AAA Diameter Research Articles

Laparoscopic Ligation of the Inferior Mesenteric Artery: A Systematic Review of an Emerging Trend for Addressing Type II Endoleak Following Endovascular Aortic Aneurysm Repair.

Background/Objectives: this systematic review aims to explore the efficacy and safety of the laparoscopic ligation of the inferior mesenteric artery (IMA) as an emerging trend for addressing a type II endoleak following endovascular aortic aneurysm repair (EVAR). Methods: A comprehensive literature search was conducted across several databases including Medline, Scopus, and the Cochrane Central Register of Controlled Trials, adhering to the PRISMA guidelines. The search focused on articles reporting on the laparoscopic ligation of the IMA for the treatment of a type II endoleak post-EVAR. Data were extracted regarding study characteristics, patient demographics, technical success rates, postoperative outcomes, and follow-up results. Results: Our analysis included ten case studies and two retrospective cohort studies, comprising a total of 26 patients who underwent a laparoscopic ligation of the IMA between 2000 and 2023. The mean age of the cohort was 72.3 years, with a male predominance (92.3%). The mean AAA diameter at the time of intervention was 69.7 mm. The technique demonstrated a high technical success rate of 92.3%, with a mean procedure time of 118.4 min and minimal blood loss. The average follow-up duration was 19.9 months, with 73% of patients experiencing regression of the aneurysmal sac, and no reports of an IMA-related type II endoleak during the follow-up period. Conclusions: The laparoscopic ligation of the IMA for a type II endoleak following EVAR presents a promising, minimally invasive alternative with high technical success rates and favorable postoperative outcomes. Despite its potential advantages, including reduced contrast agent use and radiation exposure, its application remains limited to specialized centers. The findings suggest the need for further research in larger prospective studies to validate the effectiveness of this procedure and potentially broaden its clinical adoption.

Colchicine ameliorates short-term abdominal aortic aneurysms by inhibiting the expression of NLRP3 inflammasome components in mice

BackgroundAbdominal aortic aneurysms (AAA) are often associated with chronic inflammation and pose a significant risk to affected individuals. Colchicine, known for its anti-inflammatory properties, has shown promise in managing cardiovascular diseases. However, its specific role in the development of AAA remains poorly understood. Methods and resultsIn this study, we employed a short-term AAA model induced by angiotensin II (Ang II, 1000 ng/kg/min) and calcium chloride (CaCl2, 0.5 mol/l) in male ApoE-/- and C57BL/6 mice (8–12 weeks old) to investigate the effects of colchicine on AAA progression. Colchicine (0.4 mg/kg) was administered orally once daily, starting on the same day as AAA induction. After a 4-week duration, we observed a significant reduction in AAA diameter, degradation of elastic fibers, and expression of components related to the Nucleotide-binding oligomerization domain-like receptor family protein 3 (NLRP3) inflammasome in the vessel wall of colchicine-treated mice compared to the saline group. Mechanistically, colchicine (5 μm/l, for 24h) inhibited the expression of NLRP3 inflammasome components through the P38-ERK/MicroRNA145-toll-like receptor 4 (TLR4) pathway in RAW264.7 cells. ConclusionsOur study demonstrates the effectiveness of colchicine in suppressing NLRP3 inflammasome components, thereby delaying AAA progression in the Ang II and CaCl2-induced short-term model. These findings suggest the potential of colchicine as a pharmacological treatment option for AAA.

The association of ruptured abdominal aortic aneurysm diameter with mortality in the International Consortium of Vascular Registries

BackgroundThe mortality after ruptured abdominal aortic aneurysm (rAAA) repair is high, despite improvements in perioperative care, centralization of emergency vascular surgical services, and the introduction of endovascular aneurysm repair (EVAR). The diameter of intact AAA has been shown to be a predictor of short- and long-term survival. The aim of this study was to analyze the impact of AAA diameter on mortality for rAAA repair using contemporary data collected from the International Consortium of Vascular Registries and compare outcomes by sex and the type of repair patients received. MethodsProspective registry data on repair of rAAA from seven countries were collected from 2010 to 2016. The primary outcome was perioperative mortality after EVAR and open surgical repair (OSR). Data were stratified by type of repair and sex. Logistic regression models were used to estimate odds ratio (OR) for the association between AAA diameter and perioperative mortality and the association between type of repair and mortality. Multivariable logistic regression models were used to adjust for differences in patient characteristics. ResultsThe study population consisted of 6428 patients with a mean age ranging from 70.2 to 75.4 years; the mean AAA diameter was 7.7 ± 1.8 cm. Females had a significantly smaller AAA diameter at presentation compared with males (6.9 ± 1.6 cm vs 7.9 ± 1.8 cm; P < .001). who underwent OSR had larger AAA diameters compared with those who underwent EVAR (P < .001). Females who underwent repair were significantly older (P < .001). Males were more likely to have cardiac disease, diabetes mellitus, and renal impairment. Overall, AAA diameter was a predictor of mortality in univariate and multivariate analysis. When analyzing EVAR and OSR separately, the impact of AAA diameter per cm increase on mortality was apparent in both males and females undergoing EVAR, but not OSR (EVAR: male OR, 1.09 [95% confidence interval, 1.03-1.16] and EVAR: female OR, 1.17 [95% confidence interval, 1.02-1.35]). The early mortality rate for males and females who underwent EVAR was 18.9% and 25.9% (P < .001), respectively. The corresponding mortality for males and females who underwent OSR was 30.2% and 38.6% (P < .001), respectively. ConclusionsIn these real-world international data, there is a significant association between rAAA diameters and early mortality in males and females. This association was more evident in patients undergoing EVAR, but not shown in OSR. Despite improvements in overall AAA repair outcomes, the risk of mortality after rAAA repair is consistently higher for females.

