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Mechanisms of Lower Extremity Vein Dysfunction in Chronic Venous Disease and Implications in Management of Varicose Veins. | LitMetric

Mechanisms of Lower Extremity Vein Dysfunction in Chronic Venous Disease and Implications in Management of Varicose Veins.

Vessel Plus

Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA.

Published: May 2021

AI Article Synopsis

  • - Chronic venous disease (CVD) affects the veins in the legs, often showing up as varicose veins (VVs) which can progress to chronic venous insufficiency (CVI) and even lead to venous leg ulcers (VLUs) if left untreated.
  • - Various factors contribute to the development of CVD, including genetic predispositions, lifestyle choices like obesity and sedentary behavior, and changes in the expression and activity of matrix metalloproteinases (MMPs) that affect the structural integrity of veins.
  • - Treatment options for CVD typically involve compression stockings, sclerotherapy, and surgery, with newer therapies being investigated, including the use of venotonics and inhibitors of MMP

Article Abstract

Chronic venous disease (CVD) is a common venous disorder of the lower extremities. CVD can be manifested as varicose veins (VVs), with dilated and tortuous veins, dysfunctional valves and venous reflux. If not adequately treated, VVs could progress to chronic venous insufficiency (CVI) and lead to venous leg ulcer (VLU). Predisposing familial and genetic factors have been implicated in CVD. Additional environmental, behavioral and dietary factors including sedentary lifestyle and obesity may also contribute to CVD. Alterations in the mRNA expression, protein levels and proteolytic activity of matrix metalloproteinases (MMPs) have been detected in VVs and VLU. MMP expression/activity can be modulated by venous hydrostatic pressure, hypoxia, tissue metabolites, and inflammation. MMPs in turn increase proteolysis of different protein substrates in the extracellular matrix particularly collagen and elastin, leading to weakening of the vein wall. MMPs could also promote venous dilation by increasing the release of endothelium-derived vasodilators and activating potassium channels, leading to smooth muscle hyperpolarization and relaxation. Depending on VVs severity, management usually includes compression stockings, sclerotherapy and surgical removal. Venotonics have also been promoted to decrease the progression of VVs. Sulodexide has also shown benefits in VLU and CVI, and recent data suggest that it could improve venous smooth muscle contraction. Other lines of treatment including induction of endogenous tissue inhibitors of metalloproteinases (TIMPs) and administration of exogenous synthetic inhibitors of MMPs are being explored, and could provide alternative strategies in the treatment of CVD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8270011PMC
http://dx.doi.org/10.20517/2574-1209.2021.16DOI Listing

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