BackgroundAortic aneurysms (AA), including thoracic (TAA) and abdominal (AAA) types, are life-threatening conditions with complex and poorly understood mechanisms. Metabolic alterations, particularly in amino acid and energy metabolism, have been linked to AA, but their roles remain unclear due to limited and confounded observational evidence.ObjectiveThis research aimed to comprehensively investigate the potential causal links between serum metabolites and the development of thoracic (TAA) and abdominal (AAA) aortic aneurysms.MethodsWe analyzed serum metabolites from the Metabolomics data, using datasets of 353,049 individuals for TAA (3510 cases) and 353,087 individuals for AAA (3548 cases). Mendelian randomization (MR) techniques, including MR-Egger regression and inverse-variance weighting (IVW), assessed causality, with heterogeneity tested using Cochran's Q and I2 statistics, and pleiotropy via the MR-Egger intercept. Sensitivity was further checked through leave-one-out analysis. SNP annotations identified genes linked to TAA and AAA, and metabolic pathways were also analyzed.ResultsNine metabolites were causally linked to TAA, with three as risk factors, while 18 metabolites were associated with AAA, including eight risk factors. 3-dehydrocarnitine showed contrasting effects, acting as a risk factor for TAA (OR = 2.704; P = 0.031) and a protective factor for AAA (OR = 0.303; P = 0.025). Pathway analysis revealed TAA-related pathways such as "Pyruvaldehyde degradation" and "Arginine biosynthesis," while AAA was linked to "Phenylalanine metabolism" and "Valine, leucine, and isoleucine biosynthesis." No horizontal pleiotropy was detected, and results were robust.ConclusionsIdentified metabolites and pathways may serve as potential biomarkers and therapeutic targets for the clinical assessment and prevention of TAA and AAA.

Currently, there is no effective and convenient indicator for the early differential diagnosis of ruptured abdominal aortic aneurysms (rAAAs) from unruptured abdominal aortic aneurysms (AAAs).

The aim of this study was to explore indicators for the early differential diagnosis of rAAAs in a clinical setting.

This case‒control study included 276 subjects within the last 5 years (220 patients with unruptured AAAs; 56 patients with rAAAs) in the initial analysis and 229 subjects (186 patients with unruptured AAA's; 43 patients with rAAA's) after subgroup analysis. The meaningful indicators were screened via univariate analysis and logistic regression analysis. The diagnostic performance and clinical usefulness of the indicators were assessed and compared using receiver operating characteristic (ROC) curve analysis, decision curve analysis (DCA) and clinical impact curve (CIC).

A high venous blood neutrophil counts (OR = 1.316, P = 0.007) was found to be a risk factor for rAAAs in the initial model. After subgroup analysis, the levels of neutrophils (OR = 1.394, P = 0.017) and D-dimer (OR = 1.023, P = 0.043) were both significantly greater in patients with a rAAA. Abdominal pain (OR = 32.613, P = 0.044) and back pain (OR=91.946, P = 0.036) were strongly associated with the rupture of AAA. The results of the receiver operating characteristic (ROC) analysis revealed that neutrophils (AUC: 0.847, 95% CI: 0.774-0.921) and NLR (AUC: 0.795, 95% CI: 0.717-0.873) had good diagnostic performance for rAAA. DCA demonstrated that the net benefit of neutrophils was greater than that of other indicators. The CIC confirmed that the model has good clinical usefulness.

The use of neutrophils may enhance the early diagnostic accuracy for identifying rAAAs and holds potential for clinical and scientific applications.

Abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by the pathological dilation of the abdominal aorta. Diabetes mellitus is a well-established risk factor for cardiovascular diseases, yet its relationship with AAA remains debated. We aimed to identify longitudinal associations between glycated hemoglobin A1c (HbA1c) level and the risk of AAA development.

A prospective cohort study was conducted using UK Biobank data, encompassing 326,152 participants aged 39 to 73 years, recruited from 2006 to 2010. Participants provided biological samples and completed questionnaires. AAA cases was identified via International Classification of Diseases, 10th edition, codes from linked health records. HbA1c levels and other covariates were measured. Logistic and Cox regression models were used to assess the associations between HbA1c levels and AAA prevalence and incidence. Restricted cubic spline models were applied to examine dose-response relationships. Subgroup, interaction, and sensitivity analyses were also performed.

The study revealed a nonlinear inverted U-shaped HbA1c-AAA risk relationship, with hazard ratios for AAA incidence peaking at 5.82% before declining. Compared with the lowest quartile of HbA1c levels, ascending quartiles showed progressively elevated AAA risks: Q2 = 1.14 (95% confidence interval [CI], 1.01-1.29), Q3 = 1.11 (95% CI, 0.98-1.26), Q4 = 1.27 (95% CI, 1.12-1.44; all P for trend < .05). Stratified analyses identified amplified risk escalation in younger age, elevated low-density lipoprotein cholesterol, and nondiabetic subgroups. Sensitivity analyses confirmed association robustness. Notably, younger participants (<65 years) exhibited 2.38-fold higher Q4/Q1 AAA risk (95% CI, 1.89-2.99).

This study reveals a bidirectional HbA1c-AAA incidence association, underscoring the clinical imperative for optimized glycemic control in primary AAA prevention, particularly among younger adults and hyperlipidemic patients.

Altered hemodynamics is a key factor for atherosclerosis. For decades, endothelial cell (EC) responses to fluid-generated wall shear stress have been the central focus for atherogenesis. However, circulating blood is not a cell-free fluid, it contains mechanosensitive red blood cells (RBCs) that are also subjected to altered hemodynamics and release a large amount of ATP, but their impact on atherosclerosis has been overlooked. The focus of this study is the role of shear stress (SS)-induced RBC-released ATP in atherosclerosis. Hypercholesterolemic mouse models with and without RBC-Pannexin 1 deletion were used for the study. Results showed that SS-induced release of ATP from RBCs was at µM concentrations, three-orders of magnitude higher than that from other cell types. Suppression of RBC-released ATP via deletion of Pannexin 1, a mechanosensitive ATP-permeable channel, reduced high-fat diet-induced aortic plaque burden by 40%-60%. Importantly, the location and the extent of aortic atherosclerotic lesions spatially matched with the ATP deposition profile at aortic wall predicted by a computational fluid dynamic (CFD) model. Furthermore, hypercholesterolemia increases EC susceptibility to ATP with potentiated increase in [Ca2+]i, an initial signaling for aortic EC barrier dysfunction, and an essential cause for lipid accumulation and inflammatory cell infiltration. The computational prediction also provides a physics-based explanation for RBC-released ATP-induced sex disparities in atherosclerosis. Our study reveals an important role of RBC-released ATP in the initiation and progression of atherosclerosis. These novel findings provide a more comprehensive view of how altered hemodynamics and systemic risk factors synergistically contribute to atherosclerosis.NEW & NOTEWORTHY This study reveals that, in addition to fluid-derived wall shear stress, the disturbed blood flow-induced release of ATP from mechanosensitive red blood cells (RBCs), the major cellular components of blood, along with hypercholesterolemia-induced increases in endothelial cell susceptibility to ATP contribute significantly to the initiation and progression of atherosclerosis. These novel findings advance our current understanding of how altered hemodynamics and hypercholesterolemia synergistically contribute to atherosclerosis for the first time with the inclusion of RBCs.

