Die Bedeutung einer Dilatation der Vena femoralis communis für die Pathophysiologie der chronischen Veneninsuffizienz und der Stellenwert einer Diameterbestimmung der Vena femoralis communis als diagnostisches und prognostisches Kriterium der CVI im Rahmen der degenerativen Venenerkrankungen
Background: Chronic Venous Disease (CVD) is one of the most frequent illnesses in the industrialised countries. Its prevalence within adult population exceeds in some European countries 50%. This accounts for 1.5 till 2.0 % of health care expenditures. Varicose veins (vv) and CVD decrease the quality of life of patients and their families. Venous wall degeneration is common primary cause of CVD. However, the pathophysiologic role of degenerative venodilation has not yet been finally established. In contrast to venous obstruction and venous reflux, venodilation has not been acknowledged by experts as a substrate of CVD. The aim of this study was to examine the role of dilation of Common Femoral Vein (CFV) as possible risk factor for CVD. Methods: In this cross-sectional study a total of 249 right legs (including 181 women and 68 men) were analysed. According to the CEAP classification study population was limited to primary aetiology (EP). DVT (PO) and other secondary and congenital causes of CVD (ECS) were excluded. Subjects with clinical stage 0, 1 or 2 (C0-2) were considered as non-diseased, otherwise (C3-6) as diseased. Right (n=249) and left (n=242) legs were analysed separately. Multiple logistic regression analysis was performed with the aid of SAS System. Results: The risk of CVD was around 10-fold higher in women with CFV diameter exceeding 14.0 mm as compared with those having diameter of 14.0 mm or less (adjusted for age, vv, and CFV-reflux). Based on Receiver-Operating-Characteristics curves, the ability to discriminate between diseased and non-diseased legs was higher for CFV dilation then for CFV-reflux. The curve of association between the CFV diameter and risk of CVD rose monotonically and revealed exposure-effect pattern. In women two threshold values were found for CFV diameter: at 14.0 and 17.5 mm; in men only one: at 17.5 mm. Final logistic model (women) included four covariates: age, vv, CFV-diameter and CFV-reflux duration. A probability of CVD was estimated using these parameters. Increasing body weight and height, BMI and body surface area (BSA) were associated with higher risk of CVD. However, in contrast to body weight and BMI that showed non-linear association, BSA predicted the risk of CVD in a linear manner and the association showed biological gradient. Conclusions: (1) CFV diameter is an independent risk factor of CVD of primary aetiology. Higher diameter values correspond to higher risk of clinically overt CVD. (2) CFV diameter was shown to possibly indicate the risk of CVD progression. (3) A given diameter of CFV should be interpreted in both sexes differently as the normal limits are higher in men than in women. The predictive value of CFV dilation is higher in varicose-free subjects as compared with those with vv. (4) The risk of CVD increases consistently with enlargement of CFV-diameter. In women with CFV diameter exceeding 14.0 mm the risk of CVD is markedly higher as compared with those having CFV of 14.0 mm or less. Thus, in women diameter values greater than 14.0 mm should be considered pathological. (5) The role of venodilation seems not to be restricted to predisposing to development of valvular incompetence. For making a diagnosis of CVD in women more information can be derived from the measurement of CFV diameter than from the measurement of CFV reflux. Venous valve insufficiency and ambulatory venous hypertension seem not to be necessarily involved in development of early stages of CVD. (6) Estimated probability of CVD can be utilised in phlebological evaluation of subjects, and as health index for assessing the extend of disease in the general population. This can be best estimated using four parameters: age, vv, CFV-diameter and CFV-reflux duration. These four predictors bear complementary information about risk of CVD and should be assessed together. Other parameters that have been examined in the study (including refluxes in other venous segments) do not further enhance the accuracy of diagnosis of CVD. (7) BSA is associated with both the risk of CVD and the diameter of CFV. It is hypothesised that the biological mechanism explaining the role of BSA as risk factor of CVD rely on its determining blood-volume and blood-pressure load of peripheral venous system; over time increased venous load may lead to venodilation, venous stasis and in consequence to CVD. BMI and body weight seem to represent those factors less appropriately and are related to the risk of CVD partly due to confounding by age, sedentary lifestyle, social class, immobility or hormone disorders. The risk of CVD in women depends on changes of body weight beneath the value of 80 kg, BMI beneath the value of 25 kg/m2 and body height above 160 cm. Beyond these limits, changes in these parameters do not affect the risk of CVD. (8) For the purpose of research on CVD, material should be analysed separately for each of the genders because of possible differences in the pathophysiology of CVD between the sexes.
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