Risk Of Abdominal Aortic Aneurysm Research Articles

A prospective longitudinal study of risk factors for abdominal aortic aneurysm.

The aim of this study was to identify risk factors for abdominal aortic aneurysm (AAA)from the largest Welsh screening cohort to date. Patients were recruited from 1993 (to 2015) as part of the South East Wales AAA screening programme through general practitioners. Demographic data and risk factors were collected by means of a self-report questionnaire. Statistical tests were performed to determine whether associations could be observed between AAA and potential risk factors. Odds ratios (OR) were also calculated for each of the risk factors identified. A total of 6879 patients were included in the study. Two hundred and seventy-five patients (4.0%) presented with AAA, of which 16% were female and 84% were male. Patients with AAA were older than the (no AAA) control group (p < 0.0001). The following risk factors were identified for AAA: family history of AAA (p < 0.0001); history of vascular surgery (p < 0.0001), cerebrovascular accident (p < 0.0001), coronary heart disease (p < 0.0001), diabetes (p < 0.0001), medication (p = 0.0018), claudication (p < 0.0001), smoking history (p = 0.0001) and chronic obstructive pulmonary disorder (p = 0.0007). AAA is associated with classical vascular risk factors, in addition to other less-well-documented risk factors including previous vascular surgery. These findings have practical implications with the potential to improve future clinical screening of patients in order to reduce AAA mortality.

Single-cell RNA sequencing identifies IFNICs as a cellular target for mitigating the progression of abdominal aortic aneurysm and rupture risk.

Abdominal aortic aneurysm (AAA) represents a life-threatening condition characterized by medial layer degeneration of the abdominal aorta. Nevertheless, knowledge regarding changes in regulators associated with aortic status remains incomplete. A thorough understanding of cell types and signaling pathways involved in the development and progression of AAAs is essential for the development of medical therapy. We harvested specimens of the abdominal aorta with different pathological features in Angiotensin II (AngII)-infused ApoE-/- mice, conducted scRNA-seq, identified a unique population of interferon-inducible monocytes/macrophages (IFNICs), which were amply found in the abdominal aortic aneurysms (AAAs). Gene set variation analysis (GSVA) revealed that activation of the cytosolic DNA sensing cGAS-STING and JAK-STAT pathways promoted the secretion of type I interferons in monocytes/macrophages and differentiated them into IFNICs. We generated myeloid cell-specific deletion of Sting1 (Lyz2-Cre+/-; Sting1flox/flox) mice and performed bone marrow transplantation and found that myeloid cell-specific deletion of Sting1 or Ifnar1 significantly reduced the incidence of AAA, aortic rupture rate and diameter of the abdominal aorta. Mechanistically, the activated pyroptosis- and inflammation-related signaling pathways, regulated by IRF7 in IFNICs, play critical roles in the developing AAAs. IFNICs is a unique monocyte/macrophage subset implicated in the development of AAAs and aortic rupture.

Causal relationship between immune cells and aortic aneurysms: a Mendelian randomization study.

The causal association between immune cell traits and aortic aneurysm remains unknown. We performed a bidirectional two-sample Mendelian randomization analysis to explore the causality between 731 immune cell characteristics and the risk of abdominal aortic aneurysm and thoracic aortic aneurysms through publicly available genetic data, respectively. To examine heterogeneity and horizontal pleiotropy, Cochran's Q test and MR-Egger intercept were utilized. Additionally, multivariable Mendelian randomization analysis and meta-analysis were performed in further analysis. We found that 20 immune phenotypes had a suggestive causality on abdominal aortic aneurysm, and 15 immune phenotypes had a suggestive causal effect on thoracic aortic aneurysm. After further false discovery rate adjustment (q value <0.1), CD20 on IgD+ CD38- B cell (q = 0.053) and CD127 on CD28+ CD4+ T cell (q = 0.096) were associated with an increased risk of abdominal aortic aneurysm, respectively, indicating a significant causality between them. After adjusting for smoking, there is still statistical significance between CD127 on CD28+ CD4+ T cell and abdominal aortic aneurysm. However, after adjusting for lipids, no statistical significance can be observed between CD127 on CD28+ CD4+ T cells and abdominal aortic aneurysm. Furthermore, there is still statistical significance between CD20 on IgD+ CD38- B cells and abdominal aortic aneurysm after adjusting for lipids and smoking, which was further identified by meta-analysis. We found a causal association between immune cell traits and aortic aneurysm by genetic methods, thus providing new avenues for future mechanism studies.