Abdominal aortic aneurysm (AAA) and peripheral arterial disease (PAD) are two cardiovascular diseases associated with considerable morbidity, mortality and quality of life impairment. As they are multifactorial diseases, several factors contribute to their pathogenesis, including oxidative stress and lipid peroxidation, and these may have key roles in the development of these pathologies. Alterations of the lipid metabolism and lipid profile have been reported in cardiovascular diseases but to a lesser extent in AAA and PAD. Modifications in the profile of some molecular lipid species, in particular, native phospholipid and triglyceride species were mainly reported for AAA, while alterations in the fatty acid profile were noticed in the case of PAD. Oxidized phospholipids were also reported for AAA. Although AAA and PAD have a common atherosclerotic root, lipidomics demonstrates the existence of distinct lipid. Lipidomic research regarding AAA and PAD is still scarce and should be set in motion to increase the knowledge on the lipid changes that occur in these diseases, contributing not only to the discovery of new biomarkers for diagnosis and prognosis assessment but also to tailor precision medicine in the clinical field.

For men ages 65 to 75 years without a smoking history and for women ages 65 to 75 years with a smoking history, the United States Preventative Service Task Force recommends that primary care providers (PCPs) use their clinical judgement when offering abdominal aortic aneurysm (AAA) screening. This study describes the trends in screening for these cohorts, identifies factors that may influence screening rates, and compares outcomes between screened and unscreened patients.

The TriNetX population database was queried for subjects with routine PCP visit between ages 65 to 75 from 2007 to 2023 to create cohorts of male smokers, male nonsmokers, and female smokers. Prevalence and 1- and 3-year incidences of AAA screening by ultrasound and computed tomography scans/magnetic resonance imaging (CT/MRI) were calculated. Screened and unscreened patients' demographics, diagnoses, and medications were compared. Rates of AAA diagnosis and repair were compared between unmatched screened and unscreened patients.

Screening for all groups peaked in 2023. Male smokers had the highest screening prevalence (21.2%), followed by male nonsmokers (3.1%) and female smokers (0.90%). The 1-year incidence of screening increased for male smokers, peaking at 8.2% in 2021. The 1-year incidence plateaued at 1.9% for male nonsmokers in 2020 and remained between 0.25% and 0.35% for female smokers for the whole observation period. By 2023, 23.6%, 14.3%, and 24.3% of male smokers, male nonsmokers, and female smokers had been screened via CT/MRI, respectively, with CT/MRI comprising the majority of screening events for all three cohorts. Hyperlipidemia and statin use were associated with screening for all groups (P < .05), whereas a personal history of coronary artery disease was associated with no screening. Screening for male nonsmokers was associated with hypertension, diabetes, and chronic pulmonary obstructive disease (P < .05). Screening in female smokers was associated with family history of coronary artery disease (odds ratio, 1.50; P < .001). For all groups, screening was associated with unruptured AAA diagnosis and endovascular aortic repair (P < .05). Screened female smokers had similar rates of AAA diagnosis as male nonsmokers (4.58% and 4.37%, respectively).

AAA screening in all at-risk populations increases diagnosis and treatment of AAA, but the screening rate is low for all groups, even with increasing CT/MRI use. Patients with strong risk factors for AAA are not undergoing screening. Collaboration with PCPs is necessary to increase screening rates and ensure that patients with the most clinically consequential risk factors are managed appropriately.

Determining the normal diameter of the abdominal aorta in different populations and its relationship with other demographic factors is crucial for diagnosing and managing abdominal aortic diseases. This study aimed to assess the size of the abdominal aorta in a healthy Iranian population.

This cross-sectional study included healthy individuals. Various variables including age, sex, height, and weight were measured as part of this study. We performed an echocardiographic evaluation to assess the aortic sections.

The study encompassed 167 participants, predominantly women (67.7%). Notable differences in sizes of the ascending aorta, aortic arch, sinus of Valsalva, and abdominal aorta were observed across the four age groups. Men exhibited greater sizes in multiple aortic sections within the 45-64 age group. Correlation and regression analyses demonstrated significant positive relationships between abdominal aorta size and various aortic dimensions, with a one-millimeter increase in ascending or descending aorta diameter corresponding to a 0.23 and 0.35 mm increase, respectively, in abdominal aorta diameter. The relationship between abdominal aorta size and demographic factors such as gender, age, weight, BSA, and SBP was explored, revealing age as a significant predictor.

We observed significant differences in the sizes of distinct aortic sections across different age groups, underscoring the importance of considering age-related changes when evaluating aortic characteristics. These findings contribute to our understanding of the structural changes that occur in the aorta over time. Echocardiographic screening of the abdominal aorta would enable echocardiologists to diagnose the aneurysmal aorta.

Abdominal aortic aneurysms (AAAs) possess significant patient morbidity and mortality, but diagnosis can be missed or delayed given variable presenting symptoms. Renal colic is a potential "red herring" in cases of symptomatic AAA. This case involves an atypical presentation of flank pain likely due to both nephrolithiasis and an AAA. Prompt recognition of AAAs by the emergency department (ED) is critical to prevent misdiagnosis and initiate rapid treatment when indicated.

