Background: So called “mycotic” aortic aneurysms account for only 0.7 to 1.3% of all aortic aneurysms and are commonly caused by Staphylococcus aureus and Salmonella species. Bacillus Calmette-Guérin (BCG), a live attenuated strain of Mycobacterium bovis, is part of the therapy of non-muscle-invasive bladder cancer (NMIBC). Case presentation: We report a case series of three patients with a mycobacterial graft infection related to BCG after surgical treatment of a presumed mycotic aortic aneurysm as an extremely rare complication after NMIBC treatment. All three patients developed aortic aneurysm after BCG instillation and subsequent mycobacterial graft infection. Conclusion: Diagnosis requires a high degree of suspicion because of its nonspecific symptoms and imaging. The pathogen is not detected by standard microbiological testing. Treatment includes triple antimycobacterial therapy and radical surgical interventions. Graft preservation may be considered if no anastomosis is involved.

Endovascular repair (EVAR) has become the standard procedure in treating thoracic (TAA) or abdominal aortic aneurysms (AAA). Not entirely free of complications, a persisting perfusion of the aneurysm after EVAR, called Endoleak (EL), leads to reintervention and risk of secondary rupture. How the aortic wall responds to the implantation of a stentgraft and EL is mostly uncertain. We present a pilot study to identify peptide signatures and gain new insights in pathophysiological alterations of the aortic wall after EVAR using matrix-assisted laser desorption or ionization mass spectrometry imaging (MALDI-MSI). In course of or accompanying an open aortic repair, tissue sections from 15 patients (TAA = 5, AAA = 5, EVAR = 5) were collected. Regions of interest (tunica media and tunica adventitia) were defined and univariate (receiver operating characteristic analysis) statistical analysis for subgroup comparison was used. This proof-of-concept study demonstrates that MALDI-MSI is feasible to identify discriminatory peptide signatures separating TAA, AAA and EVAR. Decreased intensity distributions for actin, tropomyosin, and troponin after EVAR suggest impaired contractility in vascular smooth muscle cells. Furthermore, inability to provide energy caused by impaired respiratory chain function and continuous degradation of extracellular matrix components (collagen) might support aortic wall destabilization. In case of EL after EVAR, this mechanism may result in a weakened aortic wall with lacking ability to react on reinstating pulsatile blood flow.

Background: Endovascular aortic aneurysm repair (EVAR) has become the standard procedure for treating infrarenal abdominal aortic aneurysms (AAA). Various associated complications can lead to open conversion (OC). Thorough follow-up after the procedure is mandatory for the early detection of complications. Persisting perfusion of the aneurysm, a so-called endoleak (EL), paired with structural instability because of aortic wall atrophy and impaired cell functionality induced by EVAR, results in a high risk for aortic rupture. Purpose: The goal of this study was to detect the risk factors for elective and urgent OC as a result of EVAR-induced pathophysiological changes inside the aortic wall. Research Design: Retrospective data analysis was performed on all open aortic repairs from January 2016 to December 2020. Data Collection and Analysis: Fifty patients were identified as treated by OC for failure of an infrarenal EVAR. The patients were divided into two subgroups, here depending on the urgency of surgery. Statistical analysis of patient characteristics and outcomes was performed. Results: The most common indications for OC were various types of EL (74%), resulting in an aortic rupture in 15 patients. Patients with insufficient or absent follow-up were treated more frequently in an emergency setting (16% vs. 63%). The mortality rate was higher in cases of emergency OC (3% vs. 26%). Conclusions: Particularly in cases of insufficient or absent follow-up, complications such as EL pose an enormous risk for fatal aortic rupture.

Introduction: Aortoesophageal fistula (AEF) after thoracic endovascular aortic repair (TEVAR) is a rare complication associated with high mortality. Most well established treatment is multi-staged surgery, including removal of infected stent graft, esophageal resection and aortic reconstruction. Presentation of case: We report on a case of a 67-year-old patient with AEF and stent graft infection. Stent removal was infeasible due to the critical condition of the patient and history of multiple vascular procedures of the thoracoabdominal aorta. Surgical management included staged right and left thoracotomy, esophagectomy, vacuum therapy (VAC) on stent prosthesis and subsequent graft coverage with omental and pleural flaps, followed by esophageal reconstruction. Discussion: An established and generally accepted treatment approach for graft infections does not exist. Graft explantation and radical surgical debridement is the therapy of choice for prosthetic infections. In comparison to previous literature, our case represents the complexity of the treatment of AEF and its enormous demands on the interdisciplinary medical team. Conclusion: Our report shows that in an emergency situation without other surgical options as in our case, it was possible to stabilize the patient through application of vacuum therapy in the infected area, with simultaneous esophagectomy, followed by secondary staged reconstruction with omentoplasty and pleura parietalis flap remaining the graft in situ. Highlights:

Vascular endothelial growth factor (VEGF) is a potent driver of angiogenesis, which may help to relieve ischemia in peripheral arterial disease (PAD). We aimed to investigate the role of intramuscular VEGF in ischemic and non-ischemic skeletal muscle in PAD patients before and after surgical or endovascular revascularization and different stages of PAD. Biopsies of the gastrocnemius and vastus muscles from twenty PAD patients with stenosis or occlusion of the superficial femoral artery were obtained both during revascularization and 8 weeks postoperatively. The gastrocnemius muscle was considered ischemic, while vastus muscle biopsies served as intraindividual controls. The levels of vascular endothelial growth factor in muscle lysates were then determined by ELISA. Preoperative VEGF levels were significantly higher in ischemic muscles compared to the controls (98.07 ± 61.96 pg/mL vs. 55.50 ± 27.33 pg/mL, p = 0.004). Postoperative values decreased significantly (p = 0.010) to 54.83 ± 49.60 pg/mL in gastrocnemius biopsies. No significant change was observed in vastus muscle biopsies, with mean postoperative VEGF values found at 54.16 ± 40.66 pg/mL. Since all patients still had indications for revascularization, impairment of angiogenesis mechanisms can be assumed. More research about angiogenesis in PAD is needed with the ultimate goal to improve conservative treatment.