Something Sweet from Uncontrolled Sugar: The Enduring Protection of Impaired Glucose Control on Abdominal Aortic Aneurysm Risk

Something Sweet from Uncontrolled Sugar: The Enduring Protection of Impaired Glucose Control on Abdominal Aortic Aneurysm Risk

Insights on P2X7 in patients with abdominal aortic aneurysm and carotid atherosclerosis

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministero della Salute, Italia, Rete Cardiologica Nazionale Background Carotid atherosclerosis and abdominal aortic aneurysm (AAA) are co-morbidities [1]. P2X-purinoceptor-7 (P2X7) is expressed both in human AAA and atherosclerotic carotid plaque (CPL) and is instability-associated in CPL [2-4]. P2X7 is functionally related to miR-150 and miR-186 (two microRNA which modulate vascular cell proliferation) [5,6], and may be shed into the bloodstream in correlation with C-reactive protein increase [7]. Little is known about the possible association between AAA risk and circulating P2X7, miR-150 and miR-186 in patients with/without hemodinamically significant CPL. Purpose Our aim is exploring the possible relationship between circulating P2X7, target miRs clinical status and lesion dimensions in patients with CPL and/or AAA. Methods Male patients with AAA and/or CPL were characterized.CPL stenosis was assessed by Ecocolordoppler-TSA. Eligible cohort included 20 patients with AAA undergoing aneurysmectomy [10 with CPL stenosis ≤40% (group A), 10with CPL stenosis &amp;gt;40% (group B)], 10 patients with hemodinamically significant CPL and small or no AAA undergoing endarterectomy (group C) donating blood and vascular samples at surgery. Twelve healthy blood donors (group D) were enrolled as controls. P2X7 protein was evaluated by ELISA. P2X7 gene, miR-150 and miR-186 were determined by RT-qPCR. Results In group A, CPL appeared mainly localized at carotid bulb, in group B extended along branches. P2X7 gene was undetermined into serum and expressed without differences among groups in patient tissues. P2X7 protein was measurable in all serum samples and was lower in group B than in the others (p=0,0117, p=0,0009, p=0,0003 vs. group A, C, D, respectively) and in group C vs. D (p=0,0006). These data differentiated patients with hemodinamically significant CPLs with severe AAA from the other patients and all those with hemodinamically significant CPLs (irrespectively from AAA severity) from healthy individuals. In group B but not in the others, serum P2X7 was linearly associated to platelet concentration. In group C the amounts of P2X7 in CPL tissue and serum were negatively associated, whereas in group A and B the P2X7 levels in AAA tissue and serum were unrelated. The miRs were detected into both serum and tissue and not correlated among them nor with circulating P2X7 protein. The serum miR-186, but not miR-150, was differentially expressed in group A vs. B (p=0,0266) and linearly related to AAA diameter in group B (p=0.0351). P2X7 content and expressed gene (p=0,015, p= 0,023, respectively) and miR expressions (p=0,0418 for miR-186, p=0,0012 for miR-150) were more elevated in AAA vs. CPL tissues, highlighting the vascular heterogenicity. Conclusions Preliminary data suggest a role for P2X7 and miR-186 in profiling patients with hemodinamically significant CPL with/without high risk AAA, deserving further investigations.

#1737 Kidney function, kidney function decline, and the risk of abdominal aortic aneurysm: the Stockholm CREAtinine Measurements (SCREAM) project