Mitochondrial dysfunction has been implicated in the pathogenesis of aortic aneurysms (AA); however, the causal role of mitochondrial-related proteins remains unclear. This study employs a Mendelian randomization (MR) approach to investigate the potential causal relationship between mitochondrial proteins and AA. Genetic instruments for mitochondrial proteins were obtained from the IEU Open genome-wide association study database, while AA-related genetic data were sourced from the FinnGen biobank. Inverse-variance weighting (IVW) served as the primary MR method, with MR-Egger and weighted median approaches utilized as complementary methods. Sensitivity analyses, including Cochran Q test, MR-Egger intercept, and MR-PRESSO, were performed to assess heterogeneity and pleiotropy. Reverse MR analysis was conducted to exclude the possibility of reverse causation. To enhance the robustness of the findings, replication was carried out using genome-wide association study Catalog data, and a meta-analysis was performed by integrating discovery and replication datasets. Gene expression validation was conducted using the Gene Expression Omnibus dataset, and gene set enrichment analysis (GSEA) was applied to explore relevant biological pathways. Additionally, in vitro experiments employing platelet-derived growth factor-BB-induced human aortic smooth muscle cells were performed to validate the expression patterns of mitochondrial-related proteins at both mRNA and protein levels. Through rigorous genetic variant selection, MR analysis using IVW, sensitivity analyses, replication, and meta-analysis, we identified iron-sulfur cluster assembly enzyme (ISCU), 39S ribosomal protein L14 (MRPL14), and mitochondrial peptide methionine sulfoxide reductase (MSRA) as mitochondrial proteins associated with AA. Sensitivity analyses confirmed the robustness of these findings, with no evidence of heterogeneity or pleiotropy. Reverse MR analysis ruled out reverse causation. Gene expression analysis demonstrated that ISCU was significantly upregulated, whereas MRPL14 and MSRA were downregulated in AA tissues. GSEA revealed that these proteins are involved in pathways related to inflammation, immune response, and vascular remodeling. In vitro experiments further corroborated these findings, demonstrating consistent expression patterns in platelet-derived growth factor-BB-induced human aortic smooth muscle cells. This study provides robust genetic and experimental evidence supporting the causal role of ISCU, MRPL14, and MSRA in AA pathogenesis. These mitochondrial proteins may serve as potential biomarkers and therapeutic targets for AA, warranting further investigation.

Diverticular disease and abdominal aortic aneurysms (AAAs) represent distinct but significant clinical entities often associated with advanced age. Diverticulitis, a common complication of diverticular disease, can result in perforation and systemic complications, while AAAs, frequently asymptomatic, carry substantial morbidity and mortality risks if undetected or untreated. Advances in imaging have improved the early identification of these conditions, yet the simultaneous management of both presents unique challenges requiring multidisciplinary coordination. A 67-year-old male with a history of ST-elevation myocardial infarction, hypertension, hyperlipidemia, and smoking presented with left lower quadrant abdominal pain and abnormal outpatient computed tomography (CT) findings. Imaging revealed Hinchey 1a diverticulitis with a microperforation and an incidental 6.5 cm saccular AAA. The patient received conservative treatment for diverticulitis with intravenous antibiotics and transitioned to oral antibiotics upon clinical improvement. Following resolution, the patient underwent successful endovascular aneurysm repair (EVAR) for the AAA, which was complicated by a type II endoleak identified postoperatively. Blood pressure management and hydration addressed acute kidney injury, and the patient recovered well with a multidisciplinary follow-up planned. This case underscores the importance of imaging in diagnosing coexisting conditions, particularly in high-risk populations. Management required balancing the risks of treating acute diverticulitis with the need for prompt intervention for a large, saccular AAA. The conservative approach to diverticulitis, followed by elective EVAR, reflects a patient-centered strategy consistent with current guidelines. Furthermore, it underscores the critical role of adhering to screening recommendations for high-risk populations, as timely detection of asymptomatic conditions like AAAs can prevent life-threatening complications.

Although diabetes has been shown to be negatively associated with development of abdominal aortic aneurysm (AAA), patients with diabetes may still develop aneurysms. In this study, we examined risk factors for the development of AAA in patients with diabetes.

Adults >50 years of age with diabetes who underwent health screening between 2009 and 2012 were followed for incident AAA until December 31, 2019. Cox proportional hazard regression models were used to calculate multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk factors associated with AAA.

Among 1,913,066 participants (55.3% men), 6996 AAA cases were identified during a mean follow-up of 7.7 years. Increased AAA risk was observed for age ≥65 years (HR, 2.69; 95% CI, 2.55-2.83), men (HR, 1.81; 95% CI, 1.69-1.94), smoking (former smoker ≥20 pack-years [PY]; HR, 1.75; 95% CI, 1.61-1.89; current smoker <20 PY; HR, 1.76; 95% CI, 1.59-1.94; current smoker ≥20 PY; HR, 2.40; 95% CI, 2.23-2.59), abdominal obesity (HR, 1.30; 95% CI, 1.23-1.38), and comorbidities, including hypertension (HR, 1.63; 95% CI, 1.53-1.73), dyslipidemia (HR, 1.35; 95% CI, 1.29-1.42), chronic kidney disease (HR, 1.52; 95% CI, 1.44-1.61), and cardiovascular disease (HR, 1.71; 95% CI, 1.58-1.86). Heavy (HR, 0.67; 95% CI, 0.61-0.74) and mild alcohol consumption (HR, 0.78; 95% CI, 0.74-0.83), overweight (HR, 0.87; 95% CI, 0.81-0.93) and obesity (HR, 0.81; 95% CI, 0.75-0.87), longer diabetes duration (≥5 years: HR, 0.74; 95% CI, 0.70-0.78), and using three or more oral hypoglycemic agents (OHA) (HR, 0.84; 95% CI, 0.79-0.90) were associated with decreased AAA risk, whereas insulin use was associated with a marginally increased risk (HR, 1.09; 95% CI, 1.00-1.18). Among the OHAs, metformin (HR, 0.95; 95% CI, 0.90-1.00), thiazolidinediones (HR, 0.87; 95% CI, 0.79-0.97), and sulfonylureas (HR, 0.88; 95% CI, 0.83-0.93) were associated with a decreased risk of AAA.

Although diabetes is associated with decreased AAA risk, those with comorbid cardiometabolic diseases, abdominal obesity, and a smoking history should be aware of an increased AAA risk. Further studies are warranted to verify the potential use of OHAs for decreasing AAA risk.

An arterial aneurysm is characterized by a localized expansion of a blood vessel relative to its original dimensions. Specifically, an abdominal aortic aneurysm (AAA) is identified as an aortic diameter measuring at least one and a half times the standard diameter at the renal artery level, approximately equivalent to 2.0 cm. In this study, we aim to evaluate the prevalence of AAA, along with the clinical features, trend, and incidence of ruptured AAA among patients undergoing surgery in our center.

The database of patients operated in Namazi Hospital from 2000 to 2021 was retrieved and patients undergoing vascular surgeries due to aneurysm were reviewed. All data were analyzed with SPSS version 26.0.

A total of 599 cases of aneurysm were operated, among which 334 were contributed to the aorta and included in our study. The average age of the participants was 69.6 (SD: 12.1, range 16-93) years and 161 (85.2%) were male. The majority of cases were in the 60 to 80 years age group (n = 205; 62.5%). There was a significant association between the age groups and the AAA rupture (p = 0.003), with the highest occurrence among the above 80 years age group (n = 37, 49.3%). Regarding the location of the aneurysm, 274 were located in the infrarenal and abdominal region, 21 in the thoracoabdominal region, and 12 in the thoracic region. Among the cases in our study, 112 were cases of ruptured aneurysms. Furthermore, the age of patients with ruptured aneurysm were significantly higher compared to non-ruptured patients (71.8 vs. 68.5; p = 0.019).

