Background This study aimed to compare early and long-term outcomes of chimney endovascular aneurysm repair (chEVAR) using a polyester endograft with a substantial oversizing strategy versus open repair (OR) for abdominal aortic aneurysms (AAAs) with challenging proximal necks, and to elucidate key determinants of successful chEVAR. Methods We retrospectively analyzed patients undergoing chEVAR (n = 112) or OR (n = 51) for AAAs with short-neck infrarenal, juxtarenal, or pararenal anatomy between May 2005 and October 2023. Primary endpoints were 30-day/in-hospital mortality and major adverse events (MAEs). Secondary endpoints included freedom from aneurysm-related adverse events and mortality, reintervention, and long-term survival. ChEVAR-specific analyses assessed freedom from type Ia endoleak (T1aEL), predictors of T1aEL, aneurysm sac behavior, and longitudinal proximal neck dilatation. Results In-hospital mortality tended to be lower with chEVAR (1.8% vs. 7.8%, P = 0.057), and 30-day MAEs were significantly reduced (10.7% vs. 37.3%, P < 0.001). Five-year freedom from aneurysm-related adverse events was higher for chEVAR (64.9% vs. 60.5%, P = 0.015). Freedom from aneurysm-related mortality, reintervention, and overall survival were similar. Three-year freedom from T1aEL was 97.5%. Predictors of T1aEL included bare metal chimney stents, multiple chimneys, larger neck diameter, shorter neck length, and reverse taper neck. Mean annual neck dilatation rate was 0.13 at the infrarenal level. Patients with or without significant neck dilatation (≥0.20; fourth quartile) had similar T1aEL rates. Conclusion ChEVAR demonstrated favorable early outcomes and comparable long-term results compared to OR. Chimney EVAR can be performed successfully without increasing the incidence of T1aEL, even in the presence of significant neck dilatation, provided that appropriate anatomical selection is applied.

Background: Environmental pollutants including particulate matter (PM) increase the morbidity and mortality for cardiovascular disorders. Recent study analyzing UK biobank datasets suggested that exposure to PM2.5 or PM10 was associated with the increased risk for abdominal aortic aneurysms (AAA). However, it has not been studied whether PM exposure alters experimental AAA formation and progression. Methods: Experimental AAAs were induced in 9-10 weeks old male C57BL/6J mice via porcine pancreatic elastase aortic wall painting procedure. Three days following AAA induction, urban particulate matter (NIST1648a, mean particulate diameter (d50): 5.87 µm, 100 µg/mouse/day) or vehicle (saline) was daily administered via intranasal installation for 11 days. Influence on experimental AAAs was assessed via serial measurements of infrarenal aortic diameter via ultrasonography and histopathological analysis at sacrifice. Results: In ultrasound imaging, no difference was noted in the baseline aortic diameter (either prior to AAA induction or PM exposure). However, PM exposure led to marked aneurysm enlargement on days 7 and 14 following AAA induction as compared to vehicle exposure. On histological analysis, PM exposure accelerated medial elastin degradation and smooth muscle cell loss as compared to vehicle exposure. Aortic accumulation of macrophages and lymphocytes were more remarkable in PM-, than those in vehicle-, exposed AAA mice. Additionally, PM exposure also substantially increased the density of CD31-positive neovessels in aneurysmal lesion as compared to vehicle exposure. Conclusion: Particulate matter exposure worsens experimental AAA progression in associated with augmented aneurysmal wall inflammation.

Background: Tripartite motif containing 59 (TRIM59) functions as an E3 ubiquitin ligase contributing to host immune responses including innate and adaptive immunity. This study investigated the influence of myeloid cell TRIM59 deletion on experimental abdominal aortic aneurysms (AAAs). Methods: Nine- to ten-week-old male, myeloid cell-specific TRIM59 deficient (Lysozyme 2 Cre + /TRIM59 flox +/+ , CKO) and TRIM59 flox +/+ (wild type, WT) mice were used in all experiments. Experimental AAAs were induced in all mice by transient intra-infrarenal aortic infusion of porcine pancreatic elastase. Experimental AAA progression was assessed via serial in vivo infrarenal ultrasonographic aortic diameter measurements and histopathologic analysis at sacrifice. Results: Major findings are summarized in the Figure. On days 7 and 14 following elastase infusion, aortic diameters were significantly larger in CKO than those in WT mice. On histological analysis, elastin degradation was enhanced in CKO mice with a trend toward aortic macrophage accumulation. Aortic accumulation of CD4 + and CD8 + T cells and B220 + B cells, as well as mural neoangiogenesis (identified by CD31 + antibody staining) were all more prominent in CKO mice. No difference in α actin-positive aortic medial smooth muscle cell depletion was noted between strains. Conclusions: Deficiency of myeloid cell TRIM59 augments progression of experimental AAAs.