Abstract Background and Aims Small, cross-sectional, cohort studies suggest a relationship between low estimated glomerular filtration rate (eGFR) and risk of developing abdominal aortic aneurysm (AAA). We here explored the possible association between eGFR and annual eGFR decline with future risk of AAA in a large community-based sample. Method Observational study from the SCREAM project, including participants free from AAA history. We used Cox regression to explore associations between eGFR and the rate of incident AAA and fatal-AAA (followed by death within 30 days). Among those with repeated eGFR tests within a year, we used linear mixed models to explore associations between the annual slope in eGFR and AAA rates. Results We included 1 586,543 eligible participants (mean age 47 years, 53% female, median eGFR 97 ml/min/1.73 m2). During median 7.6 years, 5,248 (0.34%) participants experienced AAA, of which 317 were fatal. In multivariable analyses, compared with individuals with eGFR 90 mL/min/1.73 m2, the rates of AAA and fatal-AAA were higher across lower eGFR: for eGFR 30 mL/min/1.73 m2, the HR of AAA was 1.23 (95% CI 1.09-1.39), and for fatal-AAA was 2.59 (1.71-3.90); for eGFR 15 mL/min/1.73 m2, the HR of AAA was 1.58 (1.31-1.90) and for fatal-AAA was 3.92 (2.28-6.70). Total 639 607 participants had repeated eGFR measures within a year, and experienced 3,416 AAA events during median 8.8 years of follow-up. Compared with participants showing a stable eGFR slope (−1 to 1 mL/min/y), the rate of AAA was 10% higher (HR 1.10 [1.00-1.21]) in those with an eGFR decline of 1-3 mL/min/y, and 30% higher (HR 1.30 [1.03-1.65]) in those with an eGFR decline &amp;gt;3 mL/min/y. Conclusion Both a single point eGFR and the annual slope of eGFR decline were associated with future risks of AAA. The incidence rate of AAA, and particularly fatal AAA, was higher with greater severity of chronic kidney disease or speed of eGFR decline.

Diagnostic value of uric acid to high-density lipoprotein cholesterol ratio in abdominal aortic aneurysms

Background Abdominal aortic aneurysm (AAA) is highly lethal upon onset of acute aortic diseases (AAD) or rupture. Dyslipidaemia and hyperuricaemia are important risk factors for the development of AAA and AAD as well as aortic disease-related death. The aim of this study was to explore whether uric acid (UA) to high-density lipoprotein cholesterol (HDL-C) ratio (UHR) can be used as an independent predictor of the presence of AAA or AAD. Methods Three hundred subjects, including 100 AAA patients (AAA group), 100 AAD patients (AAD group) and 100 controls (CON group), were recruited in this study. UHR and other serum samples were obtained upon the patients’ admission before any medical treatment. The optimal cut-off points of UHR were determined using receiver operating characteristic (ROC) curve analysis. Results The UHR in AAA group was significantly higher than that in CON group, but there was no significant difference between AAD group and CON group. The optimal cut-off point of UHR for AAA was 7.78 (sensitivity 84.7%, specificity 62.4%, and AUC 0.811; p < 0.001), and UHR (OR: 1.122, 95%CI: 1.064-1.184; p < 0.001) was found to be an independent factor for predicting AAA after adjusting for traditional AAA risk factor. Conclusion UHR can be widely used in clinical practice as an auxiliary tool for screening AAA. The optimal cut-off point for UHR to AAA was determined for the first time in Chinese subjects.

Identification of biomarkers for abdominal aortic aneurysm in Behçet's disease via mendelian randomization and integrated bioinformatics analyses.

Behçet's disease (BD) is a complex autoimmune disorder impacting several organ systems. Although the involvement of abdominal aortic aneurysm (AAA) in BD is rare, it can be associated with severe consequences. In the present study, we identified diagnostic biomarkers in patients with BD having AAA. Mendelian randomization (MR) analysis was initially used to explore the potential causal association between BD and AAA. The Limma package, WGCNA, PPI and machine learning algorithms were employed to identify potential diagnostic genes. A receiver operating characteristic curve (ROC) for the nomogram was constructed to ascertain the diagnostic value of AAA in patients with BD. Finally, immune cell infiltration analyses and single-sample gene set enrichment analysis (ssGSEA) were conducted. The MR analysis indicated a suggestive association between BD and the risk of AAA (odds ratio [OR]: 1.0384, 95% confidence interval [CI]: 1.0081-1.0696, p = 0.0126). Three hub genes (CD247, CD2 and CCR7) were identified using the integrated bioinformatics analyses, which were subsequently utilised to construct a nomogram (area under the curve [AUC]: 0.982, 95% CI: 0.944-1.000). Finally, the immune cell infiltration assay revealed that dysregulation immune cells were positively correlated with the three hub genes. Our MR analyses revealed a higher susceptibility of patients with BD to AAA. We used a systematic approach to identify three potential hub genes (CD247, CD2 and CCR7) and developed a nomogram to assist in the diagnosis of AAA among patients with BD. In addition, immune cell infiltration analysis indicated the dysregulation in immune cell proportions.

