First Result of a Tailored Progressive Multistep Approach for the Treatment of Aorto-esophageal Fistulae.

BACKGROUND: Aorto-esophageal fistulae (AEFs) are a rare but serious and life-threatening disease of the mediastinum. Especially, AEF in the presence of infected stent grafts, for example, after thoracic endovascular aortic repair (TEVAR) is only curable by a multistage interdisciplinary surgical approach. This study presents the results of our four-stage approach consisting of bridging TEVAR, esophagectomy, complete stent removal followed by total bovine tube aortic replacement (TBTAR), and finally esophageal reconstruction. METHODS: A case series of four patients from our department receiving a four-stage treatment of AEF is presented in this study. Retrospective database analysis focusing on overall survival, duration of intensive care unit and total hospital stay until discharge, complications, surgical time frame, and completion of chosen surgical treatment course was performed. RESULTS: Overall, four patients surgically treated for AEF since May 2015 were included. A 30-day mortality was 0%, and overall survival at 1 year was 75%. All patients survived more than 5 months and could be discharged after TEVAR and esophagectomy. TBTAR could be performed in two of four patients (50%). Esophageal reconstruction was completed in all patients. Average follow-up was 20.3 ± 1.7 months or until death. CONCLUSION: The acute management of AEF using this approach seems satisfactory, especially for reducing acute short-term mortality. Complete restoration of the circulatory system and digestive tract remains challenging and is associated with high morbidity. We support the application of bridging TEVAR with a staggered approach to further surgical treatment individually tailored to the patient.

Increase of urinary TIMP-2 and IGFBP7 as potential predictor of acute kidney injury requiring renal replacement therapy and patients' outcome following complex endovascular and open thoracic abdominal aortic aneurysm surgery - a prospective observational study.

Background: Acute kidney injury (AKI) as complication after open and endovascular repair of thoracoabdominal aortic aneurysm (TAAA) is one major predictor of mortality and postoperative complications. We evaluated tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) as combined early biomarker for AKI detection and predictor of patients' outcome. Patients and methods: Between 2014 and 2015, 52 patients have been enrolled in this observational study, of whom 29 (55.8%) underwent elective open repair and 23 (44.2%) endovascular repair. TIMP2 × IGFBP7 were measured until 48 hours after admission on intensive-care unit (ICU) and were analyzed regarding their predictive ability for AKI (defined according to the KDIGO criteria) requiring temporary renal replacement therapy (RRT) and 90-day mortality using ROC curves. Results: Mean patient age was 64.5 years (Min: 43, Max: 85), endovascular treated patients were older (p <0.0001). 40.4% (n = 21) developed AKI, and 21.2% (n = 11) required renal replacement therapy. In-hospital and total mortality rates were 7.7% (n = 4) and 9.6% (n = 5), respectively. At no time a significant difference in TIMP2 × IGFB7 levels between patients undergoing open or endovascular surgery was observed. The predictive quality of the TIMP2 × IGFBP7 value on ICU admission was sound regarding AKI requiring temporary renal replacement therapy (sensitivity: 55.56% [38.1-72.1%], specificity: 90.91% [58.7-99.8%] with an area under the curve [AUC]: 0.694 [0.543-0.820]). Mean follow-up was 13.2 months (Min: 2, Max: 20), regarding the 90-day mortality, the predictive property of the TIMP2 × IGFBP7 value was not sufficient (sensitivity: 80% [28.4-99.5%], specificity: 52.38% [36.4-68%], and AUC: 0.607 [0.454-0.746]). Conclusions: TIMP2 × IGFBP7 level measured 6-12 hrs postoperatively may be useful as an early detectable biomarker for AKI requiring temporary renal replacement therapy. It seems not suited to predict patients' outcome following complex thoracoabdominal aortic surgery, regardless if performed by open or endovascular repair.

Outcome of stenting in central venous obstruction of benign etiology.

Background: The aim of this study is to evaluate long term outcome in patients treated for benign superior vena cava (SVC) syndrome by endovascular techniques. Patients and methods: Between 2015 and 2018, 62 patients suffering from central venous obstruction of benign etiology underwent balloon angioplasty with stent placement for venous obstruction in our department. Patency was assessed clinically, using duplex ultrasound in all patients or with CT-phlebography in selected cases. Results: Median age was 60 years (23-83), forty-one patients (66%) had central venous devices. Swelling of the arm and face were the main symptoms (71%). During the median follow up of 22 months (9-38), cumulative primary patency was 71% after venous stenting. The cumulative assisted primary and the secondary patency were 85% and 92%, respectively. Conclusions: Recanalization and stenting of central vein obstruction has turned out to be the technique of reference and provides satisfactory mid-term patency rates. After adjusting for the risk factors, presence of AV-fistula remained a significant risk factor for recurrent stenosis or loss of patency after intervention.