A population-based study on hyperinsulinaemia and arterial stiffness in men with and without abdominal aortic aneurysm.

Patients with type 2 diabetes mellitus (DM) run lower risk for abdominal aortic aneurysm (AAA, aortic diameter ≥ 30 mm) and its complications. We aimed to evaluate associations between disturbances in glucose metabolism and arterial stiffness, AAA, and abdominal aortic diameter in 65-year-old men. Forty-eight 65-year-old men with screening-detected AAA and 115 men with normal abdominal aortic diameter underwent examination of glucose metabolism and arterial stiffness. Men with AAA had higher BMI, waist-hip ratio (WHR), frequency of DM, haemoglobin A1c, smoking exposure, and plasma insulin levels at 0, 60 and 120 min during OGTT compared to those without. The increase in p-insulin (P < 0.001) after OGTT was also higher in men with AAA, adjusted for smoking, WHR, and nadir value of p-insulin. In analyses adjusted for smoking, use of lipid-lowering agents, and WHR, the increase in p-insulin at 2-hours (P = 0.006) after OGTT and p-homocysteine were associated with abdominal aortic diameter. There were no differences between groups in aortic stiffness or skin autofluorescence Advanced Glycation End products. In this population-based study hyperinsulinaemia as a marker of insulin resistance, but not hyperglycaemia or aortic stiffness, was associated with AAA and abdominal aortic diameter in 65-year-old men.

Abdominal Aortic Aneurysm Diameter versus Volume: A Systematic Review

The aim of this systematic review was to analyze the results of previous studies comparing AAA diameter and volume measurements. A systematic search in PubMed, Cochrane, and EMBASE databases was performed to identify studies investigating the use of diameter and volume measurements in AAA diagnosis and prognosis in English, German, and Russian, published until December 2022. The manuscripts were reviewed by three researchers and scored on the quality of the research using MINORS criteria. After screening 752 manuscripts, 19 studies (n = 1690) were included. The majority (n = 17) of the manuscripts appeared to favor volume. It is, however, important to highlight the heterogeneity of methodologies and lack of standardized protocol for measuring both volume and diameter in the included studies, which hindered the interpretation of the results. The clinical relevance of abdominal aortic aneurysm volume measurement is still unclear, although studies show favorable and promising results for volumetric changes in AAA, especially in follow-up after EVAR.

Prophylactic Perigraft Arterial Sac Embolization During EVAR: Minimizing Type II Endoleaks and Improving Sac Regression

Type II endoleaks (ELII) are the most common complication following endovascular aneurysm repair (EVAR). Persistent type II endoleaks require continual surveillance and have been shown to increase the risk of Type I and III endoleaks, sac growth, need for intervention, conversion to open or even rupture directly or indirectly. These are often difficult to treat following EVAR and there are limited data regarding the effectiveness of prophylactic treatment of ELII. The aim of this study is to report midterm outcomes of prophylactic perigraft arterial sac embolization (pPASE) performed in patients undergoing EVAR. This is a comparison of two elective cohorts of those undergoing EVAR using the Ovation stent graft with and without prophylactic branch vessel and sac embolization. Patients who underwent pPASE at our institution had data collected in a prospective, IRB approved database. These were compared against the core lab adjudicated data from the Ovation IDE trial. Prophylactic PASE was performed at the time of EVAR with thrombin, contrast and gelfoam if lumbar or mesenteric arteries were patent. Endpoints included freedom from ELII, reintervention, sac growth, all-cause mortality (ACM) and aneurysm-related mortality (ARM). Thirty-six patients (13.1%) underwent pPASE, while 238 patients (86.9%) had standard EVAR. Median follow-up was 56 months (IQR 33-60). The 4-year freedom from ELII estimates were 84% for the pPASE vs 50.7% for the standard EVAR group (P=0.0002). All aneurysms in the pPASE group remained stable in size or demonstrated regression, whereas aneurysm sac expansion was seen in 10.9% of the standard EVAR group, P=0.03. At 4 years, mean AAA diameter decreased by 11mm (95% CI 8-15) in the pPASE group vs 5mm (95%CI 4-6) for the standard EVAR group, P=0.0005. There were no differences in the 4-year freedom from ACM and ARM. However, the difference in reintervention for ELII trended toward significance (0.0% vs 10.7%, P=0.1). On multivariable analysis, pPASE was associated with a 76% reduction in ELII [aHR(95%CI): 0.24 (0.08-0.65), P=0.005]. These results suggest that pPASE in those undergoing EVAR is safe and effective in the prevention of EII and significantly improves sac regression over standard EVAR while minimizing the need for reintervention.