Two patients treated with simultaneous EVAR and TAVI

ObjectivesThe combination of severe aortic stenosis (AS) and abdominal aortic aneurysm (AAA) is not uncommon in elderly patients and should be optimally managed. However, the guidelines do not provide recommendations for clinical practice, thus reinforcing the need for further analysis of this complex, challenging condition. MethodsWe report 2 cases of patients with severe AS patients with high surgical risk for aortic valve replacement (AVR) and AAA with a diameter of more than 5.5 cm who underwent simultaneous transcatheter aortic valve implantation (TAVI) and endovascular aneurysm repair (EVAR). ResultsThe patients were successfully treated with EVAR and TAVI and had an uncomplicated postoperative course. The importance of this combined pathological condition is emphasised as the need for simultaneous treatment with an endovascular technique, after a thorough study of the clinical and imaging data of the patients and decision-making by the teams of interventional cardiologists and vascular surgeons. The case reports are limited to one or a small number of incidents that occurred simultaneously or sequentially, without specifying the most appropriate method. ConclusionsSevere AS and AAA can be treated with combined procedures with EVAR followed by TAVI simultaneously, with a safe and effective result. The study by a multidisciplinary team highlights the importance of a thorough evaluation of all patients before intervention and the need for more studies and guidelines.

Causal association between gut microbiomes and different types of aneurysms: a Mendelian randomization study.

Previous studies suggests that gut microbiomes are associated with the formation and progression of aneurysms. However, the causal association between them remains unclear. A two-sample Mendelian randomization was conducted to investigate whether gut microbiomes have a causal effect on the risk of intracerebral aneurysm (IA), thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA), and aortic aneurysm (AA). Single nucleotide polymorphisms (SNPs) smaller than the locus-wide significance level (1 × 10-5) were selected as instrumental variables. We used inverse-variance weighted (IVW) test as the primary method for the evaluation of causal association. MR-Egger, weighted median, weighted mode, and MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) methods were conducted for sensitive analysis. The p-value was adjusted by the false discovery rate (FDR) which adjust the results of multiple comparisons, a p < 0.05 and q < 0.1 was considered a significant causal association. Additionally, a p < 0.05 and q > 0.1 was considered a suggestive causal effect. Additionally, reverse MR was also performed to exclude the possibility of reverse causality. The phylum Firmicutes (OR = 0.62; 95% CI, 0.48-0.81), class Lentisphaeria (OR = 0.75; 95% CI, 0.62-0.89), and order Victivallales (OR = 0.75; 95% CI, 0.62-0.89) have a causal protective effect on the risk of AAA. Additionally, class Verrucomicrobia, class Deltaproteobacteria, order Verrucomicrobiale, family Verrucomicrobiacea, genus Eubacterium rectale group, genus Akkermansia, and genus Clostridium innocuum group were negatively associated with the risk of different types of aneurysms, whereas class Negativicutes, order Selenomonadales, and genus Roseburia had positive causal association with different types of aneurysms (p < 0.05; q > 0.1). Further sensitivity analysis validated the robustness of our MR results, and no reverse causality was found with these gut microbiomes (p > 0.05). Our MR analysis confirmed the causal association of specific gut microbiomes with AAA, and these microbiomes were considered as protective factors. Our result may provide novel insights and theoretical basis for the prevention of aneurysms through regulation of gut microbiomes.

Uncertainty quantification of the impact of peripheral arterial disease on abdominal aortic aneurysms in blood flow simulations.

Peripheral arterial disease (PAD) and abdominal aortic aneurysms (AAAs) often coexist and pose significant risks of mortality, yet their mutual interactions remain largely unexplored. Here, we introduce a fluid mechanics model designed to simulate the haemodynamic impact of PAD on AAA-associated risk factors. Our focus lies on quantifying the uncertainty inherent in controlling the flow rates within PAD-affected vessels and predicting AAA risk factors derived from wall shear stress. We perform a sensitivity analysis on nine critical model parameters through simulations of three-dimensional blood flow within a comprehensive arterial geometry. Our results show effective control of the flow rates using two-element Windkessel models, although specific outlets need attention. Quantities of interest like endothelial cell activation potential (ECAP) and relative residence time are instructive for identifying high-risk regions, with ECAP showing greater reliability and adaptability. Our analysis reveals that the uncertainty in the quantities of interest is 187% of that of the input parameters. Notably, parameters governing the amplitude and frequency of the inlet velocity exert the strongest influence on the risk factors' variability and warrant precise determination. This study forms the foundation for patient-specific simulations involving PAD and AAAs which should ultimately improve patient outcomes and reduce associated mortality rates.

