Abstract

Chronic venous disorders are common vascular pathology of great medical and socioeconomic impact, characterized by a wide spectrum of clinical manifestations occurring with symptoms and/or signs that vary in type and severity. The predominant pathophysiological mechanisms of chronic venous disease start from the development of venous hypertension from shear stress and reflux, leading to endothelial dysfunction and venous wall dilatation. The altered hemodynamic transduces physical signals into harmful bio-molecular pathways, creating a vicious cycle among shear stress, proteolytic remodeling, and inflammatory processes. This intricate network is further exacerbated by the degradation of protective endothelial glycocalyx. In this special issue, at least three main aspects of these interactions are highlighted: the dangerous, the good, and the diverse, which may help to focus attention on the biomolecular mechanisms and the possible targeted therapy of chronic venous disorders (CVeD).

Highlights

  • Chronic venous disorders (CVeD) are common lower extremity vascular pathologies of great medical and socioeconomic impact (1–2.5% of health care budgets in developed countries), affecting a large part of the population worldwide and significantly decreasing the quality of life of affected patients [1].CVeD represents the sequelae of a general venous insufficiency that spans a wide spectrum of clinical manifestations from varicose veins to edema to skin changes to the development of venous ulceration

  • Venous diseases include clinically deteriorating conditions with morphological and functional alterations of the venous system, which occur with symptoms and/or signs that vary in type and severity as highlighted by the clinical, aetiological, anatomical, and pathological (CEAP) international classification [2]

  • The changes in hemodynamics are transmitted to the microcirculation, to endothelial cells and vessel microenvironment leading to venous microangiopathy, with dilation and tortuosity of capillary beds [3]

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Summary

Introduction

Chronic venous disorders (CVeD) are common lower extremity vascular pathologies of great medical and socioeconomic impact (1–2.5% of health care budgets in developed countries), affecting a large part of the population worldwide (prevalence as high as 73% in women and 56% in men) and significantly decreasing the quality of life of affected patients [1]. The mechano-sensors of endothelial cells, triggered by the altered hemodynamic, transduce physical signals into harmful bio-molecular pathways resulting in endothelial damages These complex biological processes activate inflammatory and proteolytic cascades in the vascular microenvironment, including leukocyte adhesion, degranulation, and release of cytoplasmic granules from neutrophils, macrophages, mastocytes, endothelial cells, and platelets [4]. All these steps lead to the formation of a deleterious network and a vicious cycle impairing microand macro-circulatory flow, creating an environment that causes remodeling of the vein walls and valves, venous hypertension, formation of varicosities, edema, and leg ulceration [3,5]. Through original research articles and reviews improving our knowledge on the pathophysiology of CVeD, at least three main aspects of these interactions are highlighted: the dangerous, the good, and the diverse, which may help to focus attention on the biomolecular mechanisms and the possible targeted therapy of CVeD

The Dangerous
The Diverse
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