Zinc supplementation ameliorates lung injury by reducing neutrophil recruitment and activity.

INTRODUCTION: Zinc is well known for its anti-inflammatory effects, including regulation of migration and activity of polymorphonuclear neutrophils (PMN). Zinc deficiency is associated with inflammatory diseases such as acute lung injury (ALI). As deregulated neutrophil recruitment and their hyper-activation are hallmarks of ALI, benefits of zinc supplementation on the development of lipopolysaccharides (LPS)-induced ALI were tested. METHODS: 64 C57Bl/6 mice, split into eight groups, were injected with 30 µg zinc 24 hours before exposure to aerosolised LPS for 4 hours. Zinc homoeostasis was characterised measuring serum and lung zinc concentrations as well as metallothionein-1 expression. Recruitment of neutrophils to alveolar, interstitial and intravascular space was assessed using flow cytometry. To determine the extent of lung damage, permeability and histological changes and the influx of protein into the bronchoalveolar lavage fluid were measured. Inflammatory status and PMN activity were evaluated via tumour necrosis factor α levels and formation of neutrophil extracellular traps. The effects of zinc supplementation prior to LPS stimulation on activation of primary human granulocytes and integrity of human lung cell monolayers were assessed as well. RESULTS: Injecting zinc 24 hours prior to LPS-induced ALI indeed significantly decreased the recruitment of neutrophils to the lungs and prevented their hyperactivity and thus lung damage was decreased. Results from in vitro investigations using human cells suggest the transferability of the finding to human disease, which remains to be tested in more detail. CONCLUSION: Zinc supplementation attenuated LPS-induced lung injury in a murine ALI model. Thus, the usage of zinc-based strategies should be considered to prevent detrimental consequences of respiratory infection and lung damage in risk groups.

Comparison of urine and serum neutrophil gelatinase-associated lipocalin after open and endovascular thoraco-abdominal aortic surgery and their meaning as indicators of acute kidney injury.

BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL) has been described as a potential biomarker of acute kidney injury (AKI) in different settings, but its behaviour under influence of open and endovascular repair of thoraco-abdominal aortic aneurysms (TAAA) has not been assessed yet. In this study, the course of NGAL was observed and differences of serum- (sNGAL) and urine-NGAL (uNGAL) levels following TAAA repair, especially with regard to AKI, were evaluated. PATIENTS AND METHODS: In this retrospective single centre study, 52 patients (mean age 64.5 years, [43-85 years]), including 39 (75 %) men, were enrolled (2014-2015, 13.2 months mean follow-up). Levels of sNGAL and uNGAL were measured perioperatively for 48 hours on intensive care unit. Twenty-three patients were treated by endovascular and 29 by open TAAA-repair. RESULTS: Logistic regression revealed an increase in NGAL (sNGAL p = 0.0263, uNGAL p = 0.0080) corresponding with an increase in serum creatinine within the first 48 hours. Fourteen patients (26.9 %) developed AKI and 11 (21.1 %) required dialysis. The course of NGAL differed significantly (uNGAL p < .0001, sNGAL p = 0.0002) between patients suffering from AKI requiring dialysis and patients without AKI. The predictive power of uNGAL was three times higher than that of sNGAL (estimate of the regression slope 0.1382 vs. 0.0460). No significant difference between patients undergoing open or endovascular TAAA repair regarding the perioperative course of sNGAL and uNGAL was observed. CONCLUSION: serum-NGAL and urine-NGAL correlate with serum creatinine levels and AKI requiring dialysis. Furthermore, the postoperative course of sNGAL and uNGAL after open and endovascular TAAA repair is not significantly different. Taken together, the results indicate that uNGAL and, to a lesser extent, sNGAL could be considered biomarkers for early detection of perioperative AKI after open and endovascular TAAA surgery.

Protective Aptitude of Annexin A1 in Arterial Neointima Formation in Atherosclerosis-Prone Mice-Brief Report.

