1. Generalities
Evolution of chronic venous disorders (CVD) from 18 to 88 years according to parental heredity. About 21 318 patients.
V. Crébassa
Data from a large French prospective, observational, multicentric study that involved 21 318 consecutive adult patients were presented. Some of the conclusions drawn from the data are unexpected. The odds ratio of chronic venous disease (CVD) is 8.6 if the patient has paternal heredity, while it is 5.0 when it is a maternal. CVD was also shown to be more frequent and symptomatic for women.
Chronic venous disease: Inherited or acquired?
P-L. Antignani, N. Labropoulos, E. Bouskela
Despite being studied for many years, the etiology and pathogenesis of chronic venous disease (CVD) remains an interesting and controversial topic for discussions. This session provided an update on the genetic and biological mechanisms of CVD, make an analysis of current knowledge on the pathways involved in the pathogenesis, and provide targets for pharmacological treatments.
The session was opened with the presentation of P-L. Antignani (Italy) entitled “Population prevalence of chronic venous disease: A question of lifestyle or valves?” The real prevalence of CVD is quite difficult to determine because the previous studies were performed in different geographical areas, they often used a nonepidemiological mode of patient recruitment, and, of course, the definition of the disease may vary especially if the Clinical, Etiologic, Anatomic, and Pathophysiologic classification (CEAP classification) was not used. Despite these issues, we know a lot about the risk factors that influence CVD manifestation. For example, we know from the Vein Consult Program that age, being overweight, and having an individual and/or family history of vein thrombosis are the risk factors in both sexes. Menopause and multiple childbirths are additional risk factors for women.
N. Labropoulos (USA) presented “Is chronic venous disease an inherited or acquired phenomenon?” and stressed the importance of epigenetic factors in CVD. There is no doubt about the role of genetic predisposition, but it cannot explain why some patients without a family history have chronic venous insufficiency that can be severe. To identify the polymorphism that is responsible, we need information from genomewide association studies, but they are expensive and have to be large enough and accurately planned.
To review the known targets of pharmacological treatments and to map out the ways of future research was the goal of E. Bouskela’s (Brazil) presentation “Therapeutic targets for chronic venous disease.” Some brilliant experimental studies from the last decade showed that the micronized purified flavonoid fraction (MPFF) is able to decrease capillary leakage, prevent remodeling of the venous wall and valves, and reduce inflammation in venous valves. These effects, resulting in clinical consequences, were confirmed in many trials. Venoactive drugs improve venous signs, such as pain, and MPFF reduces edema and the healing rate of leg ulcers. However, many details of CVD mechanisms are still poorly investigated. For this reason, E. Bouskela and her colleagues are going to perform a new study to create an experimental model of longlasting venous hypertension.
A summary was made by A. Nicolaides, the chairperson of the session. Modern consensus statements recommend MPFF with grade 1B because the benefits clearly outweigh the risks for relief of symptoms associated with CVD.