We observed an increase in the incidence of AAA surgeries in our center throughout the years, with the population growing towards younger population, while the incidence of rupture increasing towards older age groups.

Aortopathies can be congenital or acquired. Aortic atherosclerosis, abdominal aortic aneurysm, and degenerative aortic stenosis are some of the major manifestations of acquired aortopathy. Dyslipidemia, an imbalance of plasma lipid levels, is strongly associated with common aortopathies. A relationship between abdominal aortic aneurysm, degenerative aortic stenosis, and dyslipidemia has been identified in the literature but finding effective preventive strategies has been challenging. Nevertheless, lipid-lowering therapy remains a mainstay of both treatment and prevention. In patients with aortic atheroma, statins were found to be protective through the review of this study. There is currently no place for statins in the treatment or prevention of disease progression in patients with calcific aortic stenosis. Their low cost, widespread availability, and strong safety profile tip the risk-to-benefit ratio toward statins for abdominal aortic aneurysms but more research is needed. A review of proprotein convertase subtilisin/kexin type 9 inhibitors may yield similar benefits for all aortopathy patients; however, those results are not yet available.

Aortic aneurysm, the pathological dilatation of the aorta at distinct locations, can be attributed to many different genetic and environmental factors. The resulting pathobiological disturbances generate a complex interplay of processes affecting cells and extracellular molecules of the tunica interna, media and externa. In short, aortic aneurysm can affect processes involving the extracellular matrix, lipid trafficking/atherosclerosis, vascular smooth muscle cells, inflammation, platelets and intraluminal thrombus formation, as well as various endothelial functions. Many of these processes are interconnected, potentiating one another. Newer discoveries, including the involvement of odorant olfactory receptors in these processes, have further shed light on disease initiation and pathology. Olfactory receptors are a varied group of G protein coupled-receptors responsible for the recognition of chemosensory information. Although they comprise many different subgroups, some of which are not well-characterized or identified in humans, odorant olfactory receptors, in particular, are most commonly associated with recognition of olfactory information. They can also be ectopically localized and thus carry out additional functions relevant to the tissue in which they are identified. It is thus the purpose of this narrative review to summarize and present pathobiological processes relevant to the initiation and propagation of aortic aneurysm, while also incorporating evidence associating these ectopically functioning odorant olfactory receptors with the overall pathology.

Current literature reports conflicting findings regarding the effect of diabetes mellitus (DM) on outcomes of abdominal aortic aneurysm (AAA) repair. In this study we examined the effect of DM and its management on outcomes after open AAA repair (OAR) and endovascular AAA repair (EVAR).

We identified all patients undergoing OAR or EVAR for infrarenal AAA between 2003 and 2018 in the Vascular Quality Initiative registry data linked with Medicare claims. We excluded patients with missing DM status. Patients were stratified by their preoperative DM status, and then further stratified by DM management: dietary, noninsulin antidiabetic medications (NIMs), or insulin. Outcomes of interest included 1-year aneurysm sac dynamics, 8-year aneurysm rupture, reintervention, and all-cause mortality. These outcomes were analyzed with the χ2 test, Kaplan-Meier methods, and multivariable Cox regression analyses.

We identified 34,021 EVAR patients and 4127 OAR patients, of whom 20% and 16% had DM, respectively. Of all DM patients, 22% were managed by dietary management, 59% by NIM, and 19% by insulin. After EVAR, DM patients were more likely to have stable sacs, whereas non-DM patients were more likely to have sac regression at 1 year. Compared with non-DM, DM was associated with a significantly lower risk for 8-year rupture in EVAR (EVAR hazard ratio [HR], 0.68; 95% confidence interval [CI], 0.51-0.92). Compared with non-DM, NIM was associated with lower risk of rupture within 8-years for both EVAR and OAR (EVAR HR, 0.64; 95% CI, 0.44-0.94; OAR HR, 0.29; 95% CI, 0.41-0.80), whereas dietary control and insulin had a similar rupture risk compared with non-DM. However, compared with non-DM, DM was associated with a higher risk of 8-year all-cause mortality after EVAR and OAR (DM vs non-DM: EVAR HR, 1.17; 95% CI, 1.11-1.23; OAR HR, 1.16; 95% CI, 1.00-1.36). After further DM management substratification, compared with non-DM, management with NIM and insulin were associated with a higher 8-year mortality in EVAR and OAR (EVAR: NIM HR, 1.12; 95% CI, 1.05-1.20; insulin: HR, 1.40; 95% CI, 1.26-1.55; OAR: NIM HR, 1.27; 95% CI, 1.06-1.54; and insulin: HR, 1.57; 95% CI, 1.15-2.13). Finally, there was a similar risk of reintervention across the DM and non-DM populations for EVAR and OAR.

DM was associated with a lower adjusted risk of rupture after EVAR as well as OAR in patients managed with NIM. Nevertheless, just as in patients without AAA, preoperative DM was associated with a higher adjusted risk of all-cause mortality. Further study is needed to evaluate for differences in aneurysm-related mortality between DM and non-DM patients, and studies are planned to evaluate the independent effect of NIM on aneurysm-related outcomes.

Abdominal aortic aneurysm (AAA) is a common but life-threatening vascular condition in men at an advanced age. However, the underlying mechanisms of age-increased incidence and mortality of AAA remain elusive. Here, we performed RNA sequencing (RNA-seq) of mouse aortas from males (young: 3-month, n = 4 vs old: 23-month, n = 4) and integrated with the data sets of human aortas (young: 20-39, n = 47 vs old: 60-79 years, n = 92) from GTEx project and the data set (GSE183464) for AAA to search for age-shifted aortic aneurysm genes, their relevant biological processes, and signaling pathways. Angiotensin II-induced AAA in mice was used to verify the critical findings. We found 1 001 genes transcriptionally changed with ages in both mouse and human. Most age-increased genes were enriched intracellularly and the relevant biological processes included mitochondrial function and translational controls, whereas the age-decreased genes were largely localized in extracellular regions and cell periphery and the involved biological processes were associated with extracellular matrix (ECM). Fifty-one were known genes for AAA and found dominantly in extracellular region. The common age-shifted vascular genes and known aortic aneurysm genes had shared functional influences on ECM organization, apoptosis, and angiogenesis. Aorta with angiotensin II-induced AAA exhibited similar phenotypic changes in ECM to that in old mice. Together, we present a conserved transcriptional signature for aortic aging and provide evidence that mitochondrial dysfunction and the imbalanced ribosomal homeostasis act likely as driven-forces for aortic aging and age-disturbed ECM is the substrate for developing AAA.

