Abdominal Aortic Aneurysm Size Research Articles

Size thresholds for repair of abdominal aortic aneurysms warrant reconsideration

BackgroundThe historical size threshold for abdominal aortic aneurysm (AAA) repair is widely accepted to be 5.5 cm for men and 5.0 cm for women. However, contemporary AAA rupture risks may be lower than historical benchmarks, which has implications for when AAAs should be repaired. Our objective was to use contemporary AAA rupture rates to inform optimal size thresholds for AAA repair. MethodsWe used a Markov chain analysis to estimate life expectancy for patients with AAA. The primary outcome was AAA-related mortality. We estimated survival using Social Security Administration life tables and published contemporary AAA rupture estimates. For those undergoing repair, we modified survival estimates using data from the Vascular Quality Initiative and Medicare on complications, late rupture, and open conversion. We used this model to estimate the AAA repair size threshold that minimizes AAA-related mortality for 60-year-old average-health men and women. We performed a sensitivity analysis of poor-health patients and 70- and 80-year-old base cases. ResultsThe annual risk of all-cause mortality under surveillance for a 60-year-old woman presenting with a 5.0 cm AAA using repair thresholds of 5.5 cm, 6.0 cm, 6.5 cm, and 7.0 cm was 1.7%, 2.3%, 2.7%, and 2.8%, respectively. The corresponding risk for a man was 2.3%, 2.9%, 3.3%, and 3.4% for the same repair thresholds, respectively. For a 60-year-old average-health woman, an AAA repair size of 6.1 cm was the optimal threshold to minimize AAA-related mortality. Life expectancy varied by <2 months for repair at sizes from 5.7 cm to 7.1 cm. For a 60-year-old average-health man, an AAA repair size of 6.9 cm was the optimal threshold to minimize AAA-related mortality. Life expectancy varied by <2 months for repair at sizes from 6.0 cm to 7.4 cm. Women in poor health, at various age strata, had optimal AAA repair size thresholds that were >6.5 cm, whereas men in poor health, at all ages, had optimal repair size thresholds that were >8.0 cm. ConclusionsThe optimal threshold for AAA repair is more nuanced than a discrete size. Specifically, there appears to be a range of AAA sizes for which repair is reasonable to minmized AAA-related mortality. Notably, they all are greater than current guideline recommendations. These findings would suggest that contemporary AAA size thresholds for repair should be reconsidered.

Implicit screening of abdominal aortic aneurysms among veterans using lumbar spine MRI

BackgroundEarly detection of abdominal aortic aneurysms (AAAs) is critical given the high morbidity and mortality of a ruptured aneurysm. Screening ultrasound is recommended for men 65 and 75 years of age with a smoking history. However, studies have shown that the rate of ultrasound screening is low and that implicit AAA screening by abdominal imaging studies that were not originally intended for AAA screening can play a major role in AAA detection. ObjectiveThe main objective was to evaluate the role of lumbar spine MRIs as an implicit AAA screening study by assessing the detection rate of AAAs in a broader cohort of veterans that included screening and non-screening populations. Methods4085 consecutive lumbar spine MRIs from our institution between 2/2020 and 9/2023 were retrospectively reviewed. Each study was labeled AAA present, AAA not present, or indeterminate by radiologists. The correlation between the presence of AAAs and cardiovascular risk factors was assessed using multinomial logistic regression. ResultsAAAs were present in 89 studies (2.2 %) from 80 patients (mean age 75.8 (56–93), M:F 10:0) and absent in 3935 cases (96.3 %) from 3310 patients (mean age 61.7 (19–100), M:F 9:1). Indeterminate cases (n = 61, 1.5 %) were mainly due to incomplete visualization (70.5 %). Mean AAA size was 3.6 cm with most AAAs (n = 43) smaller than 3.5 cm. Sixteen AAAs were 3.5–3.9 cm, 16 between 4 and 4.9cm, and 6 between 5 and 5.9 cm. Artifact precluded measurements in 8 cases. Among the AAA-positive cases, 20 had no prior documentation of AAA. Twenty-one patients with AAAs would not have met the criteria for the routine AAA screening ultrasound. Higher rates of hypertension, hyperlipidemia, and smoking were observed for the AAA cohort at 78.8 % (OR 2.037, CI 1.160–3.576, P = .013), 82.5 % (2.808, 1.543-5.110, P < .001), and 75 % (3.340, 1.979–5.638, P < .001), respectively, compared to the matched no-AAA cohort (58.2 %, 57.6 %, and 50.8 %; n = 2055). Conclusion: Lumbar spine MRI is a valid modality for implicit screening of AAAs. Clinical impactThose interpreting lumbar spine MRIs should be vigilant about assessing for AAAs, especially in men with a history of hypertension, hyperlipidemia, or tobacco smoking.

