This series of infected EVARs is the largest group of infected AAA endografts reported to date. Because EVAR of AAAs is presently the most common method of repair, development of endograft infection, while rare, can be managed with acceptable mortality rates. Patients presenting with aortic-enteric fistula after EVAR appear to have a more virulent course.

Objective The combination of D-dimer and Wells score can exclude, but not confirm, the diagnosis of deep venous thrombosis (DVT). Since thrombosis and inflammation are interrelated, we evaluated the combination of soluble P-selectin (sPsel) with other inflammatory biomarkers for the diagnosis of DVT. Methods Sixty-two positive and 116 negative DVT patients, by duplex scan, were prospectively evaluated for sPsel, D-dimer, C-reactive protein (CRP), microparticles (total, leukocyte and platelet-derived and tissue factor positive microparticles - MP) and clinical Wells score. Results Biomarkers and clinical scores that differentiated DVT positives from negatives were sPsel (87.3 versus 53.4 ng/ml, p<0.0001), D-dimer (5.8 versus 2.1 mg/L, p<0.0001), CRP (2.1 versus 0.8 μg/ml, p<0.0005) and Wells score (3.2 versus 2.0, p<0.0001). For MP analysis, platelet-derived MP were found to differentiate DVT from negatives. Using multivariable logistic regression, a combination of sPsel and Wells score could establish the diagnosis of DVT (cut-point ≥90 ng/ml + Wells ≥2), with a specificity of 96% and positive predictive value (PPV) of 100%, and could exclude DVT diagnosis (cut-point ≤60 ng/ml and Wells <2) with a sensitivity of 99%, a specificity of 33% and a negative predictive value (NPV) of 96%. Conclusion This study establishes a biomarker and clinical profile combination that can both confirm and exclude the diagnosis of DVT.

Background Post-thrombotic syndrome (PTS) is characterized by a fibrotic vein injury following deep vein thrombosis (DVT). We sought to quantify the change in vein wall thickness in patients who fail to resolve DVT by 6 months and whether there were differences in blood or plasma levels of inflammatory proteins associated with venous remodeling. Methods Patients presenting with confirmed lower extremity DVT were prospectively recruited for this study. Duplex imaging of the lower extremity venous system was performed, and blood was collected at entrance and repeat evaluation with blood draw and ultrasound imaging at 1 and 6 months. DVT resolution and thickness of the vein wall was quantified by ultrasound imaging in each segment affected by thrombus, and a contralateral, unaffected vein wall served as a control. Gene and protein expression of inflammatory markers were examined from leukocytes and serum, respectively. ANOVA or Student’s t-tests were used, and a P <.05 was significant. N = 10 – 12 for all analyses. Results 32 patients (12 patients with DVT resolution at 6 months, 10 patients with persistent thrombus at 6 months, and 10 healthy controls) were compared. Both resolving and non-resolving DVT were associated with 1.5 – 1.8 fold increased vein wall thickness at 6 months (P = .008) as compared with non affected vein wall segments. However, the thickness of the affected segments was 1.4 fold greater in patients who had total resolution of the DVT by 6 months than in patients who had persistent chronic thrombus 6 months after presentation (P = .01). There was a 4 – 5 fold increased level of matrix metalloproteinase-9 (MMP9) in thrombosed patients compared with non-thrombosed patient controls (P <.05), while Toll like receptor-9 (TLR-9) expression was 3 fold less than controls (P <.05) at enrollment. D-dimer and P-selectin were higher in thrombosed as compared to controls at diagnosis, but not at 6 months. Both TLR4 (marker of inflammation) and P-selectin gene expression were higher in leukocytes from patients with chronic DVT compared to those who resolved at one month after diagnosis (P <.05). Conclusions This preliminary study suggests ongoing vein wall remodeling after DVT, measurable by ultrasound and associated with certain biomarkers. At 6 months, the vein wall is markedly thickened, and directly correlates with resolution. This suggests that the vein wall response is initiated early following thrombus formation, and persists even in the presence of total resolution.