Safety of Utilizing Ultrasound as the Sole Modality of Follow-Up after Endovascular Aneurysm Repair

Post-EVAR, surveillance with CTA remains the most common practice, per SVS guidelines. Chronic exposure to both radiation and IV contrast has raised concerns about long-term CTA follow-up. As we have selectively used US as a sole modality for post-EVAR surveillance, we sought to review our outcomes in this subset of patients. Retrospective review of our institution's Vascular Database identified 213 EVAR patients from 2013 to 2021. FEVAR and snorkel reconstructions were excluded. Patient demographics/outcomes, AAA characteristics, and FU modalities and outcomes were analyzed. Unpaired student t-test, ANOVA, and Chi-square test were used to assess group differences. Eighty-five of the 213 EVAR patients (39.9%) were lost to FU within 3 months. Among the 128 remaining patients, 91 underwent FU using initial US, while 37 patients underwent post-EVAR FU initially using CTA. There were no significant differences (p > 0.05) between patient age (75.5 ± 9.4 vs. 75.3 ± 8.5), BMI (27.7 ± 5.4 vs. 28.9 ± 7.4), or mean AAA size (5.6 ± 1.1 vs. 5.9 ± 1.2) in US-surveilled and CT-surveilled groups respectively. Of the 91 patients initially surveilled with US, 15 patients demonstrated endoleak and/or AAA growth (>5 mm). The 15 patients with US demonstrated-endoleak and/or growth underwent confirmatory CTA with 3 patients eventually requiring EVAR revision. Among 37 patients initially surveilled with CT, 10 demonstrated significant growth and 2 patients eventually required EVAR revision. There were no patients with AAA rupture during post-EVAR surveillance. Follow-up data was analyzed among a select lower-risk group of patients (pre-operative AAA diameter ≤ 5.5 cm, BMI ≤ 30, and no endoleak at completion of EVAR). Among this group, there were no surveilled patients that required EVAR reintervention regardless of surveillance modality (US n=32; CT n=4). The average follow-up was 29.5 ± 26.4 months in the US group and 26.4 ± 22.3 months in the CT group (p > 0.05). Although initial CT surveillance following EVAR remains ideal, in select lower-risk patients, ultrasound is a viable alternative even for the initial post-procedure study. Advantages include decreased radiation exposure and cost. Our data suggest that US is a safe sole modality for surveillance following EVAR in selective patients.

Abdominal Aortic Aneurysm and Plasminogen Activator Inhibitor 1: Correlation in the Context of Type 2 Diabetes

BackgroundAbdominal Aortic Aneurysm (AAA) is a progressive, inflammatory disease of the infrarenal aorta, characterized by irreversible aortic dilation. Despite decades of research, AAA pathogenesis remains poorly understood, and no pharmaceutical therapies to slow aortic growth have been identified. Interestingly, the only condition known to be associated with decreased rates of aortic growth and rupture in AAA patients is a diagnosis of Type 2 Diabetes Mellitus (T2DM). Our laboratory has demonstrated that streptozotocin (STZ)‐induced hyperglycemia inhibits aortic dilation in a mouse model of AAA. Plasminogen Activator Inhibitor 1 (PAI‐1), a key player in the fibrinolytic pathway, has been shown to be elevated in both Type 1 and T2DM patients and hyperglycemic mice. Additionally, studies have demonstrated that local application of PAI‐1 is effective in inhibiting AAA development in a murine model.ObjectiveThe purpose of the present study was to determine the role of PAI‐1 expression in hyperglycemic protection against AAA growth.HypothesisWe predicted that elevated PAI‐1 is responsible for decreased fibrinolysis leading to inhibited aortic growth in patients with both diabetes and AAA. Based on this hypothesis, we proposed that hyperglycemic mice deficient in PAI‐1 (PAI‐1 KO) would not demonstrate the protection from AAA growth observed in hyperglycemic C57BL/6J (C57) control mice.MethodsFasting blood glucose (BG; mg/dL) was measured in 6‐week‐old C57 and PAI‐1 KO mice at baseline on experimental day (D)0, and STZ (40 mg/kg) was intraperitoneally administered daily from D0 to D4. Sodium citrate buffer (SC; vehicle) was administered to control mice. On D14, final BG was measured to confirm hyperglycemia (≥250 mg/dL). On D21, mice underwent laparotomy: a midline abdominal incision was made and the infrarenal aorta was isolated. After measuring aortic diameter midway between the renal arteries and iliac bifurcation, pancreatic porcine elastase (PPE; 60 U/mL) was applied to the adventitial aorta for 5 minutes. The aorta and surrounding structures were then washed twice with 0.9% sterile saline. Control mice received heat‐inactivated PPE. On D49, the incision was reopened, and the aorta was isolated and measured at the widest point of dilation.ResultsSTZ‐treated C57 mice experienced significantly reduced AAA diameter compared to SC‐treated C57 controls (p&lt; 0.0001) 4 weeks post‐induction. However, differences in AAA diameter were not observed under the same treatment conditions in PAI‐1 KO mice (p= 0.290). Percent increase in aortic diameter in both STZ‐ and SC‐treated PAI‐1 KO mice induced with AAA was significantly reduced compared to that of SC‐treated C57 mice (p&lt; 0.01 and p &lt; 0.0001, respectively).ConclusionsOur study demonstrated that PAI‐1 is elevated in mice with STZ‐induced diabetes. While hyperglycemic mice show significantly reduced AAA growth compared to normoglycemic AAA controls, no difference in aortic growth is observed between hyperglycemic and normoglycemic PAI‐1 KO mice. Regardless of treatment status, PAI‐1 deficient mice experience significantly reduced AAA growth compared to C57 control mice. We conclude that while the fibrinolytic pathway and PAI‐1 are influential in AAA development, hyperglycemia‐induced elevated PAI‐1 expression does not play a crucial role in hyperglycemic inhibition of AAA growth. Conversely, PAI‐1 deficiency appears to inhibit AAA growth regardless of glycemic status.