BACKGROUND:Type 2 endoleak (T2EL) remains the most frequent complication after endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm and is associated with sac enlargement and late adverse events. Preemptive embolization of aortic side branches has been introduced to reduce its incidence. This study aimed to evaluate the mid-term outcomes of EVAR with preemptive side branch embolization and to identify factors associated with persistent T2EL. METHODS:We retrospectively reviewed 217 patients who underwent EVAR with preemptive embolization of the inferior mesenteric artery and lumbar arteries (LAs) at our institution between April 2018 and March 2025. Patient characteristics, aneurysm morphology, and procedural details were analyzed. The primary endpoint was the occurrence of T2EL during follow-up. Risk factors were evaluated using univariable and multivariable logistic regression analyses. RESULTS:During a mean follow-up of 43.0 ± 22.6 months, T2EL occurred in 25 patients (11.5%). Sac enlargement ≥5 mm was significantly more frequent in patients with T2EL (36.0% vs. 4.7%, P < 0.001), while complete sac regression was observed only in the non-T2EL group (22.9% vs. 0%, P = 0.007). Multivariable analysis identified angulated neck (OR 2.90, 95% CI 1.10-7.66, P = 0.031) and the number of residual LAs (OR 1.74, 95% CI 1.12-2.70, P = 0.013) as independent predictors of T2EL. CONCLUSION:Persistent T2EL after PBE was associated with unfavorable sac behavior and an increased need for reintervention. Residual LAs and angulated neck anatomy were independent predictors of persistent T2EL, suggesting the importance of complete embolization, particularly in patients with angulated neck anatomy.

Background: Time-restricted feeding (TRF)/intermittent fasting is associated with improved outcomes for cardiovascular and metabolic disorders and expanded lifespan. It has not been investigated whether TRF influences experimental abdominal aortic aneurysm (AAA). Methods: AAAs were induced in 9-10 weeks old male C57BL/6J mice by painting porcine pancreatic elastase on infrarenal aortic external wall. Mice were daily fasted for 16 hours (5 PM to 9 AM) starting 3 days prior to (preventive) or 4 days following (therapeutic) AAA induction, with mice without fasting serving as the controls. AAA progression was monitored via serial ultrasound measurements of maximal infrarenal aortic diameter. Fourteen days following AAA induction, mice were euthanized, and aortae were harvested for histopathological analysis. Results: TRF significantly inhibited experimental AAA enlargement as compared to non-fasting controls regardless of intervention protocol . On histological analyses, both preventive and therapeutic intervention treatment protocols improved retention of medial elastin and smooth muscle cells, reduced aortic accumulation of macrophages, T cells and B cells and attenuated aneurysmal mural neovessel formation as compared to non-fasting controls. Additionally, TRF intervention was associated with a transient but significantly slight increase in circulating ketone body levels, without recognizable impact on blood glucose. Conclusion: TRF mitigates experimental AAA progression and related pathologies. These findings suggest that TRF may present an alternative translational approach for medical management of AAA disease.

