The study compared, by a prospective, randomized method, 6 treatment options: A: Sclerotherapy; B: High-dose sclerotherapy; C: Multiple ligations; D: Stab avulsion; E: Foam-sclerotherapy; F: Surgery (ligation) followed by sclerotherapy. Results were analyzed 10 years after inclusion and initial treatment. Endpoints of the study were variations in ambulatory venous pressure (AVP), refilling time (RT), presence of duplex-reflux, and number of recurrent or new incompetent venous sites. The number of patients, limbs, and treated venous segments were comparable in the 6 treatment groups, also comparable for age and sex distribution. The occurrence of new varicose veins at 5 years varied from 34% for group F (surgery + sclero) and ligation (C) to 44% for the foam + sclero group (E) and 48% for group A (dose 1 sclero). At 10 years the occurrence of new veins varied from 37% in F to 56% in A. At inclusion AVP was comparable in the different groups. At 10 years the decrease in AVP and the increase in RT (indicating decrease in reflux), was generally comparable in the different groups. Also at 10 years the number of new points of major incompetence was comparable in all treatment groups. These results indicate that, when correctly performed, all treatments may be similarly effective. "Standard," low-dose sclerotherapy appears to be less effective than high-dose sclero and foam-sclerotherapy which may obtain, in selected subjects, results comparable to surgery.

Basic fibroblast growth factor (bFGF) and platelet-derived growth factor-BB (PDGF-BB) modulate vascular wall cell function in vitro and angiogenesis in vivo. The aim of the current study was to determine how bovine aorta endothelial cells (BAECs) respond to the simultaneous exposure to PDGF-BB and bFGF. It was found that bFGF-dependent BAEC migration, proliferation, and differentiation into tubelike structures on reconstituted extracellular matrix (Matrigel) were inhibited by PDGF-BB. The role played by PDGF receptor ␣ (PDGF-R␣) was investigated by selective stimulation with PDGF-AA, by blocking PDGF-BB-binding to PDGF-R␣ with neomycin, or by transfecting cells with dominant-negative forms of the receptors to selectively impair either PDGF-R␣ or PDGF-R␤ function. In all cases, PDGF-R␣ impairment abolished the inhibitory effect of PDGF-BB on bFGF-directed BAEC migration. In addition, PDGF-R␣ phosphorylation was increased in the presence of bFGF and PDGF, as compared to PDGF alone, whereas mitogen-activated protein kinase phosphorylation was decreased in the presence of PDGF-BB and bFGF compared with bFGF alone. In vivo experiments showed that PDGF-BB and PDGF-AA inhibited bFGF-induced angiogenesis in vivo in the chick embryo chorioallantoic membrane assay and that PDGF-BB inhibited bFGF-induced angiogenesis in Matrigel plugs injected subcutaneously in CD1 mice. Taken IntroductionThe endothelial layer represents a physical and chemical barrier between the vessel lumen and the underlying tissues. Endothelial cells (ECs) exert a variety of functions and modulate underlying smooth muscle cells by releasing molecules with vasoactive and growth-regulatory properties. 1 Endothelial cells present an active replication phenotype in vitro, but in vivo they are quiescent. 2 The different expression of membrane-bound receptors 3,4 and the in vivo action of specific inhibitors 5-7 may account, at least in part, for the different replication pattern observed.Basic fibroblast growth factor (bFGF) is a potent EC growth factor; it is known to induce a proangiogenic phenotype in ECs and is released under acidosis conditions that induce EC protection from apoptosis. 8 bFGF plays a critical role in physiologic and pathologic angiogenesis, including tumor angiogenesis. 9,10 It exerts its functions by direct action, 11 by inducing vascular endothelial growth factor (VEGF) synthesis, 12 or by potentiating VEGF activity. 13,14 Platelet-derived growth factor (PDGF) is a growth factor known to be active on ECs. Three PDGF isoforms have been identified as disulfide-linked dimers, namely PDGF-AA, PDGF-BB, and PDGF-AB, expressed by ECs under various conditions. 15-19 They interact with different affinity with 2 tyrosine-kinase receptors, PDGF-R␣ and PDGF-R␤, which are expressed on ECs in normal 4,20-22 and in pathologic conditions. [23][24][25][26] Recently, PDGF-C and PDGF-D isoforms were also identified. 27,28 PDGF isoforms are reported to exert mitogenic and chemotactic action on EC, although PDGF-AA appears to be less potent or inactive...

The biocompatibility of a new material for cardiovascular applications constituted by a poly(ether)urethane (PEtU) and a silicone [polydimethylsiloxane (PDMS)] was evaluated. The achieved material shows properties similar to both polyurethanes and silicones. The material was transformed into porous membranes by a spray-deposition technique. Since any material preparation and manufacturing procedure may introduce some toxicity, in vitro cytotoxicity screening tests were carried out. Human umbilical vein endothelial cells (HUVECs) and a mouse fibroblasts cell line (L929) were cultivated with extracts obtained from materials containing 10, 40 and 100% (w/w) of PDMS. The commercially available Estane 5714-F1 and Cardiothane 51 were used as controls. Extracts were incubated up to 72 hours with HUVECs and L929 cells. The cytotoxic effect was evaluated by light microscopy, cell viability (MTT reduction and neutral red uptake) and proliferation (5-bromo-2'-deoxyuridine incorporation) tests. In vivo studies were carried out using materials containing the same PDMS percentages as for in vitro experiments. The same commercial controls were used. Results obtained with cell culture studies agreed with those obtained in the in vivo experiments and showed that the material preparation and manufacturing procedure do not introduce any toxicity in the products at each PDMS concentration investigated.

The aim of this study was to evaluate the prevention of recurrent deep vein thrombosis (R-DVT) with an oral antithrombotic agent (sulodexide) in moderate to high-risk subjects. A group of 405 patients was included into the multicenter registry. Both compression and an exercise program were used as well as a risk-factors control plan. After diagnosis of DVT, patients were treated with oral anticoagulants for 6 months. At the end of this period a coagulation study was made and patients started treatment with oral sulodexide capsules for a period of 24 months. The femoral, popliteal, tibial, and superficial veins were scanned with high-resolution ultrasound at inclusion;scans were repeated at 6, 12, 18, and 24 months. Of the 405 subjects included into the registry 178 in the control group (mean age 52.2; SD 11; M:F=90:88) and 189 in the treatment group (mean age 53.2; SD 10.3; M:F=93:96) completed the analysis period of 24 months. At 6 and 12 months the incidence of R-DVT was lower (p<0.05) in the treatment group. At 24 months the global incidence of R-DVT was 17.9% in the control group and 7.4% in the sulodexide group (p<0.05), 2.42 times lower than in controls. The 2 groups were comparable for age and sex distribution and for the localization of the thrombi at inclusion. Also the 2 groups of dropouts were comparable. In the control group there were 32 recurrent DVTs and 24 subjects lost to follow-up (total of 56) of 202 included subjects (27.7%) in comparison with 28 failures (14 recurrent DVTs and 14 lost subjects) of 203 subjects (13.8%) in the treatment group. This difference was statistically significant. In this analysis the incidence of DVT in controls was 2.07 times higher than in the treatment group subjects. In conclusion sulodexide was effective in reducing recurrent thrombotic events in high-risk subjects.