SummarySeveral rodent models have been used to study deep venous thrombosis (DVT). However, a model that generates consistent venous thrombi in the presence of continuous blood flow, to evaluate therapeutic agents for DVT, is not available. Mice used in the present study were wild-type C57BL/6 (WT), plasminogen activator inhibitor-1 (PAI-1) knock out (KO) and Delta Cytoplasmic Tail (ΔCT). An electrolytic inferior vena cava (IVC) model (EIM) was used. A 25G stainless-steel needle, attached to a silver coated copper wire electrode (anode), was inserted into the exposed caudal IVC. Another electrode (cathode) was placed subcutaneously. A current of 250 μAmps over 15 minutes was applied. Ultrasound imaging was used to demonstrate the persence of IVC blood flow. Analyses included measurement of plasma soluble P-selectin (sP-Sel), thrombus weight (TW), vein wall morphometrics, P-selectin and Von Willebrand factor (vWF) staining, transmission electron microscopy (TEM), scanning electron microscopy (SEM); and the effect of enoxaparin on TW was evaluated. A current of 250 μAmps over 15 minutes consistently promoted thrombus formation in the IVC. Plasma sP-Sel was decreased in PAI-1 KO and increased in ΔCT vs. WT (WT/PAI-1: p=0.003, WT/ΔCT: p=0.0002). Endothelial activation was demonstrated by SEM, TEM, P-selection and vWF immunohistochemistry and confirmed by inflammatory cell counts. Ultrasound imaging demonstrated thrombus formation in the presence of blood flow. Enoxaparin significantly reduced the thrombus size by 61% in this model. This EIM closely mimics clinical venous disease and can be used to study endothelial cell activation, leukocyte migration, thrombogenesis and therapeutic applications in the presence of blood flow.

Background: Endovascular interventions for May Thurner Syndrome (MTS) have become first line therapy, often performed in a young patient population despite the lack of robust supportive data. This paper reports on long term outcomes from a large series of patients treated for de-novo or posthrombotic presentation.Methods: A retrospective review of MTS patients stented between 2006 and 2010 at two institutions. Patients who presented with acute iliofemoral DVT were treated with either catheter directed thrombolysis (CDT) and/or pharmacomechanical thrombolysis (PMT) and identified as having a venous stenosis by venogram. Patients who presented with leg pain or swelling but no DVT and evidence of MTS on duplex were evaluated by venography. IVUS was selectively utilized. Stenting of the iliocaval junction was performed in all patients with a Ͼ50% diameter stenosis on venogram, or a Ͼ70% area stenosis on IVUS.

media were harvested. TGF-␤ secretion in response to stress was determined by ELISA.Results: No difference was noted in the number of TGF-␤RI-positive and TGF-␤RII-positive cells between a-fbs and nn-fbs; however, TGF-␤RII density was reduced 40% as determined by MFI in a-fbs compared with nn-fbs (151 Ϯ 25 vs 51 Ϯ 27, n ϭ 6; P ϭ .03). In healthy commercial nn-fbs subjected to constant mechanical stress for 24 hours, there was no change in TGF-␤ secretion compared with the static (control) nn-fbs. However, there was a fourfold increase in TGF-␤ secretion (284 Ϯ 133 vs 1076 Ϯ 238 pg/mL, n ϭ 4; P ϭ 0.03) in a-fbs exposed to mechanical stress compared with their control.

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Introduction Calf muscle atrophy is commonly noted after lower-extremity immobilization. Air plethysmography (APG) provides an easily reproducible, noninvasive diagnostic test that is useful in measuring calf ejection fraction. Quantitative measurements can be preformed before and after physical therapy as a tool to evaluate effectiveness of treatment. Method We report the case of a 26-year-old woman who presented to the vascular surgery clinic with right lower extremity cyanosis, paresthesias, and swelling after hip dislocation. The patient had been immobile for a month. An arteriogram was performed to rule out arterial injury and a lower-extremity ultrasound was performed to rule out deep venous thrombosis and venous reflux. APG revealed a profoundly abnormal ejection fraction of 36%. Physical therapy was recommended, with special attention towards calf muscle strengthening. Results After 3 months of physical therapy, the APG ejection fraction increased to a normal value of 74%. In addition to normalization of the APG, all symptoms of cyanosis, paresthesias, and swelling were resolved. Conclusion APG may be a useful tool in measuring the restoration of calf muscle function in patients with injuries requiring extended immobilization.