Factors to identify patients at risk of progression chronic venous disease: have we made progress?
DOI:
https://doi.org/10.54695/mva.64.03.2086Abstract
This article will review the literature concerning the risk
factors that identify C2, C3, C4 patients, according to the
clinical, etiological, anatomical, pathophysiological (CEAP)
classification, who are at risk for progression to C6.
Evidence concerning the risk factors for progression of
chronic venous disease (CVD) is weak. There are no known
hemodynamic methods to identify which patient with primary CVD and limbs with C-class 2 to 4 will develop leg
ulcers. Duplex ultrasound scanning parameters of interest
would be the anatomic extent and distribution of reflux and
obstruction, and quantification of reflux measured at set
time intervals in prospective long-term studies with a large
sample size. History and physical examination should focus
on the appearance of new signs during the interval period,
but cannot reliably identify those patients in whom venous
reflux changes develop over time. To detect clinical progression, these patients need to be followed up using clinical severity scores, which are more sensitive than the Cclassification. Primary venous incompetence should be differentiated from secondary incompetence because the two
conditions differ in pathophysiology, management, and
prognosis.
Some clinical risk factors and clinical signs that warrant
early intervention in patients with varicose veins have been
detected, but it will probably be difficult to perform the
required prospective longitudinal studies, cross-cultural
whenever possible, to evaluate the influence of such clinical factors on disease progression. Alternative ways need to
be found.
There are gene polymorphisms and biomarkers that identify patients at high risk for progression to ulceration. In
addition, genetic variations may differ across ethnic groups.
Additional studies are needed to show if sex, age, ethnicity,
and environment influence disease progression.
So far there are no available specific inflammatory mediators for CVD or reliable methods for assessment of
endothelial function. Data regarding the deterioration of
ankle mobility, calf muscle pump function, and patient
activity need to be correlated with progression of the disease or with reversal under treatment, in order to use them
to rate the progression of venous disease. If factors for disease progression in patients with primary CVD could be
identified, a modification of these factors, if feasible, may
prevent development of venous ulcer

