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The aim of this study was to analyse and compare the outcome of open surgery (OS) and endovascular repair (ER) for the treatment of visceral artery aneurysms (VAA). A systematic literature search was carried out. 25 comparative cohort studies with 4447 patients (2469 OS and 1978 ER) were included in the meta-analysis. Mortality (ER vs OS 1.8% vs 2.1%, OR.77, 95% CI [.51; 1.17], P =.23) and technical success rates (97% vs 98%, OR.50, 95% CI [.21; 1.16], P =.11) were comparable between both groups. Lower mortality rates for ER were observed for ruptured aneurysms (4.1% vs 31%, OR.43 95% CI [.13; 1.43], P =.17). Length of stay was shorter (mean difference −4.25 days, 95% CI [−5.52; −2.98], P <.00001) and 1-year reintervention rates were higher in the ER group (9% vs 5%, OR 1.55 95% CI [.58; 4.12], P =.38. The presented evidence suggests that ER should be considered a first-line treatment for VAAs, especially in an emergency setting, due to lower morbidity and comparable mortality and technical success. Follow-up should be offered to these patients due to the higher reintervention rates. Systematic review registration: PROSPERO ID 348699 [ABSTRACT FROM AUTHOR]

Background: Popliteal artery aneurysms (PAA) were traditionally treated by open repair (OR). Endovascular repair (ER) has become a new treatment strategy. The aim of this systemic review and meta-analysis was to evaluate and compare the current outcomes of OR and ER in the emergency treatment of PAA. Methods: A systematic literature search of the PubMed/Medline database was carried out. Outcomes were 30-day mortality, morbidity, major amputation rate (30 days), major amputation rate (1 year), 1-year primary patency rate, 1-year secondary patency rate and 1-year survival. Additionally, we included clinical data of patients with popliteal aneurysms treated between 2009 and 2021 at the Martin-Luther University Halle-Wittenberg. Results: We identified two cohort studies from 2014 and 2015 with a total of 199 patients that underwent emergent surgery (39 ER and 160 OR). We also included 26 patients from our institution. For emergency treatment, 30-day major amputation rates (18% vs 3%, Odds Ratio 5.82, 95% CI [1.75; 19.30], p =.004), 30-day mortality rates (10% vs 1%, Odds Ratio 5.57, 95% CI [1.01; 30.58], p =.05), 1-year major amputation rates (15% vs 6% Odds Ratio 3.61, 95% CI [1.18; 11.09], p =.02), 1-year loss of primary patency (54% vs 23%, Odds Ratio 3.19, 95% CI [0.91; 11.20], p =.07), and 1-year loss of secondary patency (44% vs 12%, Odds Ratio 6.91, 95% CI [3.01; 15.83], p <.05) were higher in the ER group when compared to the OR group. Conclusion: Endovascular repair represents an alternative approach for the emergency treatment of PAA. Limited evidence from the available non-randomized studies shows unfavorable outcomes for patients undergoing ER. However, the results are prone to selection bias, and only randomized trials comparing ER to OR might reveal whether a subgroup of patients would benefit from ER as primary treatment of PAA in an emergency setting. [ABSTRACT FROM AUTHOR]

