Celiac revascularization as a requisite for treating the median arcuate ligament syndrome.

Median arcuate ligament syndrome (MALS) is a rare and often misunderstood condition characterized by compression of the proximal portion of the celiac artery by the median arcuate ligament. The existence of MALS, also called "celiac artery compression syndrome" or "Dunbar syndrome," has been questioned since compression of the celiac artery is often demonstrated on aortography in asymptomatic patients. Additionally, isolated stenosis of the celiac artery can be compensated for by collateral circulation from the superior mesenteric artery. Despite these dissenting arguments, there are many cases of patients with this syndrome whose symptoms have been relieved by surgical division of the median arcuate ligament. We report on a case involving a patient with similar symptoms not only to provide further support for the validity for this syndrome but also to emphasize the critical need for revascularization once pathological changes develop in the celiac artery.

Autologous platelet-rich fibrin matrix as cell therapy in the healing of chronic lower-extremity ulcers.

A novel autologous platelet-rich fibrin matrix membrane (PRFM) was assessed for the ability to facilitate healing in patients with chronic lower-extremity ulcers. Preliminary data are presented from a prospective trial (n=21). Twelve patients were identified with 17 venous leg ulcers (VLU) and nine bearing 13 nonvenous lower-extremity ulcers. Before enrollment, the patients were evaluated for vascular status and received appropriate surgical intervention to optimize arterial and venous circulatory status. None of the ulcers had responded to a variety of standard treatments from 4 months to 53 years. Initial ulcer size ranged from 0.7 to 65 cm(2) (mean, 11.2 cm(2)). Each PRFM-treated patient received up to three applications of either a 35 or 50 mm fenestrated membrane, depending on initial ulcer size. The primary endpoints were percent and rate of complete closure as measured by digital photography, computerized planimetery, and clinical examination. Patients were followed weekly for 12 weeks with a follow-up visit at 16 weeks. At each 4-week interval, the extent of healing was assessed, and those patients with >50% reduction in wound area were allowed to continue to complete closure. Patients with <50% closure received repeated applications. Complete closure was achieved in 66.7% of the VLU patients (64.7% of treated ulcers) in 7.1 weeks (median, 6 weeks) with an average of two applications per patient. Forty-four percent complete closure was seen with non-VLU patients (31% of treated ulcers). From the results of this small-scale pilot study, PRFM shows significant potential for closing of chronic leg ulcers.

Endovascular management of hepatic artery pseudoaneurysm hemorrhage complicating pancreaticoduodenectomy.

Gastrointestinal bleeding is a morbid complication of pancreaticoduodenectomy. Determining its etiology is often a daunting challenge in that both common and unusual mechanisms may be operative. Visceral artery pseudoaneurysms, although rare, must be considered in that minimally invasive means are available for effective therapy. Our recent experience with two cases highlights the importance for both general and vascular surgeons to be aware of the diagnostic and therapeutic role for early angiography and deployment of endovascular techniques to achieve a successful outcome.

Overexpression of von Willebrand factor is an independent risk factor for pathogenesis of intimal hyperplasia: preliminary studies.

OBJECTIVE: Deposition of von Willebrand factor (vWF) is increased in hyperplastic intima of grafts, vWF levels are elevated in patients with cardiovascular diseases, and there is resistance to progression of atherosclerosis in pigs with von Willebrand disease. We hypothesize that increased expression of endothelial vWF has mitogenic effects on smooth muscle cell (SMC) proliferation. METHODS: In an in vitro study, mouse aortic smooth muscle cells (SMC) were exposed to vWF in various concentrations (0, 5, 20, 100, 500, and 1000 ng/mL). DNA synthesis of SMC was measured with (3)H-thymidine incorporation. In an in vivo study, 108 mice from inbred strains of C57BL/6J (control) and RIIIS/J (characteristic of low plasma vWF) underwent carotid artery ligation (flow cessation model) and were divided into three groups: C57BL/6J, RIIIS/J, and RIIIS/J treated with desmopressin (DDAVP; intraperitoneal injection at 3 micro g/kg/d). At 2 and 4 weeks, carotid arteries were harvested for analysis with immunohistochemical analysis, morphometric studies, and reverse transcriptase polymerase chain reaction; plasma vWF was measured with an enzyme-linked immunosorbent assay. RESULTS: In vitro SMC proliferation showed a positive dose-response curve with vWF stimulation. Intimal hyperplasia (IH) in carotid arteries was prominent in C57BL/6J mice, absent in RIIIS/J mice, and moderate in RIIIS/J treated with DDAVP (intima-media ratio, 71% +/- 18%, 0, and 32% +/- 12%, respectively; P <.01). vWF deposition occurred in all hyperplastic intima subjacent to intact endothelium. Plasma vWF correlated with degree of IH (110% +/- 10%, 21% +/- 7%, and 45% +/- 8%, respectively; P <.05). vWF-messenger RNA was 9 times higher in carotid arteries of C57BL/6J mice and 4 times higher in RIIIS/J with DDAVP, compared with RIIIS/J. CONCLUSIONS: vWF directly stimulates SMC proliferation in vitro via a direct dose-response effect. In vivo low shear stress accelerates IH proportional to vWF expression. This could occur under intact endothelium without platelet activation and platelet-derived growth factor release. In effect, control of IH may entail modulation of vWF expression.