There is increasing evidence for enhanced oxidative stress in the vascular wall of abdominal aortic aneurysms (AAA). Mitochondrial damage and dysfunction are hypothesized to be actors in altered production of reactive oxygen species (ROS) and oxidative stress. However, the role of mitochondria and oxidative stress in vascular remodelling and progression of AAA remains uncertain. We here addressed whether mitochondrial dysfunction is persistently increased in vascular smooth muscle cells (VSMCs) isolated from AAA compared to healthy VSMC. AAA-derived VSMC cultures (AAA-SMC, ) and normal VSMC cultures derived from healthy donors ( ) were grown in vitro and analysed for four parameters, indicating mitochondrial dysfunction: (i) mitochondrial content and morphology, (ii) ROS production and antioxidative response, (iii) NADP+/NADPH content and ratio, and (iv) DNA damage, in the presence or absence of angiotensin II (AngII). AAA-SMC displayed increased mitochondrial circularity (rounded shape), reduced mitochondrial area, and reduced perimeter, indicating increased fragmentation and dysfunction compared to healthy controls. This was accompanied by significantly increased O₂^- production, reduced NADP+/NADPH levels, a lower antioxidative response (indicated by antioxidative response element- (ARE-) driven luciferase reporter assays), more DNA damage (determined by percentage of γ-H2A.X-positive nuclei), and earlier growth arrest in AAA-SMC. Our data suggest that mitochondrial dysfunction and oxidative stress are persistently increased in AAA-SMC, emphasizing their implication in the pathophysiology of AAA.

Summary:Background: To investigate the usability of Mixed-Reality (MR) during patient education in patients scheduled for abdominal aortic aneurysm (AAA) repair. Patients and methods: Consecutive patients scheduled for elective AAA repair were block-randomized in either the Mixed-Reality group (MR group) or the conventional group (control group). Patients of both groups were educated about open and endovascular repair of their respective AAA. The MR group was educated using a head-mounted display (HMD) demonstrating a three-dimensional virtual reconstruction of the respective patient’s vascular anatomy. The control group was educated using a conventional two-dimensional monitor to display the patient’s vasculature. Outcomes were informational gain as well as patient satisfaction with the educational process. (DRKS-ID: DRKS00025174). Results: 50 patients were included with 25 patients in either group. Both groups demonstrated improvements in scores in the Informational Gain Questionnaire (IGQ) when comparing pre- and post-education scores. (MR group: 6.5 points (±1.8) versus 7.9 points (±1.5); Control group: 6.2 points (±1.8) versus 7.6 points (±1.6); p<0.01) There was no significant difference between the MR group and the control group either in informational gain (MR group: 1.4±1.8; Control group: 1.4±1.8; p=0.5) nor in patient satisfaction scores (MR group: mean 18.3 of maximum 21 points (±3.7); Control group: mean 17 of 21 points (±3.6); p=0.1) Multiple regression revealed no correlation between the use of MR and informational gain or patient satisfaction. Usability of the system was rated high, and patients’ subjective assessment of MR was positive. Conclusions: The use of MR in patient education of AAA patients scheduled for elective repair is feasible. While patients reported positively on the use of MR in education, similar levels of informational gain and patient satisfaction can be achieved with MR and conventional methods.

Background: The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis. Reduced GLO1-activity in atherosclerotic tissue is known to be associated with diabetes. It has been shown that treatment of patients with type 2 diabetes with metformin leads to increased GLO1-activity in peripheral-blood-cells. The aim of this study was to evaluate whether metformin treatment increases GLO1-activity in atherosclerotic lesions of patients with type 2 diabetes. Patients and methods: Patients with type 2 diabetes and carotid artery disease were included into the study prospectively. Type of diabetes-medication was documented upon admission along with demographic and clinical history. Using shock frozen endarterectomy-derived carotid artery plaques, GLO1-activity as well as protein expression was measured by a spectophotometric assay and western-blotting respectively. Results: 33 patients (76 % male, mean age 71 years) were included into the study and were divided according to treatment with metformin or not (15 vs. 18 patients). GLO1-activity was increased by the factor 1.36 when treated with metformin – however, not significantly (0.86 vs. 0.63 U/mg, p = 0.056). Normalisation of GLO1-activity onto GLO1-expression level lead to a significant increase by more than twofold (8.48 vs. 3.85, p = 0.044) while GLO1-protein levels did not differ significantly. GLO1-activity correlated positively with increasing HbA1c, especially under metformin treatment. Conclusions: Treatment with metformin in patients with type 2 diabetes is associated with enhanced GLO1-activity in atherosclerotic lesions. Regarding the macro- and microvascular complications in these patients further studies are needed to gain more insight into the effect of metformin on the GLO/MG system.