OBJECTIVE: Restenosis as a consequence of arterial injury is aggravated by inflammatory pathways. Here, we investigate the role of the proresolving protein annexin A1 (AnxA1) in healing after wire injury. APPROACH AND RESULTS: Apoe-/- and Apoe-/-Anxa1-/- mice were subjected to wire injury while fed a high-cholesterol diet. Subsequently, localization of AnxA1 and AnxA1 plasma levels were examined. AnxA1 was found to localize within endothelial cells and macrophages in the neointima. Levels of AnxA1 in the plasma and its lesional expression negatively correlated with neointima size, and in the absence of AnxA1, neointima formation was aggravated by the accumulation and proliferation of macrophages. In contrast, reendothelialization and smooth muscle cell infiltration were not affected in Apoe-/-Anxa1-/- mice. CONCLUSIONS: AnxA1 is protective in healing after wire injury and could, therefore, be an attractive therapeutic compound to prevent from restenosis after vascular damage.

Extra-Thoracic Supra-aortic Bypass Surgery Is Safe in Thoracic Endovascular Aortic Repair and Arterial Occlusive Disease Treatment.

OBJECTIVE: The safety and feasibility of supra-aortic debranching as part of endovascular aortic surgery or as a treatment option for arterial occlusive disease (AOD) remains controversial. The aim of this study was to assess the clinical outcome of this surgery. METHODS: This single centre, retrospective study included 107 patients (mean age 69.2 years, 38.4% women) who underwent supra-aortic bypass surgery (carotid-subclavian bypass, carotid-carotid bypass, and carotid-carotid-subclavian bypass) because of thoracic or thoraco-abdominal endovascular aortic repair (57%; 61/107) or as AOD treatment (42.9%; 46/107) between January 2006 and January 2015. Mortality, morbidity with a focus on neurological complications, and patency rate were assessed. Twenty-six of 107 (14.2%) of the debranching patients were treated under emergency conditions because of acute type B dissection or symptomatic aneurysm. Follow up, conducted by imaging interpretation and telephone interviews, continued till March 2017 (mean 42.1, 0-125, months). RESULTS: The in hospital mortality rate was 10.2% (11/107), all of these cases from the debranching group and related to emergency procedures (p < .0001). One procedure related death of a patient in the debranching group, who had a lethal stroke 72 months post-operatively following bypass occlusion was observed. Early neurological complications were recognised in 10 patients, including two transient cases of Horner syndrome and vocal cord paralysis as well as six cases of phrenic nerve apraxia. Three cases of stenosis and one case of occlusion were successfully treated. In three AOD patients, the graft had to be exchanged because of peri-graft reaction. Primary and secondary patency rates of 96 patients after 36 months were 95% (SE 2.6%) and 98% (SE 1.8%), respectively. CONCLUSIONS: Extra-thoracic supra-aortic bypass surgery involves low complication rates and high mid-term bypass patency rates. It is a safe and feasible treatment option in the form of debranching in combination with endovascular aortic aneurysm repair and in AOD.

Editor's Choice - Open Thoracic and Thoraco-abdominal Aortic Repair After Prior Endovascular Therapy.

OBJECTIVE: The aim was to present current results of open thoracic and thoraco-abdominal aortic repair as secondary procedure after prior endovascular therapy. METHODS: This was a retrospective cross border single centre study. From 2006 to July 2017 45 open thoracic aortic (TAA) or thoraco-abdominal aortic aneurysm (TAAA) operations were performed on 44 patients (median age 58 [15-80] years) as secondary surgery after previous endovascular therapy comprising TEVAR (n = 38; 86%), EVAR (n = 3; 7%), fenestrated EVAR (n = 1; 2%) and TEVAR plus EVAR (n = 1; 2%). Eleven patients (25%) had had previous open aortic surgery at the secondary surgery site. Indications for TAA(A) repair were Type I endoleak (n = 10; 23%), post-dissection aneurysm progression due to persisting false lumen perfusion (n = 8; 18%), proximal/distal disease progression (n = 16; 36%), device fracture/dislocation (n = 4; 9%), infection (n = 5; 11%), and initial endograft misplacement (n = 1; 2%). The operations included descending thoracic aortic repair (n = 13, 29%), TAAA Type I (n = 4; 9%), Type II (n = 5; 11%), Type III (n = 13; 29%), Type IV (n = 7; 16%), and Type V repair (n = 3; 7%) with simultaneous arch repair in 18% (n = 8). The median time to secondary surgery was 36 (2-168) months. The median follow up was 39 (3-118) months. RESULTS: In hospital mortality was 20% (n = 9) due to intra-operative aneurysm rupture, pneumonia induced sepsis, hemorrhagic cerebellar infarction, mesenteric ischaemia, broncho-esophageal fistula, and multiorgan failure (1/9) as well as haemorrhage (3/9). Estimated survival was 73% at 1 year and 71% overall. The most frequent complications were pneumonia (n = 19; 43%), bleeding requiring revision (n = 11; 25%) and sepsis (n = 14; 32%). Transient dialysis was required in 32% (n = 14), permanent dialysis in 6% (n = 2). Permanent spinal cord deficit (paraparesis) occurred in 6% (n = 2). Estimated freedom from aortic re-intervention was 86%. CONCLUSION: Open TAA(A) repair as a secondary procedure after previous endovascular aortic therapy is an important treatment option even in the endovascular era. It represents a durable treatment that can produce respectable outcomes. Yet the peri-operative morbidity and mortality are relevant and a specialised team and infrastructure are mandatory for these complex procedures. Therefore, centralisation is required.