Smoking is a risk factor for cardiovascular disease, but there is currently no clinically established biomarker for its cardiovascular damage. We aimed to investigate the hypothesis that aryl hydrocarbon receptor repressor ( AHRR ) methylation at CpG site cg05575921, a biomarker of smoking behavior, is associated with the risk of peripheral artery disease (PAD) and aortic aneurysm (AA) in the general population.

In this prospective cohort study of the general population, we measured AHRR methylation in individuals from three visits to the Copenhagen City Heart Study. Information on risk factors was collected at visits with 10 years intervals; visit 1 (1991-1994), visit 2 (2001-2003), and visit 3 (2011-2015). Individuals were followed up in the Danish National Patient Register for PAD and AA until December 2018. Subhazard ratios were calculated using Fine and Gray competing risk regression. In 11 332 individuals from visit 1 ( n =9234), visit 2 ( n =5384), and visit 3 ( n =4387), there were 613 and 219 events of PAD and AA during up to 26.5 years of follow-up. AHRR hypomethylation was associated with a higher risk of PAD and AA with multivariable-adjusted subhazard ratios of 2.82 (1.91; 4.15) for PAD and 2.88 (1.42; 5.88) for AA in individuals within the lowest versus highest methylation quintile.

We found that AHRR methylation, a strong biomarker for smoking, was associated with the risk of PAD and AA. AHRR methylation could be a useful tool in more personalized risk prediction of PAD and AA.

The aim of this study is to investigate the potential causal relationships between coronary artery disease (CAD), myocardial infarction (MI), urate levels, and aortic aneurysm (AA), abdominal aortic aneurysm (AAA), thoracic aortic aneurysm(TAA), aortic dissection (AD) in individuals of European ancestry. To examine the potential causal relationships between CAD, MI, and urate levels with AA, AAA, TAA, AD, respectively, we performed a two-sample Mendelian randomization (MR) analysis. Genetic instruments that reached genome-wide significance (p < 5 × 10 - 8) for risk factors were obtained from genome-wide association studies(GWASs) conducted on individuals of European origin. On the other hand, genetic instruments of AA, AAA, TAA or AD were chosen from the FinnGen cohort. The primary analysis employed the inverse-variance weighted MR method, while sensitivity analyses were conducted using MR-Egger, weighted median MR, MR pleiotropy residual sum and outlier, and Phenoscanner searching. In addition, we performed the MR-Egger intercept analysis to identify potential pleiotropy and utilized Cochran's Q statistics to evaluate heterogeneity. Additionally, we conducted bidirectional Mendelian randomization experiments to mitigate the potential influence of reverse causation. According to the results of our study, there were statistically significant higher risks for AA in relation to CAD/MI(odds ratio (OR) with 95% confidence interval (CI): 1.309 (1.150-1.490), and 1.255 (1.147-1.373). Similarly, there were statistically significant higher risks for AAA in relation to CAD and MI (OR with 95% CI: 1.383 (1.189-1.609), and 1.352 (1.178-1.552). The sensitivity analysis demonstrated that the causative effects of CAD/MI, and AA /AAA, were robust. A positive causal link was observed between CAD/MI, and AA/AAA. Nevertheless, no causal link was found between CAD, MI, urate levels, and TAA .

An aortic aneurysm (AA) is a life-threatening condition. Oxidative stress may be a common pathway linking multiple mechanisms of an AA, including vascular inflammation and metalloproteinase activity. Endovascular aneurysm repair (EVAR) is the preferred surgical approach for AA treatment. During surgery, inflammation and ischemia-reperfusion injury occur, and reactive oxygen species (ROS) play a key role in their modulation. Increased perioperative oxidative stress is associated with higher postoperative complications. The use of volatile anesthetics during surgery has been shown to reduce oxidative stress. Individual biomarkers only partially reflect the oxidative status of the patients. A global indicator of oxidative stress (OXY-SCORE) has been validated in various pathologies. This study aimed to compare the effects of the main volatile anesthetics, sevoflurane and desflurane, on oxidative status during EVAR. Eighty consecutive patients undergoing EVAR were randomized into two groups: sevoflurane and desflurane. Plasma biomarkers of oxidative damage (protein carbonylation and malondialdehyde) and antioxidant defense (total thiols, glutathione, nitrates, superoxide dismutase, and catalase activity) were measured before surgery and 24 h after EVAR. The analysis of individual biomarkers showed no significant differences between the groups. However, the OXY-SCORE was positive in the desflurane group (indicating a shift towards antioxidants) and negative in the sevoflurane group (favoring oxidants) (p < 0.044). Compared to sevoflurane, desflurane had a positive effect on oxidative stress during EVAR. The OXY-SCORE could provide a more comprehensive perspective on oxidative stress in this patient population.

Introduction The outcome of a ruptured abdominal aortic aneurysm (AAA) without any interventions is close to uniformly fatal. The Society for Vascular Surgery suggests a door-to-intervention time of less than 90 minutes in a patient with a ruptured AAA. Admission factors associated with poor outcomes in ruptured AAAs include hypotension, renal insufficiency, severe anemia, advanced age, and cardiac arrest. Patients who are particularly at high risk for open AAA repair may be candidates for endovascular repair, which may decrease mortality. This study aimed to assess the relationship between systolic blood pressure (SBP) and serum bicarbonate levels in predicting mortality in patients with ruptured AAAs. Methods This retrospective study was performed using the United States Collaborative Network of 57 academic medical centers/healthcare organizations in the TriNetX database. A total of 4,226 patients with ruptured AAAs were identified. Patients were categorized based on SBP of ≤90 mmHg, any SBP, or >90 mmHg and further stratified by bicarbonate levels. Rounded cutoffs of the bicarbonate ranges (<10, 10.01-15; 15.01-20, >20.01) were chosen for interpretative purposes. Mortality outcome was assessed within 90 days after presentation for the ruptured AAA. Results After exclusions, 4,174 patients presented with ruptured AAA between September 30, 2003, and September 30, 2023, in the database. Overall, 90-day mortality in any SPB cohort was 28%. Patients who presented with a ruptured AAA with an SBP ≤ 90 had a 46.3% mortality. Those who presented with a SBP > 90 had a 20.1% mortality. Additionally, as bicarbonate levels decreased, mortality increased within each SBP group. Conclusions Early recognition and intervention are critical for survival in patients with ruptured AAAs. Metabolic acidosis is an important marker of the severity of hemorrhage in these patients. In this large cohort study of ruptured AAAs, mortality increases significantly with hypotension and metabolic acidosis, represented by lower bicarbonate levels. Abnormalities in the serum bicarbonate may be seen before severe changes in vital signs in hemorrhaging patients. Early recognition of metabolic acidosis may lead to earlier life-saving interventions in patients with ruptured AAAs.

To investigate the impact of national income level and sex on mortality trends from aortic aneurysm and dissection in addition to all aortic disease as a whole.