Psoas Muscle Area As A Prognostic Factor For Survival In Patients Undergoing EVAR Conversion

INTRODUCTION AND OBJECTIVES EVAR conversion (EVAR-c) is technically complex and physiologically demanding. Measures to quantify surgical frailty preoperatively may be useful prior to offering EVAR explant. There is data supporting psoas muscle area (PMA) as a prognostic factor in fenestrated endovascular and open AAA repairs. The purpose of this analysis was to use PMA as an objective measure of frailty and to determine its utility as a predictor of survival for EVAR-c. METHODS A retrospective single-center review of all AAA repairs was performed (2002-2019) and EVAR-c procedures were analyzed (n=153).Cross-sectional area of the psoas at the mid-body of the L3 vertebrae were measured. The lowest tertile of PMA in all patients was used as a cutoff value for low PMA and these patients were compared to “non-low” PMA. RESULTS Patients with low PMA tended to be older(77vs72,p=.002),less likely to be male(73%vs95%,p<.001),and have lower BMIs(26vs29%,p=.002). Time to conversion, total number of EVAR reinterventions and elective presentation as an indication for repair were similar, however; patients with low PMA had larger aneurysms(8.3vs7.5cm,p=.01)and increased post-EVAR sac growth(2.3vs1cm,p=.005). Inpatient mortality was significantly increased for those with low PMA(16%vs5%, p=.02)as well as the total number of complications (1.5±1.9vs0.9±1.5).Although MACE and need for inpatient dialysis were similar, those with low PMA had a four-fold increase in requiring dialysis at discharge(18%vs4%,p=.01).Long-term mortality was significantly reduced in those with low PMA at 68%,55%and 40% at 1,3 and 5 years, respectively, compared with 81%,69%and 69%(p=.049). CONCLUSIONS In patients with low PMA, higher complications, increased perioperative mortality and worse long-term survival may be expected. Time to conversion and endovascular remediation are equivalent but rates of sac growth and overall AAA diameter are increased. PMA evaluation offers a potential to stratify which patients may have worse short-term and late outcomes undergoing EVAR-c. EVAR conversion (EVAR-c) is technically complex and physiologically demanding. Measures to quantify surgical frailty preoperatively may be useful prior to offering EVAR explant. There is data supporting psoas muscle area (PMA) as a prognostic factor in fenestrated endovascular and open AAA repairs. The purpose of this analysis was to use PMA as an objective measure of frailty and to determine its utility as a predictor of survival for EVAR-c. A retrospective single-center review of all AAA repairs was performed (2002-2019) and EVAR-c procedures were analyzed (n=153).Cross-sectional area of the psoas at the mid-body of the L3 vertebrae were measured. The lowest tertile of PMA in all patients was used as a cutoff value for low PMA and these patients were compared to “non-low” PMA. Patients with low PMA tended to be older(77vs72,p=.002),less likely to be male(73%vs95%,p<.001),and have lower BMIs(26vs29%,p=.002). Time to conversion, total number of EVAR reinterventions and elective presentation as an indication for repair were similar, however; patients with low PMA had larger aneurysms(8.3vs7.5cm,p=.01)and increased post-EVAR sac growth(2.3vs1cm,p=.005). Inpatient mortality was significantly increased for those with low PMA(16%vs5%, p=.02)as well as the total number of complications (1.5±1.9vs0.9±1.5).Although MACE and need for inpatient dialysis were similar, those with low PMA had a four-fold increase in requiring dialysis at discharge(18%vs4%,p=.01).Long-term mortality was significantly reduced in those with low PMA at 68%,55%and 40% at 1,3 and 5 years, respectively, compared with 81%,69%and 69%(p=.049). In patients with low PMA, higher complications, increased perioperative mortality and worse long-term survival may be expected. Time to conversion and endovascular remediation are equivalent but rates of sac growth and overall AAA diameter are increased. PMA evaluation offers a potential to stratify which patients may have worse short-term and late outcomes undergoing EVAR-c.

Midterm outcomes of 455 patients receiving the AFX2 endovascular graft for the treatment of abdominal aortic aneurysm: A retrospective multi-center analysis.

Since being introduced into clinical practice the AFX family of endografts has undergone labelling updates, design and manufacturing changes to address a Type III failure mode. The published literature on the performance of the current endograft–AFX2 –is limited to small series with limited follow up. The present study reports the largest series of patients implanted with AFX2 for the treatment of abdominal aortic aneurysms. The study was a retrospective, 5 center study of patients receiving an AFX2 endograft from January 2016 until Dec 2020. Electronic case report forms were provided to four of the centers, with one additional site providing relevant outcomes in an independent dataset. Relevant outcomes were reported via Kaplan-Meier analysis and included all-cause mortality, aneurysm-related mortality, post EVAR aortic rupture, open conversion, device related reinterventions and endoleaks. Among a cohort of 460 patients, 405 underwent elective repair of an AAA, 50 were treated for a ruptured AAA, and 5 were aorto-iliac occlusive disease cases. For the elective cohort (mean age 73.7y, 77% male, mean AAA diameter 5.4cm), the peri-operative mortality was 1.7%. Freedom from aneurysm-related mortality was 98.2% at 1,2,3 and 4 years post-operatively, there were no post-operative aortic ruptures, and 2 patients required open conversion. Freedom from Type Ia endoleaks was 99.4% at 1, 2, 3 and 4 years. Freedom from Type IIIa and Type IIIb endoleaks were 100% and 100% (year 1), 100% and 99.6% (year 2), 99.4% and 99.6% (year 3), 99.4% and 99.6% (year 4) respectively. Freedom from all device-related reintervention (including Type II endoleaks) at 4 y was 86.8%. The AFX2 endograft appears to perform to a satisfactory standard in terms of patient centric outcomes in mid-term follow up. The Type Ia and Type III endoleaks rates at 4y appear to be within acceptable limits. Further follow up studies are warranted.

