Patients undergoing infrainguinal bypass are undertreated with respect to cardioprotective medications. ACE inhibitor use is associated with lower mortality, and statin drug use is associated with improved graft patency and limb salvage. Institution of consensus guidelines concerning these medications should be considered by all vascular specialists, including vascular surgeons.

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.

EVA produces successful ablation and is associated with sustained improvement in VCSS. These outcomes are independent of the presence of DVI. Finally, the use of a risk-adjusted thrombosis prevention protocol had no effect on the rate of superficial thrombus extension from EVA or EVAP in patients undergoing general anesthesia.

Objective: While rare variants in the COL5A1 gene have been associated with classical Ehlers-Danlos syndrome and rarely with arterial dissections, recurrent variants in COL5A1 underlying a systemic arteriopathy have not been described. Monogenic forms of multifocal fibromuscular dysplasia (mFMD) have not been previously defined. Approach and Results: We studied 4 independent probands with the COL5A1 pathogenic variant c.1540G>A, p.(Gly514Ser) who presented with arterial aneurysms, dissections, tortuosity, and mFMD affecting multiple arteries. Arterial medial fibroplasia and smooth muscle cell disorganization were confirmed histologically. The COL5A1 c.1540G>A variant is predicted to be pathogenic in silico and absent in gnomAD. The c.1540G>A variant is on a shared 160.1 kb haplotype with 0.4% frequency in Europeans. Furthermore, exome sequencing data from a cohort of 264 individuals with mFMD were examined for COL5A1 variants. In this mFMD cohort, COL5A1 c.1540G>A and 6 additional relatively rare COL5A1 variants predicted to be deleterious in silico were identified and were associated with arterial dissections ( P =0.005). Conclusions: COL5A1 c.1540G>A is the first recurring variant recognized to be associated with arterial dissections and mFMD. This variant presents with a phenotype reminiscent of vascular Ehlers-Danlos syndrome. A shared haplotype among probands supports the existence of a common founder. Relatively rare COL5A1 genetic variants predicted to be deleterious by in silico analysis were identified in ≈2.7% of mFMD cases, and as they were enriched in patients with arterial dissections, may act as disease modifiers. Molecular testing for COL5A1 should be considered in patients with a phenotype overlapping with vascular Ehlers-Danlos syndrome and mFMD.