Closed Incision Negative Pressure Therapy Reduces Surgical Site Infections in Vascular Surgery: A Prospective Randomised Trial (AIMS Trial).

BACKGROUND: Surgical site infections (SSIs) of the groin remain a crucial problem in vascular surgery, prompting great interest in preventative techniques, such as closed incision negative pressure therapy (ciNPT). This prospective randomised study aimed to assess the potential benefits of ciNPT application after groin incisions for vascular surgery. METHOD: The study included 204 patients who underwent vascular surgery for peripheral artery disease (PAD) at two sites between July 2015 and May 2017. These patients received post-operative treatment with ciNPT (intervention group) or standard wound dressings (control group). After exclusion, 188 patients were assessed for SSIs using the Szilagyi classification. RESULTS: The mean patient age was 66.6 ± 9.4 years (range 43-85 years), and 70% were male (n = 132). Regarding PAD stage, 52% were stage IIB, 28% stage III, and 19% stage IV. Among the patients, 45% (n = 85) had had a previous groin incision. Bacterial swabs were performed in each case of suspected SSI (22.8% [43/188]), while 76.7% (33/188) were negative, there were 5% [5/98] positive swabs in the intervention group and 5.5% [5/90] in the control group). Antibiotics were given to 13.2% of the intervention group, and 31.1% of the control group (p = .004). The control group experienced more frequent SSIs (33.3%; 30/90) than the intervention group (13.2%; 13/98; p = .0015; absolute risk difference -20.1 per 100; 95% CI -31.9 to 8.2). This difference was based on an increased rate of Szilagyi I SSI in the control group (24.6% vs. 8.1%, p = .0012). CONCLUSION: The results confirmed a reduced superficial SSI rate after vascular surgical groin incision using ciNPT compared with standard wound dressings.

Dicer generates a regulatory microRNA network in smooth muscle cells that limits neointima formation during vascular repair.

MicroRNAs (miRNAs) coordinate vascular repair by regulating injury-induced gene expression in vascular smooth muscle cells (SMCs) and promote the transition of SMCs from a contractile to a proliferating phenotype. However, the effect of miRNA expression in SMCs on neointima formation is unclear. Therefore, we studied the role of miRNA biogenesis by Dicer in SMCs in vascular repair. Following wire-induced injury to carotid arteries of Apolipoprotein E knockout (Apoe -/-) mice, miRNA microarray analysis revealed that the most significantly regulated miRNAs, such as miR-222 and miR-21-3p, were upregulated. Conditional deletion of Dicer in SMCs increased neointima formation by reducing SMC proliferation in Apoe -/- mice, and decreased mainly the expression of miRNAs, such as miR-147 and miR-100, which were not upregulated following vascular injury. SMC-specific deletion of Dicer promoted growth factor and inflammatory signaling and regulated a miRNA-target interaction network in injured arteries that was enriched in anti-proliferative miRNAs. The most connected miRNA in this network was miR-27a-3p [e.g., with Rho guanine nucleotide exchange factor 26 (ARHGEF26)], which was expressed in medial and neointimal SMCs in a Dicer-dependent manner. In vitro, miR-27a-3p suppresses ARHGEF26 expression and inhibits SMC proliferation by interacting with a conserved binding site in the 3' untranslated region of ARHGEF26 mRNA. We propose that Dicer expression in SMCs plays an essential role in vascular repair by generating anti-proliferative miRNAs, such as miR-27a-3p, to prevent vessel stenosis due to exaggerated neointima formation.

