Platelet reactivity in chronic venous insufficiency

Clin Lab. 2011;57(7-8):527-34.

Abstract

Background: Chronic venous insufficiency (CVI) is a common medical problem that may result in significant morbidity and mortality. Platelets are key players in haemostasis and thrombosis, but their role in the development of venous thrombosis is more controversial.

Aim: The purpose of this study was to investigate platelet properties in CVI and their interaction with the venular endothelium.

Methods: Human peripheral venules were explanted during leg surgery of patients with CVI and of healthy subjects (C); concurrently, the platelets were isolated from blood samples collected. The techniques used were: fluorescence and electron microscopy and Western-blotting.

Results: Compared with the C group, the platelets of patients with CVI are activated, as demonstrated by: (i) cellular modifications, such as alteration of the discoidal shape by the development of extended cytoplasmic filopodia and changes of the cells normal ultrastructure, (ii) biochemical modifications, such as the enhanced protein levels of FAK, p85 PI3K, Akt and src, accounting for activation of alphaIIbbeta3 outside-in signaling, and (iii) apparent higher adhesion to the venular endothelium. We demonstrate in addition, that CVI is accompanied by severe modifications of the ultrastructure of the cells within the venular wall.

Conclusions: In CVI, platelets circulate in an activated state and may contribute to the altered dysfunctional response of the venous wall and to the development of this pathology.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blood Coagulation Tests
  • Blood Platelets / physiology
  • Blood Platelets / ultrastructure
  • Blotting, Western
  • Cell Shape
  • Endothelium, Vascular / pathology
  • Female
  • Humans
  • Male
  • Microscopy, Electron
  • Microscopy, Fluorescence
  • Middle Aged
  • Platelet Activation*
  • Platelet Adhesiveness
  • Protein Kinases / blood
  • Signal Transduction
  • Thrombophilia / etiology*
  • Vasculitis / blood
  • Vasculitis / complications
  • Venous Insufficiency / blood*
  • Venous Insufficiency / complications
  • Venous Insufficiency / physiopathology
  • Venules

Substances

  • Protein Kinases