N6-methyladenosine-associated genetic variants in NECTIN2 and HPCAL1 are risk factors for abdominal aortic aneurysm

Although N6-methyladenosine (m6A) modification has been implicated in the pathogenesis of abdominal aortic aneurysm (AAA), the relationship between m6A-associated single nucleotide polymorphisms (m6A-SNPs) and AAA remains unknown. This study used integrative multi-omics analysis and clinical validation approaches to systematically identify potential m6A-SNPs connected with AAA risk. We found that rs6859 and rs10198139 could modulate the expression of local genes, NECTIN2 and HPCAL1, respectively, which exhibited upregulation in AAA tissues, and their risk variants were significantly correlated with an increased susceptibility to AAA. Incorporating rs6859 and rs10198139 improved the efficiency of AAA risk prediction compared to the model considering only conventional risk factors. Additionally, these two SNPs were predicted to be located within the regulatory sequences, and rs6859 showed a substantial impact on m6A modification levels. Our findings suggest that m6A-SNPs rs6859 and rs10198139 confer an elevated risk of AAA, possibly by promoting local gene expression through an m6A-mediated manner.

Antisense oligonucleotide targeting hepatic Serum Amyloid A limits the progression of angiotensin II-induced abdominal aortic aneurysm formation

Background and aimsObesity increases the risk for abdominal aortic aneurysms (AAA) in humans and enhances angiotensin II (AngII)-induced AAA formation in C57BL/6 mice. We reported that deficiency of Serum Amyloid A (SAA) significantly reduces AngII-induced inflammation and AAA in both hyperlipidemic apoE-deficient and obese C57BL/6 mice. The aim of this study is to investigate whether SAA plays a role in the progression of early AAA in obese C57BL/6 mice. MethodsMale C57BL/6J mice were fed a high-fat diet (60% kcal as fat) throughout the study. After 4 months of diet, the mice were infused with AngII until the end of the study. Mice with at least a 25% increase in the luminal diameter of the abdominal aorta after 4 weeks of AngII infusion were stratified into 2 groups. The first group received a control antisense oligonucleotide (Ctr ASO), and the second group received ASO that suppresses SAA (SAA-ASO) until the end of the study. ResultsPlasma SAA levels were significantly reduced by the SAA ASO treatment. While mice that received the control ASO had continued aortic dilation throughout the AngII infusion periods, the mice that received SAA-ASO had a significant reduction in the progression of aortic dilation, which was associated with significant reductions in matrix metalloprotease activities, decreased macrophage infiltration and decreased elastin breaks in the abdominal aortas. ConclusionsWe demonstrate for the first time that suppression of SAA protects obese C57BL/6 mice from the progression of AngII-induced AAA. Suppression of SAA may be a therapeutic approach to limit AAA progression.

Breathing danger: linking air pollution to cardiovascular disease and increased risk of abdominal aortic aneurysm.

Breathing danger: linking air pollution to cardiovascular disease and increased risk of abdominal aortic aneurysm.

Evaluation of associations between outflow morphology and rupture risk of abdominal aortic aneurysms

