Use of the AFX Stent Graft in Patients with Extremely Narrow Aortic Bifurcation: A Multicenter Retrospective Study.

INTRODUCTION: This study analyzed the patient outcomes following endovascular aortic aneurysm repair (EVAR) for infrarenal aortic pathologies with very narrow aortic bifurcations using the AFX stent graft. METHODS: The data was retrieved from the archived medical records of 35 patients treated for abdominal aortic aneurysm (AAA) (48.6%) or penetrating aortic ulcer (PAU) (51.4%) with very narrow aortic bifurcation between January 2013 and May 2020. Patient survival, freedom from endoleak (EL), and limb occlusion were estimated applying the Kaplan-Meier method. RESULTS: The mean follow-up time was 20.4 ± 22.8 months. The mean aortic bifurcation diameter was 15.8 ± 2.2 mm. Technical success was 100%, and no procedure-related deaths occurred. Two type II ELs occurred within 30-day follow-up. We observed one common iliac artery stenosis at four months and one type III EL at 54 months in the same patient, both of which required re-intervention. Overall patient survival was 95 ± 5% (AAA: 100%; PAU: 89 ± 10%), freedom from limb occlusion was 94 ± 5% (AAA: 91 ± 9%; PAU: 100%), freedom from type II EL was 94 ± 4% (AAA: 88 ± 8%; PAU: 100%), and freedom from EL type III was 83 ± 15% (AAA: 80 ± 18%; PAU: 100%) at the end of the follow-up period. CONCLUSIONS: Very narrow aortic bifurcations may predispose patients to procedure-related complications following EVAR. Our results suggest a safe use of the AFX stent graft in such scenarios. The overall short- and long-term procedure-related patient outcomes are satisfying albeit they may seem superior for PAU when compared to AAA.

Pathophysiology of chronic limb ischemia.

Chronic ischemia of the lower extremities is an everyday problem in vascular surgery clinics. In Germany, approximately 3% of all hospitalizations are due to peripheral artery disease (PAD), with critical limb ischemia (CLI) in particular showing a rapid increase. The consequences of chronic undersupply range from reduced walking distance to loss of limbs. At the beginning there are stress factors, such as hyperlipidemia (LDL), free radicals, arterial hypertension, infections or subclinical inflammation that interfere with endothelial homeostasis and cause endothelial dysfunction with increased permeability. Cells of the immune system are attracted and migrate into the vascular wall, where they lead to the degradation of matrix components and destabilization of the plaque. By changing the phenotype of smooth muscle cells and macrophages towards osteoclast-like cells, bone-like hardening of the vessel wall takes place. Above a vessel wall thickness of approximately 100 µm, hypoxia-induced factor (HIF-1α) is intensified by the lack of oxygen, which leads to an increase in growth factors, such as vascular endothelial growth factor (VEGF). This promotes angiogenesis, but it is not sufficient to compensate for a stenosed artery. Arteriogenesis refers to the growth of existing collateral vessels. The driving forces are the pressure gradient before and after the stenosis and the shear forces acting on the vessel walls. In the case of progressive stenosis, the compensatory capacities can be overtaxed and a manifest hypoxia in the tissue with regression of the obtained vascular structures and tissue atrophy occurs.

Oxidized (non)-regenerated cellulose affects fundamental cellular processes of wound healing.

In this study we investigated how hemostats such as oxidized regenerated cellulose (ORC, TABOTAMP) and oxidized non-regenerated cellulose (ONRC, RESORBA CELL) influence local cellular behavior and contraction of the extracellular matrix (ECM). Human stromal fibroblasts were inoculated in vitro with ORC and ONRC. Cell proliferation was assayed over time, and migration was evaluated by Live Cell imaging microscopy. Fibroblasts grown in collagen-gels were treated with ORC or ONRC, and ECM contraction was measured utilizing a contraction assay. An absolute pH decline was observed with both ORC and ONRC after 1 hour. Mean daily cell proliferation, migration and matrix contraction were more strongly inhibited by ONRC when compared with ORC (p < 0.05). When control media was pH-lowered to match the lower pH values typically seen with ORC and ONRC, significant differences in cell proliferation and migration were still observed between ONRC and ORC (p < 0.05). However, in these pH conditions, inhibition of matrix contraction was only significant for ONRC (p < 0.05). We find that ORC and ONRC inhibit fibroblast proliferation, migration and matrix contraction, and stronger inhibition of these essential cellular processes of wound healing were observed for ONRC when compared with ORC. These results will require further validation in future in vivo experiments to clarify the clinical implications for hemostat use in post-surgical wound healing.

Novel effects of adenosine receptors on pericellular hyaluronan matrix: implications for human smooth muscle cell phenotype and interactions with monocytes during atherosclerosis.