Using data from the World Health Organization mortality database, we conducted an analysis of mortality trends from aortic disease between 2000 and 2019, Countries were categorized into middle-income and high-income countries (MICs and HICs) on the basis of income level. Age-standardized and sex-specific age-standardized mortality rates per 100,000 persons, along with male-to-female mortality ratios, were calculated. Trends over the study period were analyzed using joinpoint regression.

Our analysis comprised 29 MICs and 46 HICs, with an average population of 595 million and 1042 million during the observation period. During the observation period, age-standardized mortality rates from aortic disease decreased to 2.21 (2.17-2.25) and 2.28 (2.26-2.30) in MICs and HICs, respectively (average annual percentage change of -0.5% in MICs and -1.8% in HICs, P < .05 for both). However, mortality rates from aortic dissection increased in HICs from 2000 to 2019 (average annual percentage change of 1.3%, P < .001). Mortality from aortic disease, aortic dissection, and aortic aneurysm were male dominant in MICs and HICs but decreasing trends during the observation periods except for aortic dissection in MICs.

We present the contemporary and comprehensive analysis of global socioeconomic status and aortic diseases mortality. Although trends of mortality from aortic diseases are on the decline in both MICs and HICs, there is a striking increase in mortality for aortic dissection, specifically in HICs.

Aortic aneurysm (AAs) is a chronic and severe aortic disease, which is extremely life-threatening due to its delayed diagnosis and a high risk of rupture. In current studies, the association between lifestyle and metabolic factors remains controversial given the complexity of pathogenesis and progression in AAs. Consequently, more reliable and robust evidence should be provided.

Genome-wide association studies summary statistics were obtained for 25 factors (6 lifestyle factors and 19 cardiometabolic factors) and AAs. Univariable Mendelian randomization (UVMR) and multivariable MR (MVMR) were used to estimate the causal effect of these factors on AAs. Meanwhile, mediation analysis was applied to assess the mediated effect of lifestyle on the association of cardiometabolic factors with AAs.

Several factors were associated with AA risk, among which triglyceride (TG) (OR = 1.32, 95 % CI = [1.18-1.47], p < 0.001) and high-density lipoprotein cholesterol (HDL-C) (OR = 0.70, 95 % CI = [0.61-0.82], p < 0.001) remain consistently associated with AA risk, with an idependent effect on AAs after adjusting for body mass index (BMI). In addition, TG mediated 15.6 % of BMI effects and 3.7 % of smoking effects on AAs, and HDL-C mediated 5.3 % of the effects of cigarette smoking on AAs.

TG and HDL-C may be the most reliable factors in the risk of AAs. More scientific management of lifestyle and regular monitoring for cardiometabolic traits may serve as a new and effective direction for the prevention and control of the occurrence of AAs.

The incidence of abdominal aortic aneurysm (AAA) is very high, but there is no risk assessment model for early identification of AAA in clinic. The aim of this study was to develop a nomogram risk assessment model for predicting AAA. The data of 280 patients diagnosed as AAA and 385 controls in The Affiliated Suzhou Hospital of Nanjing Medical University were retrospectively reviewed. The LASSO regression method was applied to filter variables, and multivariate logistic regression was used to construct a nomogram. The discriminatory ability of the model was determined by calculating the area under the curve (AUC). The calibration capability of the model is evaluated by using bootstrap (resampling = 1000) internal validation and Hosmer-Lemeshow test. The clinical utility and clinical application value were evaluated by decision curve analysis (DCA) and clinical impact curve (CIC). In addition, a retrospective review of 133 AAA patients and 262 controls from The First Affiliated Hospital of Soochow University was performed as an external validation cohort. Eight variables are selected to construct the nomogram of AAA risk assessment model. The nomogram predicted AAA with AUC values of 0.928 (95%CI, 0.907-0.950) in the training cohort, and 0.902 (95%CI, 0.865-0.940) in the external validation cohort, the risk prediction model has excellent discriminative ability. The calibration curve and Hosmer-Lemeshow test proved that the nomogram predicted outcomes were close to the ideal curve, the predicted outcomes were consistent with the real outcomes, the DCA curve and CIC curve showed that patients could benefit. This finding was also confirmed in the external validation cohort. In this study, a nomogram was constructed that incorporated eight demographic and clinical characteristics of AAA patients, which can be used as a practical approach for the personalized early screening and auxiliary diagnosis of the potential risk factors.

Atherosclerotic cardiovascular disease (ASCVD) is one of the leading causes of death worldwide and in Taiwan. It is highly prevalent and has a tremendous impact on global health. Therefore, the Taiwan Society of Cardiology developed these best-evidence preventive guidelines for decision-making in clinical practice involving aspects of primordial prevention including national policies, promotion of health education, primary prevention of clinical risk factors, and management and control of clinical risk factors. These guidelines cover the full spectrum of ASCVD, including chronic coronary syndrome, acute coronary syndrome, cerebrovascular disease, peripheral artery disease, and aortic aneurysm. In order to enhance medical education and health promotion not only for physicians but also for the general public, we propose a slogan (2H2L) for the primary prevention of ASCVD on the basis of the essential role of healthy dietary pattern and lifestyles: "Healthy Diet and Healthy Lifestyles to Help Your Life and Save Your Lives". We also propose an acronym of the modifiable risk factors/enhancers and relevant strategies to facilitate memory: " ABC2D2EFG-I'M2 ACE": Adiposity, Blood pressure, Cholesterol and Cigarette smoking, Diabetes mellitus and Dietary pattern, Exercise, Frailty, Gout/hyperuricemia, Inflammation/infection, Metabolic syndrome and Metabolic dysfunction-associated fatty liver disease, Atmosphere (environment), Chronic kidney disease, and Easy life (sleep well and no stress). Some imaging studies can be risk enhancers. Some risk factors/clinical conditions are deemed to be preventable, and healthy dietary pattern, physical activity, and body weight control remain the cornerstone of the preventive strategy.

Aortic aneurysm (AA) is an aortic disease with a high mortality rate, and other than surgery no effective preventive or therapeutic treatment have been developed. The renin-angiotensin system (RAS) is an important endocrine system that regulates vascular health. The ACE2/Ang-(1-7)/MasR axis can antagonize the adverse effects of the activation of the ACE/Ang II/AT1R axis on vascular dysfunction, atherosclerosis, and the development of aneurysms, thus providing an important therapeutic target for the prevention and treatment of AA. However, products targeting the Ang-(1-7)/MasR pathway still lack clinical validation. This review will outline the epidemiology of AA, including thoracic, abdominal, and thoracoabdominal AA, as well as current diagnostic and treatment strategies. Due to the highest incidence and most extensive research on abdominal AA (AAA), we will focus on AAA to explain the role of the RAS in its development, the protective function of Ang-(1-7)/MasR, and the mechanisms involved. We will also describe the roles of agonists and antagonists, suggest improvements in engineering and drug delivery, and provide evidence for Ang-(1-7)/MasR's clinical potential, discussing risks and solutions for clinical use. This study will enhance our understanding of AA and offer new possibilities and promising targets for therapeutic intervention.