Induction of Heme Oxygenase-1 Is Linked to the Severity of Disease in Human Abdominal Aortic Aneurysm.

BackgroundRupture of abdominal aortic aneurysm (rAAA) is associated with high case fatality rates, and risk of rupture increases with the AAA diameter. Heme oxygenase‐1 (gene HMOX1, protein HO‐1) is a stress‐induced protein and induction has protective effects in the vessel wall. HMOX1−/− mice are more susceptible to angiotensin II‐induced AAA formation, but the regulation in human nonruptured and ruptured AAA is only poorly understood. Our hypothesis proposed that HO‐1 is reduced in AAA and lowering is inversely associated with the AAA diameter.Methods and ResultsAAA walls from patients undergoing elective open repair (eAAA) or surgery because of rupture (rAAA) were analyzed for aortic HMOX1/HO‐1 expression by quantitative real‐time polymerase chain reaction and Western blot. Aortas from patients with aortic occlusive disease served as controls. HMOX1/HO‐1 expression was 1.1‐ to 7.6‐fold upregulated in eAAA and rAAA. HO‐1 expression was 3‐fold higher in eAAA specimen with a diameter >84.4 mm, whereas HO‐1 was not different in rAAA. Other variables that are known for associations with AAA and HO‐1 induction were tested. In eAAA, HO‐1 expression was negatively correlated with aortic collagen content and oxidative stress parameters H2O2 release, oxidized proteins, and thiobarbituric acid reactive substances. Serum HO‐1 concentrations were analyzed in patients with eAAA, and maximum values were found in an aortic diameter of 55 to 70 mm with no further increase >70 mm, compared with <55 mm.ConclusionsAortic HO‐1 expression was increased in eAAA and rAAA. HO‐1 increased with the severity of disease but was additionally connected to less oxidative stress and vasoprotective mechanisms.

The Short-term Predictive Value of Vessel Wall Stiffness on Abdominal Aortic Aneurysm Growth

BackgroundAbdominal aortic aneurysm (AAA) surveillance programs are currently based solely on AAA diameter. The diameter criterion alone, however, seems inadequate as small AAAs comprise 5–10 % of ruptured AAAs as well as some large AAAs never rupture. Aneurysm wall stiffness has been suggested to predict rupture and growth; this study aimed to investigate the prognostic value of AAA vessel wall stiffness for growth on prospectively collected data. MethodsAnalysis was based on data from a randomised, placebo-controlled, multicentre trial investigating mast-cell-inhibitors to halt aneurysm growth (the AORTA trial). Systolic and diastolic AAA diameter was determined in 326 patients using electrocardiogram-gated ultrasound (US). Stiffness was calculated at baseline and after 1 year. ResultsMaximum AAA diameter increased from 44.1 mm to 46.5 mm during the study period. Aneurysm growth after 1 year was not predicted by baseline stiffness (-0.003 mm/U; 95 % CI: -0.007 to 0.001 mm/U; P = 0.15). Throughout the study period, stiffness remained unchanged (8.3 U; 95 % CI: -2.5 to 19.1 U; P = 0.13) and without significant correlation to aneurysm growth (R: 0.053; P = 0.38). ConclusionsFollowing a rigorous US protocol, this study could not confirm AAA vessel wall stiffness as a predictor of aneurysm growth in a 1-year follow-up design. The need for new and subtle methods to complement diameter for improved AAA risk assessment is warranted.

An International, Multicenter Retrospective Observational Study to Assess Technical Success and Clinical Outcomes of Patients Treated with an Endovascular Aneurysm Sealing Device for Type III Endoleak

Introduction: Type III endoleaks post-endovascular aortic aneurysm repair (EVAR) warrant treatment because they increase pressure within the aneurysm sac leading to increased rupture risk. The treatment may be difficult with regular endovascular devices. Endovascular aneurysm sealing (EVAS) might provide a treatment option for type III endoleaks, especially if located near the flow divider. This study aims to analyze clinical outcomes of EVAS for type III endoleaks after EVAR. Methods: This is an international, retrospective, observational cohort study including data from 8 European institutions. Results: A total of 20 patients were identified of which 80% had a type IIIb endoleak and the remainder (20%) a type IIIa endoleak. The median time between EVAR and EVAS was 49.5 months (28.5–89). Mean AAA diameter prior to EVAS revision was 76.6±19.9 mm. Technical success was achieved in 95%, 1 patient had technical failure due to a postoperative myocardial infarction resulting in death. Mean follow-up was 22.8±15.2 months. During follow-up 1 patient had a type Ia endoleak, and 1 patient had a new type IIIa endoleak at an untreated location. There were 5 patients with aneurysm growth. Five patients underwent AAA-related reinterventions indications being: growth with type II endoleak (n=3), type Ia endoleak (n=1), and iliac aneurysm (n=1). At 1-year follow-up, the freedom from clinical failure was 77.5%, freedom from all-cause mortality 94.7%, freedom from aneurysm-related mortality 95%, and freedom from aneurysm-related reinterventions 93.8%. Conclusion: The EVAS relining can be safely performed to treat type III endoleaks with an acceptable technical success rate, a low 30-day mortality rate and no secondary ruptures at short-term follow-up. The relatively low clinical success rates, related to reinterventions and AAA enlargement, highlight the need for prolonged follow-up.