Background: Fatty acid oxidation (FAO) mitigates inflammation by supporting mitochondrial oxidative metabolism and maintaining metabolic homeostasis. The role of FAO in experimental AAAs is undetermined. We assessed the impact of FAO on experimental AAA progression by treatment with a pharmacologic inhibitor of CPT1a. Methods: AAAs were induced in 9–10-week-old male C57BL/6J mice via external application of porcine pancreatic elastase to the infrarenal aorta. Mice were treated with the CPT1a inhibitor etomoxir (20 mg/kg/day/ip) or vehicle 3 days following AAA creation. Influence on AAA progression was assessed via ultrasonography, histology and metabolite profiling Results: Major results are summarized in Figure. Progressive enlargement of aortic diameter was noted in vehicle-treated mice following topical elastase application. However, etomoxir treatment substantially diminished AAA expansion. On histologic examination, accumulation of CD4 + and CD8 + lymphocytes as well as neovessel formation were substantially diminished in etomoxir- as compared to vehicle-treated AAA mice, without significant impact on medial elastolysis, smooth muscle cell depletion or macrophage accumulation. On metabolomic assessment, distinct metabolite profiles were noted between two treatment groups. Etomoxir treatment increased pathway enrichments for linoleic and arachidonic acid metabolism in aneurysmal aortas and decreased enrichment for arachidonic acid and retinol metabolisms in sera. Conclusion: CPT1a inhibition promoted experimental AAA progression in association with increased aortic T cell accumulation, angiogenesis and distinct lipid metabolite profiles.

BACKGROUND:This study aimed to determine the prevalence and underlying causes of pedal edema (PE) in legs affected by chronic edema. METHODS:A total of 705 legs with chronic edema, defined as persistent leg edema lasting for > 3 months, were examined in 411 patients who visited our clinic between April 2009 and March 2024. Patients with known systemic edematous conditions or those with serum albumin levels <3.5 g/dL and/or an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, as confirmed during screening blood tests at their initial visits, were excluded from the study. The presence of edema in the leg, including the pedal region, was confirmed using ultrasonography to detect subcutaneous echo-free spaces (SEFS). Routine assessments included blood screening, duplex venous scans, and skin ultrasonography. Air plethysmography, lymphangioscintigraphy, and bioelectrical impedance analysis were performed whenever feasible. RESULTS:The prevalence of PE in legs with chronic edema was 64%. Multivariate analyses identified the severity of SEFS in the lateral lower calf, which correlated with the overall severity of leg edema (odds ratio [OR]: 5.62; 95% confidence interval [CI]: 2.46-14.62; P < 0.001), and serum albumin level (OR: 2.55; 95% CI: 1.31-5.05; P < 0.01) as significant risk factors for PE. CONCLUSION:PE was present in 64% of legs with chronic edema. The primary contributors to PE were the overall severity of leg edema and lower serum albumin levels, even within the normal range.

Purpose: This study retrospectively evaluated the mid-term outcomes of thromboendarterectomy (TEA) for common femoral artery (CFA) disease in a Japanese cohort by comparing patients with chronic limb-threatening ischemia (CLTI) and intermittent claudication (IC). Materials and Methods : Sixty-three TEA procedures performed between 2011 and 2024 were analyzed. The primary endpoints focused on procedure-related outcomes such as patency and limb salvage, whereas overall survival was assessed as a key secondary outcome. The patients were divided into the CLTI (n=20) and IC (n=43) groups; the anesthesia type, additional revascularization, blood loss, hospital stay, complications, and survival were compared. Multivariable Cox regression analysis was performed to identify independent predictors of mortality. Results : Patients with CLTI had higher rates of local anesthesia, additional revascularization (all performed concomitantly), greater blood loss, and longer hospital stays. Despite the 100% technical success in both groups, 30-day mortality and complications occurred only in the CLTI group. Kaplan-Meier analysis showed similar patency and limb salvage rates between groups, whereas survival rates were significantly lower in patients with CLTI (P=0.037). Multivariable analysis revealed that CLTI itself was not an independent predictor of mortality; rather, a worse systemic status (e.g., higher American Society of Anesthesiologists classification) showed a trend toward poorer outcomes (P=0.051). No significant differences were found between the patch types. Conclusion : TEA provides effective mid-term outcomes in patients with CFA disease, particularly those with IC. Although patients with CLTI show poorer survival, this appears to be driven more by systemic comorbidities than by the limb status itself. Careful preoperative assessment and holistic management of general health are essential to optimize outcomes, particularly in high-risk populations.