[Open Repair of the Thoracic Aorta Using the Clamshell Approach Because of Aortooesopheagel Fistula - a Multidisciplinary Approach]. / Offener Ersatz der gesamten thorakalen Aorta über einen "clamshell"-Zugang bei aortoösophagealer Fistel ­ eine multidisziplinäre Herausforderung.

INTRODUCTION: Aortoesophageal fistula (AEF) following open or endovascular operations of the thoracoabdominal aorta is a rare, yet life-threatening condition. In this case, the whole thoracic aorta has to be replaced using a "clamshell approach" because of an AEF following open repair of the ascending aorta after type A dissection and a thoracic endovascular aortic repair (TEVAR). CASE REPORT: In 2015 a 43-year old woman suffered a type A dissection and underwent open supracoronary ascending aortic replacement including the proximal aortic arch. In 2016, she developed severe haemoptysis. An AEF could be detected and TEVAR was performed as emergency treatment. The further steps of the repair included oesophagectomy and repair of the whole thoracic aorta using a transverse thoracotomy - a clamshell approach. CONCLUSION: The curative treatment of AEF, which is based on radical, open repair of the oesophagus and the involved aortic segments, is challenging. A clamshell approach is a feasible option when replacement of the whole thoracic aorta is required.

[Delayed Occluding Membrane (DOM) - A New Concept to Prevent Spinal Cord Ischaemia During Endovascular Aortic Aneurysm Repair]. / Delayed Occluding Membrane (DOM) ­ ein neuer Ansatz zur Protektion der spinalen Ischämie bei endovaskulärem Aortenrepair.

INTRODUCTION: The risk of spinal cord ischemia is a relevant problem in in fields of open and endovascular thoracoabdominal aortic aneurysm repair (TAAA). Despite all efforts, no therapeutical concept exists, which enables a complete treatment of the TAAA without open branches or fenestrations, and reduces the risk for a spinal cord ischemia (SCI) to the minimum. In this article, we would like to present a new concept based on slow-occluding hydrogel-textile membrane, which could help to reduce the SCI risk during endovascular TAAA repair. CONCEPT: A hydrogel textile membrane is under development, which could be used a functional unit of endovascular stentprosthesis. If in contact with blood, glutathion induces swelling of the induces ongoing swelling of the membrane because of the triggered degradation of the crosslinker. Due to the resulting water uptake of the hydrogel textile membrane and mass increase of the gel, the swelling leads to a stabilization of the membrane. In vitro studies show, that the swelling of the hydrogel textile membrane should lead to a controlled decreasing flow into the aneurysm sac. After a pre-defined period, the membrane is occluded and the aneurysm sac perfusion stops. So, by using the hydrogel textile membrane, a complete treatment of the TAAA can be realized in one procedure without further re-intervention or pre-interventional measures. Furthermore, the risk of a SCI would be minimized. As this treatment concept is under development, only interim results are presented. CONCLUSION: The successful development and usage of a slow-occluding hydrogel textile membrane as a part of endovascular stentprosthesis could help to reduce the risk SCI during endovascular TAAA surgery.

Cathepsin G Controls Arterial But Not Venular Myeloid Cell Recruitment.

BACKGROUND: Therapeutic targeting of arterial leukocyte recruitment in the context of atherosclerosis has been disappointing in clinical studies. Reasons for such failures include the lack of knowledge of arterial-specific recruitment patterns. Here we establish the importance of the cathepsin G (CatG) in the context of arterial myeloid cell recruitment. METHODS: Intravital microscopy of the carotid artery, the jugular vein, and cremasteric arterioles and venules in Apoe-/-and CatG-deficient mice (Apoe-/-Ctsg-/-) was used to study site-specific myeloid cell behavior after high-fat diet feeding or tumor necrosis factor stimulation. Atherosclerosis development was assessed in aortic root sections after 4 weeks of high-fat diet, whereas lung inflammation was assessed after inhalation of lipopolysaccharide. Endothelial deposition of CatG and CCL5 was quantified in whole-mount preparations using 2-photon and confocal microscopy. RESULTS: Our observations elucidated a crucial role for CatG during arterial leukocyte adhesion, an effect not found during venular adhesion. Consequently, CatG deficiency attenuates atherosclerosis but not acute lung inflammation. Mechanistically, CatG is immobilized on arterial endothelium where it activates leukocytes to firmly adhere engaging integrin clustering, a process of crucial importance to achieve effective adherence under high-shear flow. Therapeutic neutralization of CatG specifically abrogated arterial leukocyte adhesion without affecting myeloid cell adhesion in the microcirculation. Repetitive application of CatG-neutralizing antibodies permitted inhibition of atherogenesis in mice. CONCLUSIONS: Taken together, these findings present evidence of an arterial-specific recruitment pattern centered on CatG-instructed adhesion strengthening. The inhibition of this process could provide a novel strategy for treatment of arterial inflammation with limited side effects.

