Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class
The aim of this review is to provide a clear understanding of the pathophysiological mechanisms of chronic venous disease (CVD) at different clinical stages and the possible role of these mechanisms in the development of symptoms in C0s clinical class of the Clinical, Etiologic, Anatomic, and Pathop...
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doaj-e34dc0da01f2462d93def80179f16d952021-07-27T04:51:20ZengWolters Kluwer Medknow PublicationsVascular Investigation and Therapy2589-96862589-94812018-01-011310310910.4103/VIT.VIT_2_19Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical classAndrew NicolaidesEliete BouskelaThe aim of this review is to provide a clear understanding of the pathophysiological mechanisms of chronic venous disease (CVD) at different clinical stages and the possible role of these mechanisms in the development of symptoms in C0s clinical class of the Clinical, Etiologic, Anatomic, and Pathophysiologic classification, which consists of symptomatic patients without any visible or palpable signs of venous disease. The prevalence of C0s class in several epidemiological studies varies between 13% and 23% of the general population. Wall remodeling and valve destruction due to white cell endothelial interaction is the main cause of primary varicose veins, while deep vein thrombosis produces secondary changes leading to the postthrombotic syndrome. The underlying mechanism of the skin changes and ulceration is venous hypertension, which is transmitted to the skin microcirculation. Over the last 10 years, an improved videocapillaroscopic technique, the orthogonal polarization spectral imaging technique demonstrated that quantitative measurements in the skin microcirculation are progressively altered from C1 to C6 patients and that values in CVD patients are significantly different from healthy individuals (P < 0.05): capillary diameter increases and capillary morphology worsens from C2 to C5; diameter of the dermal papilla and diameter of the capillary bulk increase from C3 to C5; and functional capillary density (FCD) decreases from C4 to C5. In addition, significant changes have been shown between C0a and C0s patients despite the presence of normal conventional duplex scans in the latter: a decrease of FCD and an increase in the diameter of the dermal papilla. Functional abnormalities found to be present in C0s patients by recent studies include increased compliance of the venous wall (hypotonic phlebopathy), dilatation of deep veins in the calf producing an abnormally increased venous volume, reduction in emptying of venous reservoir, reduction in the venoarteriolar response on standing, and blood reflux in small venules despite a normal conventional duplex scan. However, most of the studies are small, and their findings need to be confirmed by larger series. It remains to be seen whether functional changes and microcirculatory changes respond to venoactive medications in parallel to the relief of symptoms.http://www.vitonline.org/article.asp?issn=2589-9686;year=2018;volume=1;issue=3;spage=103;epage=109;aulast=Nicolaideschronic venous diseasemicrocirculationvenous wall remodeling |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Andrew Nicolaides Eliete Bouskela |
spellingShingle |
Andrew Nicolaides Eliete Bouskela Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class Vascular Investigation and Therapy chronic venous disease microcirculation venous wall remodeling |
author_facet |
Andrew Nicolaides Eliete Bouskela |
author_sort |
Andrew Nicolaides |
title |
Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class |
title_short |
Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class |
title_full |
Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class |
title_fullStr |
Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class |
title_full_unstemmed |
Pathophysiological mechanisms of chronic venous disease and their role in C0s clinical class |
title_sort |
pathophysiological mechanisms of chronic venous disease and their role in c0s clinical class |
publisher |
Wolters Kluwer Medknow Publications |
series |
Vascular Investigation and Therapy |
issn |
2589-9686 2589-9481 |
publishDate |
2018-01-01 |
description |
The aim of this review is to provide a clear understanding of the pathophysiological mechanisms of chronic venous disease (CVD) at different clinical stages and the possible role of these mechanisms in the development of symptoms in C0s clinical class of the Clinical, Etiologic, Anatomic, and Pathophysiologic classification, which consists of symptomatic patients without any visible or palpable signs of venous disease. The prevalence of C0s class in several epidemiological studies varies between 13% and 23% of the general population. Wall remodeling and valve destruction due to white cell endothelial interaction is the main cause of primary varicose veins, while deep vein thrombosis produces secondary changes leading to the postthrombotic syndrome. The underlying mechanism of the skin changes and ulceration is venous hypertension, which is transmitted to the skin microcirculation. Over the last 10 years, an improved videocapillaroscopic technique, the orthogonal polarization spectral imaging technique demonstrated that quantitative measurements in the skin microcirculation are progressively altered from C1 to C6 patients and that values in CVD patients are significantly different from healthy individuals (P < 0.05): capillary diameter increases and capillary morphology worsens from C2 to C5; diameter of the dermal papilla and diameter of the capillary bulk increase from C3 to C5; and functional capillary density (FCD) decreases from C4 to C5. In addition, significant changes have been shown between C0a and C0s patients despite the presence of normal conventional duplex scans in the latter: a decrease of FCD and an increase in the diameter of the dermal papilla. Functional abnormalities found to be present in C0s patients by recent studies include increased compliance of the venous wall (hypotonic phlebopathy), dilatation of deep veins in the calf producing an abnormally increased venous volume, reduction in emptying of venous reservoir, reduction in the venoarteriolar response on standing, and blood reflux in small venules despite a normal conventional duplex scan. However, most of the studies are small, and their findings need to be confirmed by larger series. It remains to be seen whether functional changes and microcirculatory changes respond to venoactive medications in parallel to the relief of symptoms. |
topic |
chronic venous disease microcirculation venous wall remodeling |
url |
http://www.vitonline.org/article.asp?issn=2589-9686;year=2018;volume=1;issue=3;spage=103;epage=109;aulast=Nicolaides |
work_keys_str_mv |
AT andrewnicolaides pathophysiologicalmechanismsofchronicvenousdiseaseandtheirroleinc0sclinicalclass AT elietebouskela pathophysiologicalmechanismsofchronicvenousdiseaseandtheirroleinc0sclinicalclass |
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1721280003165913088 |