Effect of Abdominal Aortic Aneurysm Size on Mid-Term Mortality After Endovascular Repair

BackgroundPrevious studies have suggested that large preoperative AAA size may impact late survival after elective EVAR. It is unclear, however, whether this association applies to patients with smaller AAA between 5.0-5.5 cm, who constitute a substantial portion of patients undergoing elective EVAR. The purpose of this study was to delineate the effect of AAA size between 5.0 and 5.5 cm on mid-term mortality after EVAR by analyzing a large national cohort, the Vascular Quality Initiative (VQI) database. MethodsUsing the Vascular Quality Initiative (VQI) national database, patients who underwent EVAR for intact AAA between 2003 and 2018 were identified and stratified based on maximal AAA diameter into 3 groups: Group 1 (4.0 cm ≤ AAA <5.0 cm); Group 2 (5.0 cm ≤ AAA < 5.5 cm); and Group 3 (AAA ≥ 5.5 cm). Cox proportional hazard model and propensity score matching method were used to estimate AAA size effect on all-cause mortality at 1, 3, and 5 years after EVAR while adjusting for potential confounders. ResultsThe study included 32,398 patients, of whom 81% were men with a mean age of 74. The most common group who underwent EVAR was Group 2 (5.0 cm ≤ AAA < 5.5 cm). Larger AAA size was associated with male sex (75% versus 79% versus 84%, for Groups 1, 2, and 3 respectively; P < 0.0001) and with coronary artery disease (27% versus 29% versus 31%, for Groups 1, 2, and 3 respectively, P< 0.0001); but was negatively associated with active smoking (33% versus 31% versus 30%, for Groups 1, 2, and 3, respectively, P< 0.001). While 10% of the largest and smallest AAA groups (Groups 3 and 1, respectively) were symptomatic, only 5% of patients in Group 2 were symptomatic (P < 0.01). Adjusted Cox proportional hazard modeling revealed that patients in Group 2 were at significantly lower risk of 5-year mortality when compared to patients in Group 3 (HR 0.66, 95% CI 0.61-0.72, P< 0.01), while similar in risk when compared to patients in Group 1 (HR 1.11, 95% CI 0.93-1.32, P= 0.26). ConclusionOur analysis found that over 40% of EVAR in the national VQI cohort were performed for AAA < 5.5 cm, with the greatest number of patients undergoing EVAR at AAA size 5.0-5.5cm. Patients with AAA size 5.0-5.5 cm had better 5-year survival outcomes than patients with AAA ≥ 5.5 cm, and similar survival to patients with small AAA between 4.0-5.0 cm.

Simple diameter measurements with ultrasound can be safely used to follow the majority of patients after infrarenal endovascular aneurysm repair

The optimal imaging follow-up after infrarenal EVAR is still undefined. The aim of this study was to analyze the outcome of a personalized follow-up program after infrarenal EVAR based on ultrasound AAA diameter measurements for low-risk patients.All consecutive patients followed-up locally after elective and acute infrarenal EVAR between 2010 and 2015 were retrospectively reviewed. Patients underwent CTA at 1-month post-EVAR whereby the attending surgeon defined the subsequent follow-up. Patients considered at low risk were followed with ultrasound only assessing AAA diameter at 1, 2, 3 and every 5 years postoperatively (group A). Low risk required a favorable pre-operative anatomy especially regarding the aneurysm neck, satisfactory intraoperative result and uneventful 1 month CTA (type 2 endoleaks acceptable). Patients not fulfilling the criteria for group A were followed with yearly 3-phase-CTAs (group B).Two hundred twenty-two patients with a AAA median diameter of 58 (54-68) mm were included. One hundred ninety-one were allocated into group A and 31 in group B. Median follow-up time was 36 (24-59) months. Five-year primary and primary-assisted success was 82±5% and 93±3% for group A and 70±13% and 93±5% for group B, respectively (P=0.042 and P=0.504, respectively). Sixteen late aneurysm-related reinterventions were performed in 12 patients (7 in group A and 9 in group B). In group A, 5 reinterventions were rupture-preventing and 2 were symptomatic. All late reinterventions in group B were performed following findings on follow-up imaging. Five-year late reintervention-free survival was 95±2% and 84±7% for groups A and B, respectively (P=0.046). Five-year survival was 80±3% and 63±10% for group A and B, respectively (P=0.024).A customized follow-up program after infrarenal EVAR based on ultrasound AAA diameter measurements in low-risk patients seems to be effective in maintaining a very high mid-term clinical success rate.