Annexin A1 counteracts chemokine-induced arterial myeloid cell recruitment.

RATIONALE: Chemokine-controlled arterial leukocyte recruitment is a crucial process in atherosclerosis. Formyl peptide receptor 2 (FPR2) is a chemoattractant receptor that recognizes proinflammatory and proresolving ligands. The contribution of FPR2 and its proresolving ligand annexin A1 to atherosclerotic lesion formation is largely undefined. OBJECTIVE: Because of the ambivalence of FPR2 ligands, we here investigate the role of FPR2 and its resolving ligand annexin A1 in atherogenesis. METHODS AND RESULTS: Deletion of FPR2 or its ligand annexin A1 enhances atherosclerotic lesion formation, arterial myeloid cell adhesion, and recruitment. Mechanistically, we identify annexin A1 as an endogenous inhibitor of integrin activation evoked by the chemokines CCL5, CCL2, and CXCL1. Specifically, the annexin A1 fragment Ac2-26 counteracts conformational activation and clustering of integrins on myeloid cells evoked by CCL5, CCL2, and CXCL1 through inhibiting activation of the small GTPase Rap1. In vivo administration of Ac2-26 largely diminishes arterial recruitment of myeloid cells in a FPR2-dependent fashion. This effect is also observed in the presence of selective antagonists to CCR5, CCR2, or CXCR2, whereas Ac2-26 was without effect when all 3 chemokine receptors were antagonized simultaneously. Finally, repeated treatment with Ac2-26 reduces atherosclerotic lesion sizes and lesional macrophage accumulation. CONCLUSIONS: Instructing the annexin A1-FPR2 axis harbors a novel approach to target arterial leukocyte recruitment. With the ability of Ac2-26 to counteract integrin activation exerted by various chemokines, delivery of Ac2-26 may be superior in inhibition of arterial leukocyte recruitment when compared with blocking individual chemokine receptors.

Editor's Choice - Open Thoracic and Thoraco-abdominal Aortic Repair in Patients with Connective Tissue Disease.

OBJECTIVE/BACKGROUND: The aim is to present current results of open complex aortic repair in patients with connective tissue disease (CTD). METHODS: This was a retrospective cross-border, single centre study. From February 2000 to April 2016 72 aortic operations were performed on 65 patients with CTD (41 male, median age 41 years [range 19-70 years]). Fifty-six patients (86%) underwent at least one previous aortic repair (71 open, four endovascular), including 33 patients (51%) operated before at the site of the procedure reported here. The open procedures, counting eight emergency operations (11%), included aortic arch revision (n = 1; 1%), descending thoracic aortic repair (n = 11; 15%), TAAA type I repair (n = 12; 17%), type II repair (n = 29; 40%), type III repair (n = 12; 17%), and type IV repair (n = 5; 7%). Simultaneous repair of the ascending aorta and/or the aortic arch was performed in two (3%) and eight cases (11%), respectively. Seven patients (10%) underwent staged procedures. Median follow-up was 42 months (0.5-180 months). RESULTS: The in hospital mortality was 14% (n = 9) as a result of haemorrhage (n = 3/9), neurological (n = 3/9), cardiac (n = 2/9), and pulmonary (n = 1/9) complications. Paraplegia and paraparesis occurred in one (2%) and three patients (5%), respectively. Seven patients (11%) required temporary dialysis; none needed permanent dialysis. Major complications were revision surgery for bleeding or haematoma (n = 20/65), sepsis (n = 10/65), myocardial infarction/severe cardiac arrhythmia (n = 2/65), stroke (n = 2/65), as well as multiorgan failure, abdominal compartment syndrome, mesenteric and peripheral ischaemia (all n = 1/65). Multivariate analysis identified an operating time > 7 hours (p = .006) as an independent predictor of increased mortality. Freedom from re-intervention was 85%, 1 year survival was 80%, and overall survival was 75%. CONCLUSION: Open TAA(A) repair is a durable therapy for patients with CTD. Often being performed as revision surgery, it can be associated with relevant risks and should therefore be reserved for specialised centres. Staged procedures and thus reducing operating time, if applicable, should be preferred.