Simple Summary: This review delves into metabolic reprogramming in pancreatic cancer and its development, with a special emphasis on the mevalonate pathway, encompassing cholesterol biosynthesis, transport, targeting approaches, and clinical investigations. It describes how cancer cells manipulate cholesterol metabolism to fuel their proliferation, outlining the specific metabolic routes employed by pancreatic cancer cells for cholesterol production and the potential of inhibiting these processes to decelerate cancer progression. The paper elucidates intracellular cholesterol storage, inter-cellular transport, and its correlation with cancer metastasis. Moreover, the review highlights promising pharmaceutical candidates for pancreatic cancer therapy. Overall, this comprehensive review provides valuable insights into the prospects of combating pancreatic cancer by selectively addressing cholesterol-related processes. Pancreatic cancer's substantial impact on cancer-related mortality, responsible for 8% of cancer deaths and ranking fourth in the US, persists despite advancements, with a five-year relative survival rate of only 11%. Forecasts predict a 70% surge in new cases and a 72% increase in global pancreatic cancer-related deaths by 2040. This review explores the intrinsic metabolic reprogramming of pancreatic cancer, focusing on the mevalonate pathway, including cholesterol biosynthesis, transportation, targeting strategies, and clinical studies. The mevalonate pathway, central to cellular metabolism, significantly shapes pancreatic cancer progression. Acetyl coenzyme A (Acetyl-CoA) serves a dual role in fatty acid and cholesterol biosynthesis, fueling acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN) development. Enzymes, including acetoacetyl-CoA thiolase, 3-hydroxy-3methylglutaryl-CoA (HMG-CoA) synthase, and HMG-CoA reductase, are key enzymes in pancreatic cancer. Inhibiting HMG-CoA reductase, e.g., by using statins, shows promise in delaying PanIN progression and impeding pancreatic cancer. Dysregulation of cholesterol modification, uptake, and transport significantly impacts tumor progression, with Sterol O-acyltransferase 1 (SOAT1) driving cholesterol ester (CE) accumulation and disrupted low-density lipoprotein receptor (LDLR) expression contributing to cancer recurrence. Apolipoprotein E (ApoE) expression in tumor stroma influences immune suppression. Clinical trials targeting cholesterol metabolism, including statins and SOAT1 inhibitors, exhibit potential anti-tumor effects, and combination therapies enhance efficacy. This review provides insights into cholesterol metabolism's convergence with pancreatic cancer, shedding light on therapeutic avenues and ongoing clinical investigations. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to analyze the outcome of emergency thoracic endovascular aortic repair (TEVAR) in the treatment of "primary aortic" (aneurysm, aortic dissection, penetrating aortic ulcer (PAU)) and "secondary aortic" (iatrogenic, trauma, and aortoesophageal fistula) pathologies. Methods: Retrospective review of a cohort of patients treated at a single tertiary referral center from 2015 to 2021. The primary end point was postoperative in-hospital mortality. Secondary end points were the duration of the procedure, duration of postoperative intensive care treatment, length of hospital stay, and the nature and severity of postoperative complications according to the Dindo–Clavien classification. Results: A total of 34 patients underwent TEVAR for emergency indications. Twenty-two patients were treated for primary and twelve patients for secondary aortic pathologies. Concerning in-hospital mortality, no statistically significant difference could be observed between the primary and secondary aortic groups (27.3% vs. 33.3%, p = 0.711). Patients with an aortoesophageal fistula had a mortality rate of 66.7%. Postoperative morbidity (Dindo–Clavien > 3) was also not statistically significantly different between the primary and secondary aortic groups (36.4% vs. 33.3%, p = 0.86). Preoperative hemoglobin level (p < 0.001 for mortality, p = 0.002 for morbidity), hemoglobin level difference (p = 0.022, p = 0.032), postoperative creatinine level (p = 0.009, p = 0.035), and pre- and postoperative lactate levels (p < 0.001 for both mortality and morbidity) were found to be independent factors associated with postoperative mortality and morbidity (Dindo–Clavien > 3), respectively. The preoperative creatinine level was found to be associated with mortality (p = 0.024) but not morbidity. Conclusions: Morbidity and in-hospital mortality are still considerable after emergency TEVAR for both primary and secondary aortic indications. Pre- and postoperative levels of hemoglobin, creatinine, and lactate may be valuable to predict patient outcomes. [ABSTRACT FROM AUTHOR]

Objectives: Based on the angiogenetic, transcriptional profile of non-diseased and arteriosclerotic vessels, we aim to identify the leucocytic markers as a potential, minimal invasive tool supporting diagnosis of vascular pathology. Methods: Transcriptional profiling was performed with Angiogenesis RT2 Profiler PCR (Polymerase Chain Reaction) array on three non-pathological and three arteriosclerotic vessels, followed by immunohistochemical staining. Based on these screening results, selected transcripts were employed for qPCR with specific primers and investigated on the blood RNA (RiboNucleic Acid) obtained from nine healthy controls and 29 patients with cardiovascular disorders. Thereafter, expression of these transcripts was investigated in vitro in human monocytes under calcification-mimicking conditions. Results and Conclusions: Transcriptional profiling on the vessels revealed that out of 84 targets investigated two were up-regulated more than 100-fold, 18 more than 30 and 15 more than 10, while the most noticeable down-regulation was observed by ephrin-A3 and platelet-derived growth factor alpha (PDGFA) genes. Based on the vessel results, investigations of the selected blood transcripts revealed that thrombospondin 1 (THBS1), thrombospondin 3 (THBS3), transforming growth factor, beta receptor 1 (TGFBR1), platelet-derived growth factor alpha, plasminogen activator, urokinase (PLAU) and platelet/endothelial cell adhesion molecule 1 (PECAM-1) were significantly elevated in cardiovascular blood as compared to corresponding controls. Induction of calcification-related conditions in vitro to human THP-1 monocytes led to noticeable modulation of these transcripts. Taken together, these data demonstrate that leucocytic THBS1, THBS3, TGFBR1, platelet-derived growth factor alpha, PLAU and PECAM-1 have a correlation with cardiovascular disorders and could be used as a supportive tool predicting development of this pathological condition. [ABSTRACT FROM AUTHOR]