Ultrasonographic hemodynamical and epidemiological factors in advancement of clinical manifestations in primary varicose veins.

BACKGROUND: Primary varicose veins (PVV) represent the most prominent clinical manifestation of chronic venous disease (CVD) and has a complex pathophysiological background. The aim of our study was to investigate the impact of sonographic hemodynamical and contemporary epidemiological factors on the clinical severity of PVV. METHODS: We analyzed the sonographic hemodynamical and clinical parameters from 159 consecutive CVD patients and 233 lower limbs with PVV of clinical stages C2, C3 and C4. Univariate and logistic regression analysis was performed between patients of C2 (N.=70 - 30.0%) and C3 - 4 stages and between subgroups C3 (N.=101 - 43.3%) and C4 (N.=62 - 26.6%). RESULTS: Reflux of common femoral vein and saphenofemoral junction was detected in 43.3% and 65.7%. High venous reflux rates were found at the great saphenous above and below knee (90.1% - 53.2%) and in Cockett perforators (80.5%). Logistic regression revealed that factors associated with the symptomatic C3; 4 stages were the duration of disease >10 years (P=0.015, insufficiency in two or more perforators (P<0.001) and history of 2 pregnancies (P=0.001). Analysis C3 vs. C4 showed that insufficiency in two or more perforators increased the likelihood of advanced C4 clinical stage by 2.2 times, (P=0.037). An additional significant factor was the presence of at least one incompetent Cockett perforator. CONCLUSIONS: Clinical severity of PVV is correlated with a plethora of complex anatomical, hemodynamical and epidemiological factors. Insufficiency in two or more perforators seems to play the most important role and this highlights the value of preoperative venous ultrasound mapping.

The role of Visfatin in atherosclerotic peripheral arterial obstructive disease.

Visfatin is an adipokine molecule acting as an essential coenzyme in multiple cellular redox reactions. The increased serum levels of Visfatin have been correlated with metabolic syndrome and endothelial homeostasis. In this study we investigate the possible relationship of Visfatin serum levels with the severity and location of atherosclerotic peripheral arterial occlusive disease (PAOD). Study protocol included 45 consecutive PAOD and 20 Control patients with age >55years old. Definition of PAOD was based in Rutherord's classification (RC). End-stage PAOD patients (RC-V & -VI) were excluded from study. Data were collected prospectively and included age, gender, atherosclerotic risk factors and the body mass index (BMI). In PAOD patients recorded the PAOD's clinical stage and the presence of carotid stenosis >50%. PAOD patients divided in two subgroups, those with mild (RC-I & -II) and moderate disease (RC-III & -IV). In all serum samples Visfatin was measured, blindly, twice by anosoenzymatic technique. Statistical analysis was performed by non-parametric Mann-Whitney U test, Pearson's chi-square, One Way Anova and Kruskall-Wallis tests, as appropriate. The mean Visfatin value in PAOD and Control groups were 38.5±16.0 and 13.9±3.8ng/ml respectively (p<0.0005). In-PAOD subgroup of patients the visfatin values were not affected by demographics, BMI and atherosclerotic risk factors (p>0.05). Univariate analysis showed that severity of PAOD (mild vs severe), presence of carotid stenosis >50% and multilevel disease significantly affected outcomes (p=0.018, p=0.010 and p=0.006 respectively). In multivariate regression analysis severity of PAOD was the solely factor with strong correlation with high visfatin values (p=0.001). High Visfatin levels seem to be strongly correlated with the presence and severity of PAOD. Further and in depth investigation is needed to define the possible role of Visfatin in atherosclerosis and it's value as a potential prognostic biomarker of PAOD.