Sarcoidosis-Associated Aortoesophageal Fistula-Multistage Interdisciplinary Surgical Therapy for a Rare and Life-Threatening Condition.

Aortoesophageal fistulas (AEFs) are rare and life-threatening conditions. Till date, an association between an AEF and sarcoidosis has not been reported yet. The aim of this report is to demonstrate a case of AEF secondary to sarcoidosis and its multistage interdisciplinary surgical therapy. A 66-year-old male was diagnosed with sarcoidosis in 2014. He has been treated with glucocorticoids since then and no severe health restrictions due to the disease have occurred. In December 2015, the patient presented with acute thoracic pain and hematemesis: an esophagogastroscopy revealed an AEF. First, stent-graft implantation in the thoracic aorta was urgently performed as a "bridging" procedure. Second, esophagectomy and local debridement were performed, followed by explantation of the stent graft and reconstruction by means of xenograft replacement of the stented aorta in a third operation. Finally, retrosternal gastric pull-up was performed in a fourth operative procedure. Sixteen days after the last operation the patient could be discharged to a rehabilitation clinic. Follow-up is uneventful so far; the antibiotic therapy was stopped at the time of hospital discharge. The pathogenesis of sarcoidosis, a rare autoimmunological disease, has not been completely clarified yet. The diagnosis relies on clinical symptoms and radiological as well as histopathological findings. Many cases of sarcoidosis show spontaneous regression, but severe complications may occur. While tracheoesophageal fistulas have been described in the literature, AEFs related to sarcoidosis have not been mentioned yet. Despite surgical and antibiotic treatment, the morbidity and mortality rates of AEF are high. Because the endovascular treatment has been established for emergency procedures of the aorta, it is considered as an appropriate first-line "bridging" treatment option. To achieve good long-term results, surgical treatment has to involve esophagectomy with secondary reconstruction of the upper gastrointestinal tract, as well as open aortic replacement using xenograft or homograft material. Sarcoidosis may lead to AEF as demonstrated in this case. Successful treatment can be realized by a multistage interdisciplinary surgical approach.

Functional Assessment and Evaluation of Outcome After Endovascular Therapy With Coverage of the Left Subclavian Artery in Case of Blunt Thoracic Aortic Injury.

BACKGROUND: Patients suffering blunt thoracic aortic injury (BTAI) can be treated by use of thoracic endovascular aortic repair (TEVAR). In this setting, the coverage of the left subclavian artery (LSA) is frequently necessary. Nevertheless, the functionality of the upper left extremity after TEVAR had been rarely analyzed. Thus, this study intends to underline the safety of TEVAR as well as to determine the functionality of the left arm after coverage of the LSA. METHODS: All patients suffering from BTAI treated by endovascular means in 3 centers (Aachen [Germany], Maastricht [Netherlands], and Innsbruck [Austria]) between 1996 and 2009 were retrospectively analyzed. The safety of the procedure had been assessed by the morbidity and mortality rate. The mid-term functional status of the upper left extremity was evaluated by using the DASH score (disabilities of the arm shoulder and hand). RESULTS: Forty-six patients (40 male, 6 female), mean age 39.4 ± 16.9 years suffered from BTAI caused by traffic accident (n = 31 [67.39%]), by skiing injury (n = 8 [17.39%]), and by fall (n = 7 [15.21%]). All patients underwent TEVAR, the technical success rate was 100%; 1 carotid-carotid subclavian bypass implantation was necessary. LSA coverage was performed in 76% (35/46) of the cases. Total complication rate was 17.3% (8/46); the endoleak rate was 8.6% (4/46) (2 × Ib, 1 × IIa, 1 × IV). Further complications were bypass and endograft occlusion. The postoperative mortality rate was 6% (3/46), the DASH score was completed in 65% (30/46). The study population reached a mean value of 17 ± 20, which is comparable to a nonharmed reference group (10.10 ± 14.68). A significant correlation between the DASH score and patients age could be demonstrated (2-sided P value: 0.0213). CONCLUSIONS: Endovascular therapy of BTAI revealed a good primary success rate. An adequate mid-term functional status of the upper left extremity could be assessed in comparison to a nonharmed reference group.

