) classically result from venous hypertension owing to incompetence of the major communications between the superficial and deep veins of the lower extremity. In a significant number of patients, there is no demonstrable truncal saphenous reflux and varicosities are the result of isolated perforating and nonsaphenous vein incompetence. The clinical and histologic features of VVs are the result of disruption of the normal architectural structure of the venous wall as a consequence of remodeling of the extracellular matrix (ECM) in response to increased venous distention and altered hemodynamic shear stress. Although a number of genes, growth factors, proteases, and their inhibitors known to modulate the ECM have been implicated in the pathogenesis of VVs, their etiology remains unknown. The complex variations in venous anatomy in patients with VVs require detailed vein mapping to determine the source and drainage locations of reflux if the rates of residual and recurrent varicosities are to be reduced. The distinct pathogenic mechanisms involved in the development of VVs have important implications for the management of VVs that include a wide spectrum of treatment modalities ranging from reassurance, alternative medicines, conservative management or compression therapy, and surgical or endovascular therapy.