The Harborview Risk Score (HRS) was recently proposed as scoring tool to predict 30-day mortality in patients with ruptured abdominal aortic aneurysms (rAAAs). The HRS assigns 1 point for each of the following preoperative characteristics: age > 76 years, pH < 7.2, creatinine level > 2 mg/dL (> 176.8 μmol/L), and systolic blood pressure < 70 mm Hg, resulting in scores from 0 to 4. The 30-day mortality risk increases with every point. Primarily, we aimed to validate the HRS for the first time in a Dutch study population. A second objective was to identify other clinically relevant predictors for 30-day mortality after repair of rAAA.

Retrospective data from patients who underwent open repair or endovascular aortic repair for a rAAA between January 2009 and February 2022 were reviewed. Patients were grouped by HRS category (score 0-4). The 30-day mortality rate was calculated for each HRS category. Determinants for 30-day mortality were tested for significance and validated for HRS.

In total, data from 135 patients were included. Open repair was performed in 95 patients and 40 patients underwent endovascular aortic repair. Univariate logistic regression identified pH < 7.2, systolic blood pressure < 70 mm Hg, female sex, performance status, and increase per HRS unit as significant determinants for 30-day mortality. After adjusting for sex and performance status in the multivariate analysis, the association between the HRS per-unit increase and 30-day mortality remained significant (odds ratio 2.532 (95% confidence interval: 1.437-4.461)). The 30-day mortality rate for HRS score 0 was 15.2%, while for HRS score 3 and 4 the mortality was 80% and 100% respectively.

The Harborview Risk Score was validated in this single-center Dutch population. Results were concordant with data presented in earlier studies. Therefore, the HRS seems accurate and accessible as preoperative tool. For now, the HRS should guide as an insightful tool to indicate the chances of postoperative mortality during the preoperative conversations in the emergency room, rather than as a decision-making tool whether to operate or not. Our results suggest that female sex and performance status are also relevant predictors that should be assessed in other populations to improve preoperative scoring systems.

Aortic aneurysm (AA) refers to the persistent dilatation of the aorta, exceeding three centimeters. Investigating the pathophysiology of this condition is important for its prevention and management, given its responsibility for more than 25000 deaths in the United States. AAs are classified based on their location or morphology. various pathophysiologic pathways including inflammation, the immune system and atherosclerosis have been implicated in its development. Inflammatory markers such as transforming growth factor β, interleukin-1β, tumor necrosis factor-α, matrix metalloproteinase-2 and many more may contribute to this phenomenon. Several genetic disorders such as Marfan syndrome, Ehler-Danlos syndrome and Loeys-Dietz syndrome have also been associated with this disease. Recent years has seen the investigation of novel management of AA, exploring the implication of different immune suppressors, the role of radiation in shrinkage and prevention, as well as minimally invasive and newly hypothesized surgical methods. In this narrative review, we aim to present the new contributing factors involved in pathophysiology of AA. We also highlighted the novel management methods that have demonstrated promising benefits in clinical outcomes of the AA.

Abdominal Aortic Aneurysm (AAA) is a disease characterized by localized dilation of the abdominal aorta, involving multiple factors in its occurrence and development, ultimately leading to vessel rupture and severe bleeding. AAA has a high mortality rate, and there is a lack of targeted therapeutic drugs. Epigenetic regulation plays a crucial role in AAA, and the treatment of AAA in the epigenetic field may involve a series of related genes and pathways. Abnormal expression of these genes may be a key factor in the occurrence of the disease and could potentially serve as promising therapeutic targets. Understanding the epigenetic regulation of AAA is of significant importance in revealing the mechanisms underlying the disease and identifying new therapeutic targets. This knowledge can contribute to offering AAA patients better clinical treatment options beyond surgery. This review systematically explores various aspects of epigenetic regulation in AAA, including DNA methylation, histone modification, non-coding RNA, and RNA modification. The analysis of the roles of these regulatory mechanisms, along with the identification of relevant genes and pathways associated with AAA, is discussed comprehensively. Additionally, a comprehensive discussion is provided on existing treatment strategies and prospects for epigenetics-based treatments, offering insights for future clinical interventions.

Abdominal aortic aneurysm (AAA) is one of the most important cardiovascular diseases, especially in the elderly. People with this disease are at risk of rupture of the abdominal aorta and death. The present study was conducted with the aim of analyzing the cost-effectiveness of endovascular repair compared to open surgery in AAA patients in Iran.

A Markov chain model was developed based on the use of endovascular repair and open surgery. The base-case patient was defined as a 65-year-old man presenting with AAA diameter greater than 5 cm. The determination of costs was from the perspective of the public sector provider. QALY was used to calculate the effectiveness. Incremental cost-effectiveness ratio (ICER) and TreeAge software were used for cost-effectiveness analysis. The follow-up period was 10 years and the willingness to pay (WTP) was determined as three times the Gross domestic product (GDP) per capita.

At the end of year 10, the endovascular aneurysm repair (EVAR) strategy gained 1 318 313 559 Iranian Rial (IRR) (67 885.29$) in cost and 3.57 QALYs in effectiveness. In contrast, the use of the open surgery repair (OSR) strategy gained 1 186 761 858 IRR (61 111.16$) in cost and 3·32 QALYs in effectiveness. The incremental cost-effectiveness ratio, comparing EVAR versus OSR, was 53, 346, 3757 IRR (178.36$) per QALYs, which is lower than the proposed WTP, indicating that EVAR is more expensive and more effective. Based on the Monte Carlo simulation test, EVAR is the preferred strategy in 58.6% of the population.

Endovascular repair has a relative superiority compared to open surgery, and the probability of the effectiveness of endovascular repair compared to open surgery does not change with increasing willingness to pay.

This umbrella meta-analysis aims to investigate two surgical treatments for abdominal aortic aneurysm (AAA): endovascular aneurysm repair (EVAR) and open surgery repair (OSR). Our study aims to elucidate the 30-day mortality rate, reintervention rates, and aneurysm-related mortality in EVAR versus OSR for AAA.  We conducted a comprehensive assessment of meta-analyses (n = 34 articles) comparing EVAR and OSR for AAA. We adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol and considered statistical significance at P ≤ 0.05. For the 30-day mortality rate, a pooled odds ratio (pOR) of 0.59 (95% confidence interval [CI] 0.45-0.77, P = 0.0001, and I2 = 98%) indicates that EVAR was associated with a lower risk of mortality compared to OSR. For reintervention rates, a pOR of 1.33 (95% CI = 0.98-1.82, P = 0.11, and I2 = 90%). In aneurysm-related mortality, a pOR of 0.78 (95% CI = 0.63-0.97, P = 0.03, and I2 = 43%). In postoperative rupture of aneurysm, a pOR of 3.28 (95% CI = 2.16-4.98, P < 0.00001, and I2 = 50%). Furthermore, when analyzing systemic complications, only for visceral ischemia, significant results showed lower odds for EVAR, with a pOR of 0.57 (95% CI = 0.40-0.80, P = 0.001, and I2 = 0%) was found.  EVAR is better in terms of short-term mortality rate and aneurysm-related mortality. Furthermore, EVAR is still a safer procedure in elective settings, as the studies we included recruited patients for this setting. However, given the high reintervention rates and recent developments in surgical techniques and materials, more recent data and extensive research are needed.