Macrophage Migration Inhibitory Factor Predicts Outcome in Complex Aortic Surgery.

The perioperative inflammatory response is associated with outcome after complex aortic repair. Macrophage migration inhibitory factor (MIF) shows protective effects in ischemia-reperfusion (IR), but also adverse pro-inflammatory effects in acute inflammation, potentially leading to adverse outcome, which should be investigated in this trial. This prospective study enrolled 52 patients, of whom 29 (55.7%) underwent open repair (OR) and 23 (44.3%) underwent endovascular repair (ER) between 2014 and 2015. MIF serum levels were measured until 72 h post-operatively. We used linear mixed models and ROC analysis to analyze the MIF time-course and its diagnostic ability. Compared to ER, OR induced higher MIF release perioperatively; at 12 h after ICU admission, MIF levels were similar between groups. MIF course was significantly influenced by baseline MIF level (P = 0.0016) and acute physiology and chronic health evaluation (APACHE) II score (P = 0.0005). MIF level at 24 h after ICU admission showed good diagnostic value regarding patient survival [sensitivity, 80.0% (28.4-99.5%); specificity, 51.2% (35.1-67.1%); AUC, 0.688 (0.534-0.816)] and discharge modality [sensitivity, 87.5% (47.3-99.7%); specificity, 73.7% (56.9-86.6%), AUC, 0.789 (0.644-0.896)]. Increased perioperative MIF-levels are related to an increased risk of adverse outcome in complex aortic surgery and may represent a biomarker for risk stratification in complex aortic surgery.

[Deep Veins: Hybrid Procedure for Treatment of Iliofemoral Obstruction]. / Tiefes Venensystem: Hybridverfahren zur Therapie der iliofemoralen chronischen venösen Obstruktionen.

Background Endovascular recanalisation of chronic obstruction of iliofemoral or caval veins gives very good patency. However, patency decreases if the common femoral vein and its side branches are also involved. Endophlectomy during a hybrid procedure can improve outcome and avoid early reocclusion due to restored inflow. The review presents the technical details and the published results of this technique. Results The hybrid procedure combines venous recanalisation and stent angioplasty with endophlebectomy. There have only been 4 studies with more than 10 patients and follow-up between 6 and 24 months. Primary and secondary patency ranges from 0 to 70% and 30 to 93%, respectively, but most patients showed clinical benefit. Conclusion Although there have only been a few studies on the hybrid procedure with endophlebectomy, this technique seems to improve the outcome of venous recanalisation if femoral inflow is disturbed.

Vitamin K antagonism aggravates chronic kidney disease-induced neointimal hyperplasia and calcification in arterialized veins: role of vitamin K treatment?

Arteriovenous fistula (AVF) is the common vascular access type for a hemodialysis patient. Its failure is due to neointimal hyperplasia. Vitamin K antagonists are given to lower thrombosis tendency, but have side effects that enhance arterial calcifications. Here, we investigated the effects of vitamin K antagonists and vitamin K2 (K2) treatment on neointimal hyperplasia development and calcification in rats and in arterialized human veins. AVF was generated in female rats while chronic kidney disease (CKD) was induced using an adenine-enriched diet. Arterialization, CKD, and vitamin K antagonists all significantly enhanced venous neointimal hyperplasia. K2 treatment, additional to vitamin K antagonists, significantly reduced neointimal hyperplasia in arterialized veins in healthy rats but not in rats with CKD. Arterialization, CKD, and vitamin K antagonism all significantly increased, whereas K2 supplementation attenuated calcification in healthy rats and rats with CKD. K2 significantly enhanced matrix Gla protein carboxylation in control rats and rats with CKD. Arterialized human vein samples contained inactive matrix Gla protein at calcification and neointimal hyperplasia sites, indicating local vitamin K deficiency. Thus, vitamin K antagonists have detrimental effects on AVF remodeling, whereas K2 reduced neointimal hyperplasia and calcification indicating vasoprotective effects. Hence, K2 administration may be useful to prevent neointimal hyperplasia and calcification in arterialized veins