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Background: An intraluminal, non-occlusive thrombus (ILT) is a common feature in an abdominal aortic aneurysm (AAA). This study investigated the relative progression of ILT vs. AAA volume using a novel parameter, the so-called thrombus burden ratio (TBR), in non-treated AAAs. Parameters potentially associated with TBR progression were analyzed and TBR progression in large vs. small and fast- vs. slow-growing AAAs was assessed. Methods: This retrospective, single-center study analyzed sequential contrast-enhanced computed tomography angiography (CTA) scans between 2009 and 2018 from patients with an AAA before surgical treatment. Patients' medical data and CTA scans were analyzed at two given time points. The TBR was calculated as a ratio of ILT and AAA volume, and relative TBR progression was calculated by normalization for time between sequential CTA scans. Spearman's correlation was applied to identify morphologic parameters correlating with TBR progression, and multivariate linear regression analysis was used to evaluate the association of clinical and morphological parameters with TBR progression. Results: A total of 35 patients were included. The mean time between CT scans was 16 ± 15.9 months. AAA volume progression was 12 ± 3% and ILT volume progression was 36 ± 13%, resulting in a TBR progression of 11 ± 4%, suggesting overproportioned ILT growth. TBR progression was 0.8 ± 0.8% per month. Spearman's correlation verified ILT growth as the most relevant parameter contributing to TBR progression (R = 0.51). Relative TBR progression did not differ significantly in large vs. small and fast- vs. slow-growing AAAs. In the multivariate regression analysis, none of the studied factors were associated with TBR progression. Conclusion: TBR increases during AAA development, indicating an overproportioned ILT vs. AAA volume growth. The TBR may serve as a useful parameter, as it incorporates the ILT volume growth relative to the AAA volume, therefore combining two important parameters that are usually reported separately. Yet, the clinical relevance in helping to identify potential corresponding risk factors and the evaluation of patients at risk needs to be further validated in a larger study cohort.
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Introduction: The use of 3D-printed aortic models for the creation of surgeon-modified endoprostheses represents a promising avenue in aortic surgery. By focusing on the potential impact of sterilization on model integrity and geometry, this report sheds light on the suitability of these models for creating customized endoprostheses. The study presented here aimed to investigate the safety and viability of 3D-printed aortic models in the context of sterilization processes and subsequent remodeling. Methods: The study involved the fabrication of 3D-printed aortic models using patient-specific imaging data and established additive manufacturing techniques. Five identical aortic models of the same patient were printed. Two models were subjected to sterilization and two to disinfection using commonly employed methods, and one model remained untreated. The models were checked by in-house quality control for deformation (heat map analyses) after the sterilization and disinfection processes. Three models (sterilized, disinfected, and untreated) were sent for ex-house (Lufthansa Technik, AG, Materials Technologies and Central Laboratory Services, Hamburg, Germany) evaluation and subsequent quantification of possible structural changes using advanced imaging and measurement technologies (macroscopic and SEM/EDX examinations). After sterilization and disinfection, each aortic model underwent sterility checks. Results: Based on macroscopic and SEM/EDX examinations, distinct evidence of material alterations attributed to a treatment process, such as a cleaning procedure, was not identified on the three implants. Comparative material analyses conducted via the EDX technique yield consistent results for all three implants. Disinfected and sterilized models tested negative for common pathogens. Conclusions: The evaluation of 3D-printed aortic models' safety after sterilization as well as their suitability for surgeon-modified endoprostheses is a critical step toward their clinical integration. By comprehensively assessing changes in model integrity and geometry after sterilization, this research has contributed to the broader understanding of the use of 3D-printed models for tailor-made endovascular solutions. As medical technologies continue to evolve, research endeavors such as this one can serve as a foundation for harnessing the full potential of 3D printing to advance patient-centered care in aortic surgery.
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BACKGROUND: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. METHODS: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. RESULTS: RNA-Seq identified LGALS9 (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (p < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with LGALS9 in different gene sets. Of the top 100 genes potentially interacting with LGALS9, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. CONCLUSION: Nic exposure of HAoECs causes a significant increase in LGALS9 at a transcriptional level. LGALS9 itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies.