BACKGROUND: Given changes in intervention guidelines and the growing popularity of endovascular treatment for aortic aneurysms, we examined the trends in admissions and repairs of abdominal aortic aneurysms (AAA), thoracoabdominal aortic aneurysms (TAAA), and thoracic aortic aneurysms (TAA).
METHODS: We identified all patients admitted with ruptured aortic aneurysms and intact aortic aneurysms repaired in the Nationwide Inpatient Sample (NIS) between 2004-2019. We then examined the utilization of open, endovascular, and complex endovascular repair (OAR,EVAR,cEVAR) for each aortic aneurysm location (AAA,TAAA,TAA), alongside their resulting in-hospital mortality, over time. cEVAR included branched, fenestrated, and physician modified endograft.
RESULTS: 715,570 patients were identified with AAA (87% Intact-Repairs, 13% Rupture-Admissions). Both intact AAA repairs and ruptured AAA admissions decreased significantly between 2004 and 2019 (intact 41,060-34,215,p<.01; ruptured 7,175-4,625,p=.02). Out of all AAA repairs done in a given year, the use of EVAR increased (2004-2019: intact 45%-66%,p<.01; ruptured 10%-55%,p<.01) as well as cEVAR (2010-2019: intact 0%-23%,p<.01; ruptured 0%-14%,p<.01). Mortality after EVAR of intact AAAs decreased significantly by 29% (2004-2019, 0.73%-0.52%,p<.01) while mortality after OAR increased significantly by 16% (2004-2019, 4.4%-5.1%,p<.01). In the study, 27,443 patients were identified with TAAA (80% Intact, 20% Ruptured). In the same period, intact TAAA repairs trended upwards (2004-2019 1,435-1,640,p=.055) and cEVAR became the most common approach (2004-2019, 3.8%-72%,p=.055). 141,651 patients were identified with ascending, arch, or descending TAA (90% Intact, 10% Ruptured). Intact TAA repairs increased significantly (2004-2019 4,380-10,855,p<.01). From 2017-2019, the mortality after OAR of descending TAAs increased and mortality after TEVAR decreased (2017-2019: OAR 1.6%-3.1%; TEVAR 5.2%-3.8%).
CONCLUSIONS: Both intact AAA repairs and ruptured AAA admissions significantly decreased between 2004 and 2019. The use of endovascular techniques for the repair of all aortic aneurysm locations, both intact and ruptured, increased over the past two decades. Most recently in 2019, 89% of intact AAAs repairs, infrarenal through suprarenal, were endovascular (EVAR or cEVAR, respectively). cEVAR alone has risen to 23% of intact AAA repairs in 2019, from 0% a decade earlier. In this period of innovation, with many new options to repair aortic aneurysms while maintaining arterial branches, endovascular repair is now used for the majority of all intact aortic aneurysm repairs. Long-term data are needed to evaluate the durability of these procedures.

OBJECTIVE: In the endovascular aneurysm repair (EVAR) era, open surgical repair (OSR) is performed for ruptured abdominal aorta aneurysm (RAAA) in patients with complex aneurysm neck and technical difficulties. Understanding the risk factors of OSR is essential for the clinical selection of the ideal surgical procedure. We aimed to re-evaluate the outcomes of OSR and treatment options for RAAA.
METHODS: Patients who underwent OSR for RAAA between January 2010 and December 2022 were enrolled in this single-center, retrospective observational study. Preoperative status, operative findings, and postoperative course were retrospectively reviewed. The Cox proportional hazards model was used to evaluate the association between age and early postoperative mortality.
RESULTS: Among 142 patients, 43 (30.3%) and 99 (69.7%) were aged ≥80 and <80 years, respectively. Postoperative mortality within 30 days occurred in 24 (16.9%) patients (11/43 [25.6%] and 13/99 [13.1%] patients aged ≥80 and <80 years, respectively; hazard ratio [HR]=1.95; P=0.069). In a multivariable analysis, increased postoperative mortality within 30 days was associated with age ≥80 years (adjusted HR, aHR=2.36; P=0.049), the presence of pre- or intraoperative cardiopulmonary arrest (aHR=12.0; P<0.001), and postoperative gastrointestinal disorder (aHR=4.42; P=0.003).
CONCLUSIONS: EVAR may be preferable in older people; however, its use in cases of pre- or intraoperative cardiopulmonary arrest or perioperative gastrointestinal disorders remains controversial, and a careful discussion on the surgical indications is needed in such cases.

OBJECTIVE: Assess subsequent cardiovascular events and all-cause mortality in patients with intact AAA treated by EVAR according to the existence of isolated EL2 at 1 year after EVAR implantation.
METHODS: This retrospective, single-centre study included patients treated with EVAR between 2010 and 2017 in the vascular surgery department of the University Hospital of Lyon with a infrarenal AAA > 50 mm. The baseline clinical characteristics collected just before EVAR were retrieved from electronic patient records of our institution. AAA characteristics, procedure and the one-year post-operative CTA were reported. Study endpoints, major adverse cardiovascular events (MACE), major adverse lower extremity events (MALE) and all-cause mortality, were recorded during follow-up. Patients were divided into 2 groups according to the presence of isolated EL2 (EL2 +) or absence (EL2 -) of any endoleak on CTA at 1 year. MACE, MALE and all-cause mortality were compared between both groups.
RESULTS: During the study period, 589 patients were treated by endovascular surgery and 207 were included. According to the CTA results at 1 year, 60 patients (29%) were included in the EL2 + group, and 147 patients (71%) in the EL2 - group. A total of 109 patients (53%) experienced a MACE or MALE; significantly fewer patients in the EL2 + than in the EL2 - group did so (p = .009). There were 47 patients (23%) who experienced at least one MALE, and the frequency was significantly lower in the EL2 + group (p = .017).
CONCLUSIONS: Patients with AAA treated by EVAR who did not develop EL2 at one year, were at higher risk of MALE during follow-up. This might be explained by more frequent symptomatic LEPAD at baseline in this group. These patients therefore require a closer follow-up and strict control of cardiovascular risk factors to prevent cardiovascular morbi-mortality.

Abdominal aortic aneurysm (AAA) is a cardiovascular disease that seriously threatens human health and brings huge economic burden. At present, its pathogenesis remains unclear and its treatment is limited to surgical treatment. With the deepening and analysis of studies on the mechanism of ferroptosis, a new idea has been provided for the clinical management of AAA patients, including diagnosis, treatment and prevention. Therefore, this paper aims to construct a competitive endogenous RNA (ceRNA) regulatory axis based on ferroptosis to preliminarily explore the pathogenesis and potential therapeutic targets of AAA. We obtained upregulated and downregulated ferroptosis-related DEGs (FRGs) from GSE144431 dataset and 60 known ferroptosis-related genes. Pearson correlation analysis was used to find aldoketone reductase 1C (AKR1C1) in AAA samples. Enrichment analysis of these genes was performed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Correlation test between immune cells and AKR1C1 was investigated through single-sample gene set enrichment analysis (ssGSEA). The AKR1C1-miRNA pairs were predicted by the TargetScan database and miRWalk database. Circular RNA (CircRNA)-miRNA pairs were selected by the CircInteractome database. Overlapping miRNA between circRNA-miRNA and AKR1C1-miRNA pairs was visualized by Venn diagram. Finally, the circRNA-miRNA-mRNA axis was constructed by searching for upstream circRNA and downstream mRNA of overlapping miRNA. Only one downregulated AKR1C1 gene was found in GSE144431 and 60 ferroptosis-related genes. Functional Enrichment and Pathway Analysis of AKR1C1-related genes were further explored, and it was observed that they were mainly enriched in \"response to oxidative stress,\" \"glutathione biosynthetic process\" and \"nonribosomal peptide biosynthetic process,\" \"Ferroptosis,\" \"Glutathione metabolism\" and \"Chemical carcinogenesis-reactive oxygen species.\" They were also found to be significantly associated with most immune cells, including Activated Dendritic cells, CD56dim Natural killer cells, Gamma Delta T cells, Immature B cells, Plasmacytoid dendritic cell, Type 2 T helper cell, Activated CD4 T cell and Type 1 T helper cell. Has_circ_0005073-miRNA-543 and AKR1C1-miRNA-543 were identified by Online Database analysis. Therefore, we have established the has_circ_0005073/miRNA-543/AKR1C1 axis in AAA. We found AKR1C1 was differentially expressed between normal and AAA groups. Based on AKR1C1, we constructed the has_circ_0005073/miRNA-543/AKR1C1 axis to analyze AAA.

Abdominal aortic aneurysm (AAA) is a life-threatening disease that remains undetected until it acutely ruptures. Due to lack of effective pharmaceutic therapies, it is urgent to explore new prevention and treatment strategies. Metabolic reprogramming is a cellular process through which cells change their metabolic patterns to meet material and energy requirements, including glucose metabolism, lipid metabolism and amino acid metabolism. Recently, the regulatory role of metabolic reprogramming in cardiovascular diseases, especially AAA, has attracted significant attention. This review article focuses on the research progress regarding the effects of metabolic reprogramming of vascular smooth muscle cells (VSMCs) and macrophages on the occurrence and development of AAA, especially their roles in major pathological processes such as VSMCs apoptosis and phenotype transformation, extracellular matrix remodeling, oxidative stress, and inflammatory response. The aim is to provide new clues for the mechanism research and clinical treatment of AAA from the perspective of metabolism.