A morphovolumetric analysis of aneurysm sac evolution after elective endovascular abdominal aortic repair

ObjectiveAbdominal aortic aneurysm (AAA) sac shrinkage after endovascular aortic repair (EVAR) has been regarded as positive marker of EVAR success durability. The purpose of this study was to describe the morphovolumetric changes of the AAA sac during follow-up after elective EVAR and to analyze sac shrinkage-related variables. MethodsThis is a single-center, retrospective, observational cohort study from a tertiary referral university hospital. All patients treated with EVAR between January 2013 and December 2018 were identified. Inclusion criteria were elective EVAR for AAA, preoperative computed tomography angiography within 6 months before EVAR and at least one postoperative computed tomography angiography during the follow-up, using a standardized protocol. Aneurysm sac shrinkage was defined as diameter decrease of 1 cm or more, volume shrinkage threshold was identified by a 16% decrease compared with the preoperative value. Primary outcomes were early (≤30 days) and late survival, and freedom from aneurysm-related mortality (ARM), and aortic reintervention. ResultsThere were 149 of the 325 patients (45.8%) who met the inclusion criteria: 133 (89.3%) were male and 16 (10.7%) female. The mean age was 74 ± 7 years (range, 55-87 years); the median AAA diameter was 56 mm (interquartile range, 50.0-61.2 mm) and the median volume was 138.8 cm3 (range, 99.0-178.3 cm3). Primary technical success was achieved in 145 patients (97.3%). The in-hospital mortality rate was 1.3%. The median follow-up was 42 months (interquartile range, 22.5-58.0 months). Both AAA diameter and volume decreased (P = .001 and P = .035, respectively) compared with preoperative measurements. Diameter shrinkage was adjudicated in 27 patients (18.1%), volume shrinkage was observed in 42 patients (28.2%). A Cox regression analysis demonstrated an association between the AAA diameter shrinkage and the preoperative diameter (P = .002; hazard ratio, 1.03; 95% confidence interval [CI], 1.011-1.052). The presence of a persistent endoleak predicted the absence of volume shrinkage (P = .001; hazard ratio, 7.75; 95% CI, 2.282-26.291). The estimated freedom from ARM was 97.5 ± 1.0% (95% CI, 93-99) at 12 months, and 96 ± 2% (95% CI, 90-98) at both 36 and 60 months. Aortic reintervention during the follow-up period was necessary in 7 patients (4.7%). ARM was only observed in the group characterized by the concomitant absence of diameter and volume shrinkage. ConclusionsVolumetric analysis showed to have higher sensitivity than the simple two-dimensional measurement of the diameter to study AAA sac changes after EVAR. Although no predictor was found to be associated with AAA volume shrinkage, ARM occurred only in the group of AAAs with the absence of volume shrinkage.

Favorable Outcomes in Octogenarians With Hostile Neck Undergoing Endovascular Repair Using EndoAnchors

ObjectivesStandard endovascular repair (EVAR) is not suitable in patients with hostile aortic anatomy. Open aneurysm repair (OAR) has been the gold-standard approach in managing these patients. EndoAnchors have been introduced as a technique to make EVAR in patients with short and angulated necks possible. The use of EndoAnchors in managing hostile aneurysms in octogenarians has not been studied before. Thus, the purpose of this study is to evaluate both short and long-term outcomes in octogenarians versus nonoctogenarians patients with hostile aortic anatomy undergoing EVAR using EndoAnchors. MethodsOnly patients enrolled in the primary arm of the ANCHOR registry were included and stratified into octogenarians (80–89 years) and nonoctogenarians (<80 years). Standard univariate (chi-square, fisher's exact, student's t-tests) and multivariable (logistic, cox-regression) analysis was used to evaluate patients’ characteristics and outcomes between octogenarians versus nonoctogenarians as appropriate. ResultsOf 461 patients, 21% (N = 97) were octogenarians. Compared to nonoctogenarians, octogenarians were more likely to have a history of renal (32.0% vs. 18.4%) and genitourinary (30.9% vs. 21.2%) disease (both P < 0.05). They were also more likely to have an AAA diameter greater than 55 mm compared to nonoctogenarians (59% vs. 46%), had increased neck tortuosity index (mean [S.D.] 1.07 [0.08] vs. 1.05 [0.05]), greater proximal neck angulation (mean [S.D.]: 28.2 [17.3] vs. 23.7 [16] degrees) and were more likely to have localized (29.3% vs. 18.7%) and diffuse (25.6% vs. 20.7%) neck calcification (All P < 0.05). The overall procedural success was similar between both groups. However, octogenarians had higher rates of endoleaks at completion (32.0% vs. 21.2%, P = 0.03) and 30-day bleeding (12.4% vs. 5.8%) and cardiac (13.4% vs. 5.2%) complications (All P < 0.05). Additionally, compared to nonoctogenarians, octogenarians had lower freedom from all-cause mortality (87.90% vs. 96.50%) and type II endoleak (73.30% vs. 88.60%) based on Kaplan Meier estimates through one year (Both P < 0.05). In multivariable cox-regression analysis, octogenarians demonstrated a 5-fold increase in all cause mortality (HR [95% CI]: 5.19 [1.92–14], P = 0.001) and a 3-fold increase in type II endoleak (HR [95% CI]: 2.99 [1.54–5.81], P = 0.001) at 1-year. However, no significant difference was seen in aneurysm/device related mortality (HR [95% CI]: 1.42 [0.14–14.7], P = 0.77) and type I endoleak (HR [95% CI]: 1.71 [0.31–9.55], P = 0.54) at 1-year. ConclusionsDespite a worse aortic neck anatomy, octogenarians undergoing EVAR using EndoAnchors showed acceptable short and long-term outcomes. The results of our study could expand the utilization of EVAR in octogenarians with hostile neck.

Prediction of Abdominal Aortic Aneurysm Growth Using Geometric Assessment of Computerized Tomography Images Acquired During the Aneurysm Surveillance Period.