PurposeThis study aimed to evaluate the association between the outflow morphology and abdominal aortic aneurysm (AAA) rupture risk, to find risk factors for future prediction models. Materials and methodsWe retrospectively analyzed 46 patients with ruptured AAAs and 46 patients with stable AAAs using a 1:1 match for sex, age, and maximum aneurysm diameter. The chi-square test, paired t-test, and Wilcoxon signed-rank test were used to compare variables. Logistic regression was performed to evaluate variables potentially associated with AAA rupture. Receiver operating characteristic curve analysis and the area under the curve (AUC) were used to assess the regression models. ResultsRuptured AAAs had a shorter proximal aortic neck (median (interquartile range, IQR): 24.0 (9.4–34.2) mm vs. 33.3 (20.0–52.8) mm, p = 0.004), higher tortuosity (median(IQR): 1.35 (1.23–1.49) vs. 1.29 (1.23–1.39), p = 0.036), and smaller minimum luminal area of the right common iliac artery (CIA) (median (IQR): 86.7 (69.9–126.4) mm2 vs. 118.9 (86.3–164.1)mm2, p = 0.001) and left CIA (median(IQR): 92.2 (67.3,125.1) mm2 vs. 110.7 (80.12, 161.1) mm2, p = 0.010) than stable AAA did. Multiple regression analysis demonstrated significant associations of the minimum luminal area of the bilateral CIAs (odds ratio [OR] = 0.996, 95 % confidence interval [CI] 0.991–0.999, p = 0.037), neck length (OR = 0.969, 95 % CI 0.941–0.993, p = 0.017), and aneurysm tortuosity (OR = 1.031, 95 % CI 1.003–1.063, p = 0.038) with ruptured AAAs. The AUC of this regression model was 0.762 (95 % CI 0.664–0.860, p < 0.001). ConclusionsThe smaller minimum luminal area of the CIA is associated with an increased risk of rupture. This study highlights the potential of utilizing outflow parameters as novel and additional tools in risk assessment. It also provides a compelling rationale to further intensify research in this area.

The associations among peptic ulcer disease, Helicobacter pylori infection, and abdominal aortic aneurysms: A nationwide population-based cohort study

BackgroundThere are overlapping risk factors and underlying molecular mechanisms for both peptic ulcer disease (PUD) and abdominal aortic aneurysm (AAA). Despite improvements in the early diagnosis and treatment of AAA, ruptured AAAs continue to cause a substantial number of deaths. Helicobacter pylori are Gram-negative, microaerophilic bacteria that are now recognized as the main cause of PUD. H. pylori infection (HPI) is associated with an increased risk of certain cardiovascular diseases. HPIs can be treated with at least two different antibiotics to prevent bacteria from developing resistance to one particular antibiotic. MethodsWe conducted a population-based cohort study using the National Health Insurance Research Database to evaluate whether associations exist among PUD, HPI, and eradication therapy for HPI and AAA. The primary outcome of this study was the cumulative incidence of AAA among patients with or without PUD and HPI during the 14-year follow-up period. ResultsOur analysis included 7003 patients with PUD/HPI, 7003 patients with only PUD, and another 7003 age-, sex-, and comorbidity-matched controls from the database. We found that patients with PUD/HPI had a significantly increased risk of AAA compared to those with PUD alone and matched controls. The patients who had PUD/HPI had a significantly higher cumulative risk of developing AAA than those with PUD and the comparison group (2.67 % vs. 1.41 % vs. 0.73 %, respectively, p < 0.001). Among those patients with PUD/HPI, patients who had eradication therapy had a lower incidence of AAA than those without eradication therapy (2.46 % vs. 3.88 %, p = 0.012). ConclusionsWe revealed an association among PUD, HPI, and AAA, even after adjusting for age, sex, comorbidities, and annual medical follow-up visits. Notably, we found that HPI eradication therapy reduced the incidence of AAA among patients with PUD.

Effects of preoperative aortic tortuosity and postoperative hypertension on patient-specific hemodynamics of abdominal aortic aneurysm

Abdominal aortic aneurysm (AAA) is a serious dilated vascular disease. The risk factors of aneurysm rupture and postoperative blood pressure are the major clinical concerns. The purpose of this work is to analyze the hemodynamic difference between preoperative and postoperative AAA using patient-specific boundary conditions and explore the rupture risk of AAA with different torsion and to simulate the blood flow of different degrees of hypertension. A three-element Windkessel model is utilized as the outlet boundary condition. 20-sim software and self-developed user-defined functions are used to calibrate the parameters. To analyze the influence of aortic tortuosity on hemodynamics, five AAA geometries with different torsion degrees are modified and obtained. We also grade the hypertension and explore the effect of hypertension after operation. The analysis results are consistent with the patient-specific situation. The results show that stent implantation for aneurysms reduces the pressure at the lesion site and increase the speed and wall shear stress. Vessels with high torsion have lower time-averaged wall shear stress (TAWSS), higher oscillatory shear stress index (OSI) and relative retention time, and more disordered blood flow. After stent implantation, with the increase in blood pressure, TAWSS and OSI continue to increase, and the blood flow speed is also faster. AAA with high torsion is more likely to rupture. In clinical practice, attention should be paid to the degree of torsion of the lesion site. Furthermore, blood pressure should be monitored and controlled in time to prevent postoperative complications.