暂无摘要。

UNASSIGNED: Abdominal aortic aneurysm (AAA) is an important cause of cardiovascular mortality.
UNASSIGNED: The authors aimed to explore the associations between sleep patterns and genetic susceptibility to AAA.
UNASSIGNED: We included 344,855 UK Biobank study participants free of AAA at baseline. A sleep pattern was defined by chronotype, sleep duration, insomnia, snoring, and daytime sleepiness, and an overall sleep score was constructed with a range from 0 to 5, where a high score denotes a healthy sleep pattern. Polygenic risk score based on 22 single nucleotide polymorphisms was categorized into tertiles and used to evaluate the genetic risk for AAA. Cox proportional hazards regression models were used to assess the association between sleep, genetic factors, and the incidence of AAA.
UNASSIGNED: During a median of 12.59 years of follow-up, 1,622 incident AAA cases were identified. The HR per 1-point increase in the sleep score was 0.91 (95% CI: 0.86-0.96) for AAA. Unhealthy sleep patterns, defined as a sleep score ranging from 0 to 3, were found to be associated with a higher risk of AAA for the intermediate (HR: 1.18, 95% CI: 1.06-1.31) and poor sleep patterns (HR: 1.40, 95% CI: 1.13-1.73), respectively, compared to the healthy pattern. Participants with poor sleep patterns and high genetic risks had a 2.5-fold higher risk of AAA than those with healthy sleep patterns and low genetic risk.
UNASSIGNED: In this large prospective study, healthy sleep patterns were associated with a lower risk of AAA among participants with low, intermediate, or high genetic risk.

暂无摘要。

BACKGROUND: Thoracic endovascular aortic repair (TEVAR) is a minimally invasive technique used to treat type B aortic dissections. Left subclavian artery (LSA) reconstruction is required when treating patients with involvement of LSA. The best antiplatelet therapy after LSA reconstruction is presently uncertain.
METHODS: This study retrospectively analyzed 245 type B aortic dissection patients who underwent left subclavian artery revascularization during TEVAR. Out of 245 patients, 159 (64.9%) were in the single antiplatelet therapy (SAPT) group, receiving only aspirin, and 86 (35.1%) were in the dual antiplatelet therapy (DAPT) group, receiving aspirin combined with clopidogrel. During the 6-month follow-up, primary endpoints included hemorrhagic events (general bleeding and hemorrhagic strokes), while secondary endpoints comprised ischemic events (left upper limb ischemia, ischemic stroke, and thrombotic events), as well as death and leakage events. Both univariate and multivariate Cox regression analyses were performed on hemorrhagic and ischemic events, with the Kaplan-Meier method used to generate the survival curve.
RESULTS: During the six-month follow-up, the incidence of hemorrhagic events in the DAPT group was higher (8.2% vs. 30.2%, P < 0.001). No significant differences were observed in ischemic events, death, or leakage events among the different antiplatelet treatment schemes. Multivariate Cox regression analysis showed that DAPT (HR: 2.22, 95% CI: 1.07-4.60, P = 0.032) and previous chronic conditions (HR:3.88, 95% CI: 1.24-12.14, P = 0.020) significantly affected the occurrence of hemorrhagic events. Chronic conditions in this study encompassed depression, vitiligo, and cholecystolithiasis. Carotid subclavian bypass (CSB) group (HR:0.29, 95% CI: 0.12-0.68, P = 0.004) and single-branched stent graft (SBSG) group (HR:0.26, 95% CI: 0.13-0.50, P < 0.001) had a lower rate of ischemic events than fenestration TEVAR (F-TEVAR). Survival analysis over 6 months revealed a lower risk of bleeding associated with SAPT during hemorrhagic events (P = 0.043).
CONCLUSIONS: In type B aortic dissection patients undergoing LSA blood flow reconstruction after synchronous TEVAR, the bleeding risk significantly decreases with the SAPT regimen, and there is no apparent ischemic compensation within 6 months. Patients with previous chronic conditions have a higher risk of bleeding. The CSB group and SBSG group have less ischemic risk compared to F-TEVAR group.

BACKGROUND: The surgical evaluation and management of non-A non-B aortic dissections, in the absence of ascending aortic involvement, remains a grey area. It is in these scenarios when thorough evaluation of patient/family history, clinical presentation, but also overall lifestyle, is of immense importance when determining an optimal intervention.
METHODS: We present a 38-year-old patient with a physically demanding lifestyle as a professional wrestler, uncontrolled hypertension due to history of medical non-adherence, and family history of aortic dissection who presented with acute non-A non-B aortic dissection. He was spared a total arch replacement by undergoing a hybrid approach of complete aortic debranching with antegrade Thoracic Endovascular Aortic Repair (TEVAR). The patient was able to benefit from reduced cardiopulmonary bypass (CPB) time, avoidance of aortic cross clamp, circulatory arrest, and hypothermic circulation.
CONCLUSIONS: This patient\'s unique composition of a physically demanding lifestyle, personal history of medical non-adherence, family history of aortic dissection, and clinical presentation required a holistic approach to understanding an ideal intervention that would be best suited long-term. Due to this contextualization, the patient was able to be spared a total arch replacement, or suboptimal medical management, by instead undergoing a hybrid-approach with total aortic arch debranching with antegrade TEVAR.