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Abstracts
Journal of Vascular Surgery November 2017
through the Swedvasc database. The mandatory national health care registries and medical records provided data on comorbidities, mortality, and major amputations. Results: A total of 16,889 patients with PAD (IC, n = 6272; CLI, n = 10,617) were studied. The incidence of amputations in IC patients was 0.4% (range 0.3%e0.5%) per year. Among CLI patients, the amputation rate during the first 6 months following revascularisation was 12.0% (95% CI 11.3e12.6). Thereafter, the incidence declined to approximately 2% per year. The cumulative combined incidence of death or amputation 3 years after revascularisation was 12.9% (95% CI 12.0e13.9) in IC patients and 48.8% (95% CI 47.7e49.8) in CLI patients. Among CLI patients, compared with IC patients, the prevalence of diabetes, ischaemic stroke, heart failure, and atrial fibrillation was approximately doubled and renal failure was nearly tripled, even after age standardisation. Conclusion: The risk of amputation is particularly high during the first 6 months following revascularisation for CLI. IC patients have a benign course in terms of limb loss. Mortality in both IC and CLI patients is substantial. Revascularised CLI patients have different comorbidities from IC patients.
Reconstruction of the femoro-ilio-caval outflow by percutaneous and hybrid interventions in symptomatic deep venous obstruction van Vuuren TMAJ, de Wolf MAF, Arnoldussen CWKP, Kurstjens RLM, van Laanen JHH, Jalaie H, de Graaf R, Wittens CHA. Eur J Vasc Endovasc Surg 2017;54:495-503. Objective/Background: Deep venous obstruction is relatively prevalent in patients with chronic venous disease. Endovascular treatments and hybrid interventions can be used to relieve venous outflow obstructions. This paper assesses mid-term clinical outcomes and patency rates in a large cohort after percutaneous and hybrid interventions. Methods: This was a prospectively analysed cohort study. Patients with symptomatic deep venous obstruction who presented at a tertiary referral hospital were divided into three groups: patients who underwent percutaneous stenting for non-thrombotic iliac vein compression syndrome (IVCS group); patients with post-thrombotic syndrome (PTS) treated by percutaneous stent placement (P-PTS group); and PTS patients with obstruction involving the veins below the saphenofemoral junction in which a hybrid procedure was performed, combining stenting with open surgical disobliteration (H-PTS group). Patency rates, complications, and clinical outcomes were analysed. Results: A total of 425 lower extremities in 369 patients were treated. At 60 months, primary patency, assisted primary patency, and secondary patency rates were 90%, 100%, and 100% for IVCS, and 64%, 81%, and 89% for the P-PTS group, respectively. The H-PTS group, showed patency rates of 37%, 62%, and 72%, respectively, at 36 months. Venous claudication subsided in 90%, 82%, and 83%, respectively. At the 24 month followup, mean Venous Clinical Severity Score decreased for all patients and improvement in Villalta score was seen in post-thrombotic patients.
The number of complications was related to the extent of deep venous obstruction in which patients in the H-PTS group showed the highest complication rates (81%) and re-interventions (59%). Conclusion: Percutaneous stent placement to treat non-thrombotic iliac vein lesions, and post-thrombotic ilio-femoral obstructions are safe, effective, and showed patency rates comparable with previous research. Patients with advanced disease needing a hybrid procedure showed a lower patency rate and more complications. However, when successful, the clinical outcome was favourable at mid-term follow-up and the procedure may be offered to selected patients.
TIMP3 is Regulated by Pericytes upon Shear Stress Detection Leading to a Modified Endothelial Cell Response Schrimpf C, Koppen T, Duffield JS, Böer U, David S, Ziegler W, Haverich A, Teebken OE, Wilhelmi M. Eur J Vasc Endovasc Surg 2017;54:524-33. Objectives: Atherosclerosis is a hallmark of cardiovascular disease. Shear stress on endothelial cells has been linked to atherogenesis and to fibrous cap thinning and rupture. Pericytes reside in the sub-endothelial space of vessels and have vasoprotective effects. They are subjected to shear stress when endothelial cell integrity is disrupted. The aim was to investigate the susceptibility and response of pericytes to shear stress. Methods: Endothelial cells and pericytes were seeded in two dimensional monocultures and co-cultures, and in a novel three dimensional co-culture system and were subjected to no, low and high shear stress (0, 10, 30 dyne/cm2) for 48 h. The morphological response to flow was assessed by histology and the expression of extracellular matrix proteins was analysed using quantitative polymerase chain reaction, immunoblotting, and ELISA. Results: While endothelial cells aligned into flow direction, pericytes aligned perpendicularly (p < .001), indicating that they must be capable of sensing flow. When pericytes were embedded into a 3D matrix they showed similar alignment and pericytes built long processes towards the lumen. Under shear stress endothelial cells upregulated “a disintegrin and metalloproteinase with thrombospondin motif 1” (ADAMTS-1) (p < .01) and pericytes upregulated “tissue inhibitor of matrix metalloproteinase” (TIMP) 3 (p < .05), an inhibitor of ADAMTS-1, meanwhile differential expression of extracellular matrix (ECM) proteins could be detected in co-cultures of both cells. For TIMP3 expression direct cellecell contact between endothelial cells and pericytes was required. Conclusion: The experiments highlight that pericytes are able to sense direct flow thereby regulating ECM proteins known to be involved in vascular remodelling. Furthermore, pericytes counter-regulate endothelial ADAMTS-1 by protective TIMP3 expression to prevent matrix degradation and maintain vascular stability. For this protective effect direct cell contact was necessary. This observation might represent an adaptive, protective mechanism of pericytes to counteract endothelial damage in the onset of atherosclerosis.