INTRODUCTION:Lymphedema is generally managed with conservative therapy. However, in cases of severe fibrosclerotic lymphedema, debulking surgery is required, although rarely. We present a case of massive lymphedema in the left calf complicated by severe skin fibrosclerosis that was successfully managed with debulking surgery. CASE PRESENTATION:A 58-year-old woman presented to our clinic with bilateral leg swelling, which was particularly massive in the left calf. She could hardly walk independently and experienced cellulitis 2 to 4 times a year. The patient was admitted, and aggressive decongestion with compression therapy was attempted initially. However, this was unsuccessful due to severe skin hardening caused by abnormal dermal thickening. We then performed partial subcutaneous tissue resection and wrapping with the redundant skin, but this resulted in extensive skin necrosis. Finally, resection of the whole skin and subcutaneous tissue down to the deep fascia in the left calf was performed, followed by split-thickness skin grafting harvested from the left thigh. At present, one year after the surgery, the patient is capable of performing light exercise and has not experienced a recurrence of cellulitis. CONCLUSIONS:When preoperative conservative therapy is unsuccessful due to severe skin fibrosclerosis, earlier surgical intervention, including debulking, is beneficial in the management of massive lymphedema.

Background: This study aimed to determine the prevalence and underlying causes of pedal edema (PE) in legs affected by chronic edema. Methods: A total of 705 legs with chronic edema, defined as persistent leg edema lasting for > 3 months, were examined in 411 patients who visited our clinic between April 2009 and March 2024. Patients with known systemic edematous conditions or those with serum albumin levels <3.5 g/dL and/or an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m(2), as confirmed during screening blood tests at their initial visits, were excluded from the study. The presence of edema in the leg, including the pedal region, was confirmed using ultrasonography to detect subcutaneous echo-free spaces (SEFS). Routine assessments included blood screening, duplex venous scans, and skin ultrasonography. Air plethysmography, lymphangioscintigraphy, and bioelectrical impedance analysis were performed whenever feasible. Results: The prevalence of PE in legs with chronic edema was 64%. Multivariate analyses identified the severity of SEFS in the lateral lower calf, which correlated with the overall severity of leg edema (odds ratio [OR]: 5.62; 95% confidence interval [CI]: 2.46-14.62; P < 0.001), and serum albumin level (OR: 2.55; 95% CI: 1.31-5.05; P < 0.01) as significant risk factors for PE. Conclusion: PE was present in 64% of legs with chronic edema. The primary contributors to PE were the overall severity of leg edema and lower serum albumin levels, even within the normal range.

Objectives: Peri-aortitis following endovascular aneurysm repair (EVAR) is a rare phenomenon with unclear pathogenesis. In this study, we investigated its clinical features and sac prognosis. Methods: A retrospective analysis was conducted on 1369 EVAR. Peri-aortitis was defined using post-EVAR computed tomography. Clinical and imaging data were assessed. Results: Peri-aortitis following EVAR was identified in 12 patients (0.89%) with a mean age of 74 ± 8.9 years; 83.3% were male, and 41.7% had allergic or autoimmune histories. There were eight symptomatic cases (66.7%), including seven with fever, three with back or abdominal pain, and one with hydronephrosis. Precautionary antibiotic treatment was administered in five febrile cases. Although persistent and recurrent inflammation was observed in two cases (16.7%) each, inflammation resolved spontaneously in seven patients (58.3%). One (8.3%) needed steroid therapy for severe back pain. Aneurysm shrinkage was observed in seven cases (58.3%), while enlargement was noted in one case (8.3%) with type II endoleak. No correlation was found between aneurysm growth and peri-aortitis development. Conclusions: Peri-aortitis following EVAR may present significant challenges, including differentiation from infection, management of symptomatic cases requiring medical therapy, and addressing recurrences. Accurate diagnosis, individualized treatment, and meticulous follow-up are essential for favorable outcomes.

Background: Intermittent fasting and ketogenic diet may improve cardiovascular health. We studied the impact of ketogenic dietary intervention on experimental abdominal aortic aneurysms (AAAs). Methods: AAAs were induced in male mice via topical abluminal porcine pancreatic elastase (PPE) application at laparotomy in C57BL/6J, and 28 day administration of exogenous angiotensin (Ang) II in apolipoprotein E deficient strains, respectively. As feeding regimens, mice were fed standard or ketogenic diets 3 days prior to or 3 days following, AAA induction. Influence on AAA development was assessed by serial transabdominal ultrasonography and histopathologic analysis at sacrifice. Results: Ketogenic diet promotes cardiovascular health in part by increasing ketone body production. The Figure summarizes the influence of ketogenic diet on experimental AAAs in two distinct models. Following PPE application, subsequent aortic diameter enlargement was significantly reduced in mice receiving ketogenic vs. standard diets at 7 and 14 days regardless of specific feeding regimen. On histologic analysis, ketogenic diet feeding resulted in improved aortic medial elastin and smooth muscle cell retention, reduced mural macrophage, CD4 + and CD8 + T and B cell infiltration, and attenuated mural angiogenesis. In the Ang II infusion model, ketogenic diet limited Ang II-induced aortic diameter expansion, lowered AAA incidence and reduced AAA severity. Conclusion: Ketogenic dietary intervention suppressed experimental AAA progression in complementary murine modeling systems. Already popular clinically, this dietary modification may prove effective in limiting clinical AAA disease progression as well as other cardiovascular disease endpoints.