Hyaluronan (HA) is responsive to pro-atherosclerotic growth factors and cytokines and is thought to contribute to neointimal hyperplasia and atherosclerosis. However, the specific function of the pericellular HA matrix is likely depend on the respective stimuli. Adenosine plays an important role in the phenotypic regulation of vascular smooth muscle cells (VSMC) and is thought to inhibit inflammatory responses during atherosclerosis. The aim of this study was to examine the regulation and function of HA matrix in response to adenosine in human coronary artery SMC (HCASMC). The adenosine receptor agonist NECA (10 µM) caused a strong induction of HA synthase (HAS)1 at 6 h and a weaker induction again after 24 h. Use of selective adenosine receptor antagonists revealed that adenosine A2(B) receptors (A2(B)R) mediate the early HAS1 induction, whereas late HAS1 induction was mediated via A2(A)R and A3R. The strong response after 6 h was mediated in part via phosphoinositide-3 kinase- and mitogen-activated protein kinase pathways and was inhibited by Epac. Functionally, NECA increased cell migration, which was abolished by shRNA-mediated knock down of HAS1. In addition to HA secretion, NECA also stimulated the formation of pronounced pericellular HA matrix in HCASMC and increased the adhesion of monocytes. The adenosine-induced monocyte adhesion was sensitive to hyaluronidase. In conclusion, the current data suggest that adenosine via adenosine A2(B)R and A2(A)R/A3R induces HAS1. In turn a HA-rich matrix is formed by HCASMC which likely supports the migratory HCASMC phenotype and traps monocytes/macrophages in the interstitial matrix.

[Endovascular treatment of traumatic ruptures of the thoracic aorta]. / Endovaskuläre Versorgung der traumatischen thorakalen Aortenruptur.

Traumatic rupture of the descending aorta is an acute life-threatening event. The most common cause is deceleration trauma resulting in a sudden stretching of the aortic isthmus as for example in car and motorcycle accidents and falls from a great height. Exemplified by a case report of a multiply injured 57-year-old male the diagnostic pathways, therapy and postoperative complications are presented.

[Influence of fixation mechanism on changes of the supra- and infrarenal segment of the aorta after endovascular treatment of infrarenal aortic aneurysm]. / Einfluss des Verankerungsmechanismus auf Veränderungen des supra- und infrarenalen Aortensegments nach endovaskulärer Ausschaltung infrarenaler Bauchaortenaneurysmen.

INTRODUCTION: Dilatation of the infrarenal aortic segment determines the long-term outcome after endovascular repair of abdominal aortic aneurysms. This segment is crucial for sealing and preventing stent-graft migration. The purpose of this study was to evaluate influence of fixation mechanism on changes of supra- and infrarenal aortic diameters over a 10-year period. METHODS: We reviewed all our endovascular procedures for abdominal aortic aneurysms and follow-up CT scans between 1998 and 2008. Only patients with the three most frequently implanted self-expandable stent-graft types and a minimal follow-up of three months were included in this study. Further inclusion criteria were elective repair and follow-up at our department to consistent data formats. A total of 103 patients, 35 with suprarenal fixation without hooks (Medtronic Talent®, Medtronic World Medical, Sunrise, FL, USA), 29 with suprarenal fixation with hooks (Cook Zenith®, Cook Inc. Bloomington, IN, USA) and 39 with infrarenal fixation with anchors (Gore Excluder®, W. L. Gore & Associates, Flagstaff, Ariz, USA) met the inclusion criteria. All measurements were performed in duplicate by two different investigators to determine intra- and interobserver errors. Based on this error a minimal change of 2 mm of infrarenal aortic neck diameter was determined as aortic neck dilatation. RESULTS: During a mean follow-up time of 39.4 (3-108.8) months, infrarenal aortic neck dilatation was found in 28.57% in the Medtronic group, 10.26% in the Gore group and 31.03 in the Cook group. Suprarenal changes were 17.14%, 20.51% and 17.24%, respectively. Reduction of the maximal diameter could be achieved in 74.3% (Medtronic), 79.5% (Gore), and 75.8% (Cook). Seven of 23 patients with a notable dilatation of the infrarenal neck required reintervention. All of them were stent-grafts with suprarenal fixation. No statistical significance was found between the 3 groups regarding changes of suprarenal or infrarenal diameters or migration rates. CONCLUSION: Although no statistical significance was found among the groups, infrarenal fixation showed the lowest rate of infrarenal dilatation.

Ten years of endovascular treatment of traumatic aortic transection--a single centre experience.

BACKGROUND: Aim of the study was to present the 10-year results after endovascular repair of acute traumatic rupture of the descending aorta in a single centre. METHODS: Forty-eight consecutive patients (35 men and 13 women; mean age 39.8 +/- 18 years) with traumatic lesions of the descending aorta were treated between March 1999 and November 2008. All patients were treated within 24 hours of admission. RESULTS: Thirty-one Gore TAG, 13 Medtronic Valiant, 6 Cook Zenith TX2 were used. The technical success rate was 100%, the conversion rate was 0%. Thirty-day mortality rate was 8.3%; overall procedure-related mortality was 2.1% due an acute stent graft compression syndrome. Infolding endografts were observed in 3 patients (6.25%). The left subclavian artery was covered in 35 cases (70%), in one patient revascularisation was necessary. No neurological deficit was reported. Mean follow-up was 51.9 months (4-116 months). No late complications occurred. CONCLUSION: Endovascular treatment of acute traumatic rupture of the thoracic aorta is a safe method, with a lower morbidity and mortality than open repair.