Methods: A prospective study was designed in which 165 patients with symptomatic,

unilateral, first-episode DVT were randomized to a long-term anticoagulant treatment with coumarin or enoxaparin during at least 3 months. The rate of thrombus regression was defined as the difference in Marder score after 3 months of treatment by venography. Follow-up was performed at 3, 6, and 12 months, and yearly thereafter for 5 years. Venous disease was related to pathologic severity of PTS according to the validated scale of Villalta as rated by a physician blinded to treatment. Recurrence of symptomatic venous thromboembolism was documented objectively.

Results. The 5-year follow-up period was completed for 100 patients (enoxaparin, 56; coumarin, 44). A lesser incidence this website of PTS was observed in the enoxaparin group (39.3% absent, 19.6% severe) than in the coumarin group (29.5% absent, 29.5% severe), although this difference

was not statistically significant. The accumulated recurrence rate was 19.3% with enoxaparin compared with 36.6% with coumarin (P =.02). Although the mean Marder score was significantly improved in both groups (49.1% for enoxaparin vs 24.0% for coumarin; P =.016), a lower Angiogenesis inhibitor reduction in thrombus size was associated with higher clinical events of recurrence (hazard ratio = 1.97; 95% CI, 1.06-3.66; P =.032). A significant inverse correlation was also found between the degree of thrombus regression at 3 months and the incidence at 5 years of PTS (P =.007).

Conclusions: Residual venous thrombosis is an important risk factor for recurrent thromboembolism and PTS. A greater reduction in thrombus size was associated with lesser clinical events of recurrence and consequently a lesser rate of PTS. However, despite a greater recanalization with enoxaparin, the incidence of PTS was similar between both treatment groups, probably because of the small sample size. Further investigations are needed to clarify the implication

of the anticoagulant treatment in the severity of PTS.”
“Background: Lower extremity chronic venous disease is due to venous hypertension resulting from reflux and/or obstruction. Studies of venous valvular Angiogenesis chemical function have validated and quantified valve closure times defining normal and abnormal valve function, and investigators have categorized the amount of venous reflux with validated criteria. However, hemodynamics; of venous outflow obstruction remains poorly defined. The purpose of this study is to assess whether chronic venous disease alters arterial inflow at rest or during hyperemic limb challenge, and whether there are differences in patients with primary chronic venous insufficiency (1 degrees CVI) versus those with postthrombotic venous disease.

Methods. Twenty-two normal limbs and 32 limbs in patients with chronic venous disease (C-3 or greater) were examined between September 2006 and January 2008.