We investigated the utility of geometric features for future AAA growth prediction. Novel methods for growth prediction of AAA are recognized as a research priority. Geometric feature have been used to predict cerebral aneurysm rupture, but not examined as predictor of AAA growth. Computerized tomography (CT) scans from patients with infra-renal AAAs were analyzed. Aortic volumes were segmented using an automated pipeline to extract AAA diameter (APD), undulation index (UI), and radius of curvature (RC). Using a prospectively recruited cohort, we first examined the relation between these geometric measurements to patients' demographic features (n = 102). A separate 192 AAA patients with serial CT scans during AAA surveillance were identified from an ongoing clinical database. Multinomial logistic and multiple linear regression models were trained and optimized to predict future AAA growth in these patients. There was no correlation between the geometric measurements and patients' demographic features. APD (Spearman r = 0.25, P < 0.05), UI (Spearman r = 0.38, P < 0.001) and RC (Spearman r =-0.53, P < 0.001) significantly correlated with annual AAA growth. Using APD, UI, and RC as 3 input variables, the area under receiver operating characteristics curve for predicting slow growth (<2.5 mm/yr) or fast growth (>5 mm/yr) at 12 months are 0.80 and 0.79, respectively. The prediction or growth rate is within 2 mm error in 87% of cases. Geometric features of an AAA can predict its future growth. This method can be applied to routine clinical CT scans acquired from patients during their AAA surveillance pathway.

Integrated Plasma and Tissue Proteomics Reveals Attractin Release by Intraluminal Thrombus of Abdominal Aortic Aneurysms and Improves Aneurysm Growth Prediction in Humans.

Discovery of novel biomarkers for AAA growth prediction. Novel biomarker of AAA growth is a recognized priority in research. Our prior work implicated intraluminal thrombus (ILT) in AAAs to be a potential source of systemic mediators during AAA progression. Here we applied a mass spectrometry proteomics pipeline to discover novel biomarkers for AAA growth prediction. Patients were prospectively recruited. Plasma samples were collected at baseline (n = 62). AAA growth was recorded at 12 months. In Experiment 1, plasma samples from the fastest and slowest growth patients (n = 10 each) were compared. In Experiment 2, plasma samples were collected before and at 10-12 weeks after surgery (n = 29). In Experiment 3, paired ILT and omental biopsies were collected intra-operatively during open surgical repair (n = 3). In Experiment 4, tissue secretome was obtained from ex-vivo culture of these paired tissue samples. Samples were subjected to a liquid chromatography tandem mass spectrometry workflow to discover novel biomarkers. We discovered 3 proteins that are: (i) present in ILT; (ii) released by ILT; (iii) reduced in circulation after AAA surgery; (iv) differs between fast and slow growth AAAs. One of these is Attractin. Plasma Attractin correlates significantly with future AAA growth (Spearman r = 0.35, P < 0.005). Using Attractin and AAA diameter as input variables, the area under receiver operating characteristics for predicting no growth and fast growth or AAA at 12 months is 85% and 76%, respectively. We show that ILT of AAAs releases mediators during the natural history of AAA growth. These are novel biomarkers for AAA growth prediction in humans.

Predictors of Aneurysm Sac Shrinkage Utilizing a Global Registry

Aneurysm sac remodeling is a complex multifactorial process with unknown factors influencing sac regression after endovascular aortic aneurysm repair (EVAR). We sought to identify factors associated with this process by analyzing data obtained from patients treated with the GORE EXCLUDER endovascular aneurysm repair (EVAR) endoprosthesis from December 2010 to October 2016 enrolled in the Global Registry for Endovascular Aortic Treatment (GREAT). All patients enrolled in GREAT with three years CT angiography (CTA) follow-up in each of the three successive years after EVAR were included. The percentage of sac size reduction toward device diameter was calculated and used as a surrogate for sac regression with the formula used being: sac size reduction = ((AAA baseline diameter - AAA diameter at follow-up)/(AAA baseline diameter - device diameter))∗100. The cohort was divided into two groups in accordance with the percentage of aneurysm sac reduction at three years; one with the top quartile of patients and the other with the lowest three quartiles. Demographic and procedural variables were analyzed using univariate and regression modeling to determine factors predictive of sac regression. There were 3265 subjects enrolled with follow-up as of May 2018 of which 526 (16.2%) had three years of CTA surveillance. Overall aneurysm sac size decreased from a mean of 58.0mm (Std Dev: 10.4, range: 34.2, 100.0) to a mean of 49.3mm (Std Dev: 14.1, range: 0, 140) for a percentage reduction toward device diameter of a mean 28.2% (Std Dev: 39.0, range: -103.7, 183.9). On multivariate logistic regression model; two factors proved to be statistically significant contributors to a larger percentage reduction in aneurysm sac: a conical neck (odds ratio [OR]=1.64, P-value=0.023) and a larger proximal device diameter (OR=1.09, P-value=0.023). On the other hand, two factors were negative predictors of sac shrinkage, namely: old age (OR=0.96, P-value=0.002) and larger baseline aneurysm sac diameter (OR=0.98, P-value=0.028). Aneurysms with conical necks and larger proximal device neck diameters have an increased percentage change in sac size over time after EVAR. Older age and larger initial diameters of aneurysms were negatively associated with percentage change in sac size as well as sac regression. Further study is needed to determine the clinical utility of these observations and applicability across multiple endoprosthesis platforms.