IntroductionType II endoleak (T2EL) is the most common type of endoleak after endovascular aneurysm repair (EVAR) and a common indication for reintervention due to late sac enlargement. Although pre-emptive embolization of the inferior mesenteric artery (IMA) has been proposed to prevent this, no studies have prospectively demonstrated its efficacy. This study aimed to prove the validity of IMA embolization during EVAR in selective cases by analyzing the mid-term outcomes of a randomized clinical trial (RCT).MethodsThis single-center, parallel-group, non-blinded RCT included participants at high risk of T2EL, characterized by a patent IMA in conjunction with one or more following risk factors: a patent IMA ≥3 mm in diameter, lumbar arteries ≥2 mm in diameter, or an aortoiliac-type aneurysm. The participants were randomly assigned to two groups in a 1:1 ratio: one undergoing EVAR with IMA embolization and the other without. The primary endpoint was T2EL occurrence. The secondary endpoints included aneurysm sac changes and reintervention. In addition to RCT participants, outcomes of patients with low-risk of T2EL were also analyzed.ResultsThe embolization and non-embolization groups each contained 53 patients. Five-year follow-up after the last patient enrolment revealed that T2ELs occurred in 28.3% and 54.7% of patients in the IMA embolization and non-embolization groups, respectively (P=.006). Both freedom from T2EL-related sac enlargement ≥5 mm and cumulative incidence of sac shrinkage ≥5 mm were significantly higher in the IMA embolization group than in the non-embolization group (95.5% vs. 73.6% at 5 years; P=.021, 54.2% vs. 33.6% at 5 years; P=.039). The freedom from T2EL-related sac enlargement ≥10 mm, an alternative indicator for T2EL-related reintervention, showed similar results (100% vs. 90.4% at 5 years; P=.019). Outcomes in the low-risk group were preferable than those in the non-embolization group and comparable to those in the IMA embolization group.ConclusionA lower threshold for pre-emptive IMA embolization when implementing EVAR would be more appropriate if limited to patients at high risk of T2ELs.

Abdominal aortic aneurysm (AAA) is a chronic aortic disease that lacks effective pharmacological therapies. This study was performed to determine the influence of treatment with the gasdermin D inhibitor necrosulfonamide on experimental AAAs. AAAs were induced in male apolipoprotein E-deficient mice by subcutaneous angiotensin II infusion (1000 ng/kg body weight/min), with daily administration of necrosulfonamide (5 mg/kg body weight) or vehicle starting 3 days prior to angiotensin II infusion for 30 days. Necrosulfonamide treatment remarkably suppressed AAA enlargement, as indicated by reduced suprarenal maximal external diameter and surface area, and lowered the incidence and reduced the severity of experimental AAAs. Histologically, necrosulfonamide treatment attenuated medial elastin breaks, smooth muscle cell depletion, and aortic wall collagen deposition. Macrophages, CD4+ T cells, CD8+ T cells, and neovessels were reduced in the aneurysmal aortas of necrosulfonamide- as compared to vehicle-treated angiotensin II-infused mice. Atherosclerosis and intimal macrophages were also substantially reduced in suprarenal aortas from angiotensin II-infused mice following necrosulfonamide treatment. Additionally, the levels of serum interleukin-1β and interleukin-18 were significantly lower in necrosulfonamide- than in vehicle-treated mice without affecting body weight gain, lipid levels, or blood pressure. Our findings indicate that necrosulfonamide reduced experimental AAAs by preserving aortic structural integrity as well as reducing mural leukocyte accumulation, neovessel formation, and systemic levels of interleukin-1β and interleukin-18. Thus, pharmacologically inhibiting gasdermin D activity may lead to the establishment of nonsurgical therapies for clinical AAA disease.

