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The Morphofunctional Changes in the Wall of Varicose Veins

Jeļena Birdina1, Māra Pilmane2, Artūrs Ligers1

  • 1Department of Morphology, Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia.

Annals of Vascular Surgery
|March 17, 2017
PubMed

Insights

Varicose veins show damaged smooth muscle and altered basement membranes, indicating significant blood vessel remodeling. These histological changes in great saphenous veins are linked to chronic venous insufficiency.

Area of Science:

  • Vascular Biology
  • Histopathology
  • Venous Disease Research

Background:

  • Varicose vein (VV) disease is a common lower extremity pathology.
  • Chronic venous insufficiency stems from venous hypertension and venous wall changes.
  • The precise pathogenesis of varicosity remains incompletely understood.

Purpose of the Study:

  • To investigate the histological and immunohistochemical alterations in great saphenous veins (GSVs) of patients with chronic venous insufficiency.

Main Methods:

  • Histopathological analysis of GSV tissues from 20 varicose vein patients and 4 control subjects.
  • Immunohistochemical staining for vascular endothelial growth factor (VEGF), adhesion molecules (ICAM-1, VCAM-1), PGP 9.5, collagen type IV, laminin, and fibronectin.
  • Semiquantitative evaluation of stained tissue sections.

Main Results:

  • Varicose veins exhibited damaged endothelium, disorganized smooth muscle, increased vasa vasorum, and neoangiogenesis compared to normal veins.
  • Significant differences were observed in PGP 9.5 positive structures and subendothelial laminin.
  • A trend towards increased VEGF and decreased collagen IV was noted, though not statistically significant for all markers.

Conclusions:

  • Varicose GSVs demonstrate disrupted basement membrane integrity, smooth muscle disorganization, and active neoangiogenesis, indicative of vascular remodeling.
  • Alterations in PGP 9.5 innervation and extracellular matrix components like laminin and collagen IV confirm the remodeling of damaged vessels.
Abstract

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