Association of metformin use with abdominal aortic aneurysm: A systematic review and meta-analysis.

Abdominal aortic aneurysm (AAA) is a cardiovascular disease characterized by a high mortality rate when ruptured. Some studies suggest a potential inverse correlation between AAA and diabetes patients, especially those undergoing metformin treatment. However, this relationship remains unclear. This paper offers a systematic review and meta-analysis with the objective of clarifying the influence of metformin on AAA. A search for relevant articles was performed across multiple databases including PubMed, ScienceDirect, Cochrane and Scopus. The focus was on studies that examined the comparative effects of metformin and non-metformin treatments on AAA patients. Data from appropriate studies were consolidated to estimate the effects. Our study encompassed 11 articles, comprising 13 cohorts that compared metformin (n = 32,250) with a control group (n = 116,339). The random effects meta-analysis revealed that metformin was associated with a slower growth rate (weighted mean difference (WMD) -0.86 mm; 95% CI: -1.21 to -0.52; p < 0.01; I2: 81.4%) and fewer AAA-related events (OR: 0.54; 95% CI: 0.34 to 0.86; p = 0.01; I2: 60.9%). The findings suggest that metformin may be linked to a reduced risk of aortic aneurysm. A meta-regression analysis indicated that the association between metformin and AAA growth was significantly influenced by male gender (p = 0.027), but not by age (p = 0.801), hypertension (p = 0.256), DM (p = 0.689), smoking history (p = 0.786), use of lipid-lowering agents (p = 0.715), or baseline diameter (p = 0.291). These results hint at a potential role for metformin in limiting annual AAA growth, AAA-related events, and the risk of AAA.

Air pollutants, genetic susceptibility, and abdominal aortic aneurysm risk: a prospective study.

Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown. This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset. Long-term exposure to particulate matter with an aerodynamic diameter <2.5 µm [PM2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10 µm [PM10, 1.21 (1.16, 1.27)], nitrogen dioxide [NO2, 1.16 (1.11, 1.22)], and nitrogen oxides [NOx, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM2.5, 3.09 (2.39, 4.00) for PM10, 2.41 (1.86, 3.13) for NO2, and 2.01 (1.55, 2.61) for NOx. In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence.

Development and validation of a machine-learning prediction model to improve abdominal aortic aneurysm screening

ObjectiveDespite recommendations by the United States Preventive Services Task Force and the Society for Vascular Surgery, adoption of screening for abdominal aortic aneurysms (AAAs) remains low. One challenge is the low prevalence of AAAs in the unscreened population, and therefore a low detection rate for AAA screenings. We sought to use machine learning to identify factors associated with the presence of AAAs and create a model to identify individuals at highest risk for AAAs, with the aim of increasing the detection rate of AAA screenings. MethodsA machine-learning model was trained using longitudinal medical records containing lab results, medications, and other data from our institutional database. A retrospective cohort study was performed identifying current or past smoking in patients aged 65 to 75 years and stratifying the patients by sex and smoking status as well as determining which patients had a confirmed diagnosis of AAA. The model was then adjusted to maximize fairness between sexes without significantly reducing precision and validated using six-fold cross validation. ResultsValidation of the algorithm on the single-center institutional data utilized 18,660 selected patients over 2 years and identified 314 AAAs. There were 41 factors identified in the medical record included in the machine-learning algorithm, with several factors never having been previously identified to be associated with AAAs. With an estimated 100 screening ultrasounds completed monthly, detection of AAAs is increased with a lift of 200% using the algorithm as compared with screening based on guidelines. The increased detection of AAAs in the model-selected individuals is statistically significant across all cutoff points. ConclusionsBy utilizing a machine-learning model, we created a novel algorithm to detect patients who are at high risk for AAAs. By selecting individuals at greatest risk for targeted screening, this algorithm resulted in a 200% lift in the detection of AAAs when compared with standard screening guidelines. Using machine learning, we also identified several new factors associated with the presence of AAAs. This automated process has been integrated into our current workflows to improve screening rates and yield of high-risk individuals for AAAs.