Background: Indoleamine 2,3-dioxygenase (IDO) promotes immunosuppression. Genetic IDO deficiency limits angiotensin II-induced abdominal aortic aneurysms (AAAs) in hyperlipidemic mice. We investigated the influence of IDO inhibition or IDO-catabolized tryptophan catabolite on elastase-induced AAAs in normolipidemic mice. Methods: AAAs were induced in male C57B/6J mice via intra-aortic porcine pancreatic elastase (PPE) infusion. Mice were treated with IDO inhibitor 1-methyl-DL-tryptophan (MT, 2 mg/ml in drinking water), tryptophan metabolite 3-hydroxyanthranilic acid (HAA, 200 mg/kg, oral gavage), or vehicle, starting 3 days prior to PPE infusion for 17 days. AAAs were assessed via ultrasonography and histopathology at sacrifice. Results: The Figure summarizes aortic diameters and histopathology in differentially treated PPE-infused mice. Rapid aortic enlargement was noted in MT-, as compared to vehicle-treated mice following PPE infusion. AAA rupture, unusual for this model, was noted in MT-treated AAA mice. No difference was noted between groups in medial elastin degradation, smooth muscle cell depletion, or macrophage accumulation. However, mural neoangiogenesis and lymphocyte accumulation were remarkably augmented in MT-treated mice. HAA Treatment attenuated aortic enlargement in conjunction with improved medial elastin and smooth muscle cell retention and reduced aortic leukocyte accumulation and neovessels. Conclusion: IDO activity and its tryptophan metabolite HAA limit experimental AAA progression in the PPE model. These results provide further support for investigating tryptophan metabolites in clinical AAA disease suppression.

Purpose: To compare the outcomes of endovascular aortic aneurysm repair using a chimney technique (ch-EVAR) with those of the standard EVAR (st-EVAR) for ruptured abdominal aortic aneurysms (RAAA).Materials and Methods: We implemented ch-EVAR for juxtarenal RAAA based on obvious anatomical indications after converting the strategy for RAAA from open repair to EVAR. A retrospective, cohort-based study was conducted on patients with RAAA who were treated using EVAR in our hospital between July 2011 and March 2022. EVAR cases were extracted, and outcomes were compared between ch-EVAR and st-EVAR. Patient clinical status, anatomical variables, treatment, and follow-up data were evaluated.Results: A total of 56 (82%) and 12 (18%) patients were treated by st-EVAR and ch-EVAR, respectively. Thirty-day mortality rates were comparable between the 2 groups [8.9% in st-EVAR vs 8.3% in ch-EVAR (p= 0.95)]. Short-term outcomes showed that no type Ia endoleak occurred in either group. Midterm outcomes, including sac enlargement [7.5% in st-EVAR vs 0% in ch-EVAR (p= 0.37)], shrinkage [77.5% in st-EVAR vs 80.0% in ch-EVAR (p= 0.86)], and overall survival and freedom from aneurysm-related reintervention at 3 years [64.7% and 96.4% in the EVAR group vs 91.7% and 100% in the ch-EVAR group, respectively (p= 0.30 and 0.52)], were not significantly different between the 2 groups.Conclusion: Ch-EVAR for RAAA showed remarkably excellent outcomes, comparable to those of st-EVAR. Ch-EVAR is considered technically feasible in experienced centers. The indications for EVAR for RAAA may be further expanded using the chimney technique, resulting in overall improved outcomes for RAAA.Clinical Impact This is a retrospective, single-center analysis of 68 patients with ruptured abdominal aortic aneurysms (RAAAs) treated by endovascular repair (EVAR) to investigate the efficacy of the chimney technique for juxtarenal RAAA. Thirty-day mortality rate was 8.3% for the chimney EVAR group, which was equivalent to that in the standard EVAR group. Mid-term outcomes including sac enlargement/shrinkage, overall survival, and freedom from aneurysm-related reintervention were comparable between the two groups. This report suggests the possibility of broadening the selection criteria of the current endovascular strategy using the chimney technique.