The potential role of smoking as a risk factor for thoracic aortic aneurysm is still a subject of debate. Therefore, it is important to systematically investigate the causal relationship between smoking and thoracic aortic aneurysm using Mendelian randomization methods. Genetic data were obtained from genome-wide association studies using the inverse variance weighting method as the primary approach. A thorough sensitivity analysis was conducted to ensure the reliability of the findings. Instrumental variables were assessed using the F statistic, and meta-analysis was employed to assess the average genetic predictive effect between smoking and thoracic aortic aneurysm. Our Mendelian randomization study found a positive association between smoking and thoracic aortic aneurysm. The odds ratios (OR) in the inverse variance weighting method were OR = 1.23 (95% confidence interval [CI] = 1.00-1.51; P = .053) and OR = 2.07 (95% CI = 1.10-3.91; P = .024). Furthermore, meta-analyses consistently demonstrated a positive causal relationship between ferritin and myocardial infarction, although statistical significance was not observed. The analysis results did not indicate any horizontal pleiotropy. Despite the presence of heterogeneity, the Mendelian randomization analysis still yielded significant results. This study employed Mendelian randomization to establish a positive association between smoking levels and the risk of thoracic aortic aneurysm. The genetic evidence reveals a causal relationship between the two, offering new insights for future interventions targeting thoracic aortic aneurysms.

Abdominal aorta calcium (AAC) burden and dilatation are associated with an increased risk of mortality. The purpose of this study was to investigate determinants of AAC and abdominal aorta size in patients with essential hypertension.

Patients with uncomplicated essential hypertension who had undergone non-enhanced abdominal CT to rule out secondary hypertension in addition to biological test were recruited between 2010 and 2018. A semi-automatic system was designed to estimate the aortic size (diameter, length, volume) and quantify the AAC from mesenteric artery to bifurcation using the Agatston score. Determinants of aortic size and those related to AAC were searched for using uni- and multivariables analyses.

Among 293 randomly selected patients with hypertension (age 52 ± 11 [SD] years) included, 23% had resistant hypertension. Mean abdominal aorta diameter was 20.1 ± 2.1 (SD) mm. Eight (3%) patients had abdominal aorta aneurysm ≥ 30 mm and 58 (20%) had dilated abdominal aorta ≥ 27 mm. Median AAC score was 38 and calcifications were detected in the infra- and supra-renal abdominal aortic portions in 59% and 26% of the patients, respectively. After adjustment for age, male sex and body surface area, abdominal aorta diameter was positively associated with diastolic blood pressure (P = 0.0019). Smoking was the single variable associated with calcified abdominal aorta (P < 0.001) after adjustment for cofactors. In patients with calcifications of abdominal aorta, the score increased with smoking history (P < 0.001), statins treatment (P < 0.01), greater number of anti-hypertensive drugs (P < 0.01), larger abdominal aorta (P < 0.05) and greater systolic blood pressure (P < 0.05). Patients with resistant hypertension had more AAC in the supra-renal abdominal aorta portion than those without resistant hypertension (P < 0.01).

In patients with essential hypertension, abdominal aorta dilation is related with diastolic blood pressure while AAC is associated with smoking history and resistant hypertension when located to the supra-renal abdominal aorta portion.

Thoracic aortic aneurysms are often an accidental finding and result from a degenerative process. Medical therapy includes pharmacological control of arterial hypertension and smoking cessation, that slows the growth of aneurysms. An association between the dilatation of the ascending and abdominal aorta has been already reported. The aim of the study was to identify possible demographic and clinical factors that may implicate further imaging diagnostics in patients with ascending aorta dilatation.

There were 181 (93 (53%) males and 88 (47%) females) patients with a median age of 54 (41-62) years who underwent cardiac magnetic resonance due to non-vascular diseases, were enrolled into retrospective analysis.

Multivariable analysis revealed ascending aorta dilatation (odds ratios (OR) = 7.45, 95% confidence interval (CI): 1.98-28.0, p = 0.003) and co-existence of coronary artery disease (OR = 8.68, 95% CI: 2.15-35.1, p = 0.002) as significant predictors for thoracic descending aorta dilatation. In patients with abdominal aorta dilatation, the multivariable analysis showed a predictive value of ascending aortic dilatation (OR = 14.8, 95% CI: 2.36-92.8, p = 0.004) and age (OR = 1.04, 95% CI: 1.00-1.08, p = 0.027). In addition, cut-off values were established for age groups determining the risk of thoracic aorta dilatation over 49 years and abdominal aorta dilatation over 54 years.

The results of our analysis showed predictive factors, including ascending aorta dilatation and co-existence of coronary artery disease, particularly over 49 years of age for thoracic, while ascending aorta dilatation and age, particularly over 54 years, for abdominal aorta dilatation. These features may be considered to increase clinical vigilance in patients with aortic diameter abnormalities.

Heritable thoracic aortic disease puts patients at risk for aortic aneurysms, rupture, and dissections. The diagnosis and management of this heterogenous patient population continues to evolve. Last year, the American Heart Association/American College of Cardiology Joint Committee published diagnosis and management guidelines for aortic disease, which included those with genetic aortopathies. Additionally, evolving research studying the implications of underlying genetic aberrations with new genetic testing continues to become available. In this review, we evaluate the current literature surrounding the diagnosis and management of heritable thoracic aortic disease, as well as novel therapeutic approaches and future directions of research.

The retroperitoneum is an important space in the human body that is often implicated in a range Epub ahead of print of acute medical conditions, some of which can be life-threatening. Ultrasonography may serve as a pivotal first-line imaging technique when assessing patients with suspected retroperitoneal abnormalities. Effective ultrasonography of the retroperitoneum requires a comprehensive grasp of its anatomy, adjacent structures, and potential pathologies. Being well-acquainted with the imaging characteristics of acute conditions can meaningfully assist in an accurate diagnosis and guide subsequent management. This review article summarizes and illustrates the acute conditions involving the retroperitoneum through the lens of ultrasound imaging.