Association of women-specific size threshold and mortality in elective abdominal aortic aneurysm repair.

It is unclear whether women derive mortality benefit from early repair of abdominal aortic aneurysms (AAA). The aim of this study was to compare short- and mid-term mortality for women treated at small versus large diameters. Women receiving elective repair of AAA at small (49-54 mm) and large (≥55 mm) diameters from 2008 to 2022 were extracted from the Swedish National Registry for Vascular Surgery (n = 1642 women). The effect of diameter on 90-day, 1- and 3-year mortality was studied in logistic regression and propensity score models. Age, co-morbidities, smoking and repair modality were considered as confounders. Men (n = 9047) were analysed in parallel. Some 1642 women were analysed, of whom 34% underwent repair at small diameters (versus 52% of men). Women with small (versus large) AAAs were younger (73 versus 75 years, P < 0.001), and 63% of women in both size groups had endovascular repairs (P = 0.120). Mortality was 3.5% (90 days), 7.1% (1 year) and 15.8% (3 years), with no differences between the size strata. There was no consistent association between AAA size and mortality in multivariable models. Sex differences in mortality were almost entirely due to mortality in younger-than-average women versus men (3-year mortality: small AAAs 11.1% versus 7.3%, P < 0.030, or large 14.4% versus 10.7%, P < 0.038). Mortality in women is high and unaffected by AAA size at repair. The optimal threshold for women remains undefined. The higher rupture risk in women should not automatically translate into a lower, women-specific threshold.

Влияние диаметра инфраренальной аневризмы брюшной аорты на исход лечения

INTRODUCTION: Abdominal aortic aneurysm (AAA) is usually asymptomatic, and its first manifestation in most cases is a dissection or rupture, with a mortality rate exceeding 90%. Until now, the aspect of the possible effect of the diameter of the AAA on mortality after surgical treatment has not been practically studied. AIM: To study the influence of the size of AAA as a risk factor for fatality in its surgical treatment. MATERIALS AND METHODS: This study is retrospective. The study included 226 patients who underwent open and endovascular procedures for an infrarenal abdominal aortic aneurysm (iAAA) in the period 2011–2015 on the basis of the Department of Cardiovascular Surgery of the Ryazan State Medical University (Ryazan, Russia) and in 2011–2017 at the Republican Scientific Center of Cardiovascular Surgery (RSCSC) (Dushanbe, Tajikistan). There were 60 patients from Dushanbe and 166 from Ryazan. The work is part of a study on the treatment of patients with AAA and registered on the platform ClinicalTrials.gov (NCT04935268). RESULTS: Of the total number of patients with iAAA (n = 226), the number of males and females was 174 (77%) and 52 (23%), respectively, and the average age was 69.4 ± 2.6 years. The diameters of aneurysms in the RT and in the RF did not differ statistically significantly, the comorbidity rate per patient reached 1.84. In the RF and RT the number of operated patients for AAA was 31.3% and 26.7% (p &gt; 0.05), respectively. The average diameter of the AAA in patients who survived surgery for the treatment of iAAA was 57.0 mm [53.5; 60.5] and 59.0 mm [48.0; 73.0] (p &gt; 0.05, U = 2953.5; Z = 0.91), respectively. The diameter of the AAA in deceased patients after surgery (planned and rupture) in the RT and the RF is 60.0 mm [55.0; 65.5] and 72.0 mm [53.5; 80.5] (p &gt; 0.05, U = 129.0; Z = 1.14), respectively. In the RT, the size of the AAA is not associated with a fatal outcome (57.0 mm [53.5; 60.5] and 60.0 mm [55.0; 65.5]; p &gt; 0.05 (U = 207.0; Z = 1.49)). In the RF the size of the AAA in deceased patients was statistically significantly larger than in survivors — 72.0 mm [53.5; 80.5] and 59.0 mm [48.0; 73.0], respectively; p = 0.029 (U = 1394.5; Z = 2.18). The 30-day mortality rate after planned and emergency operations was comparable between the patients of the two clinics. CONCLUSION: The diameter of the AAA is a risk factor for the development of a fatal outcome after treatment.

WTP1.13 The A-HeAD Study: Effects of socio-economic deprivation on modifiable preoperative health behaviours and outcomes after aortic aneurysms repair. A retrospective review

Abstract Aims Social Deprivation is associated with health inequalities and poor clinical outcomes. As yet outcomes for aneurysm surgery are not well understood. This study aims to explore the association of Abdominal Aortic Aneurysm (AAA) surgery and socio-economic status on postoperative complications and outcome. Methods All elective AAA repair (open and endovascular) performed between January 2015 and January 2020 at a tertiary vascular centre were analysed. Deprivation (index of multiple deprivation (IMD)) data was sourced from the English indices of deprivation 2019, by postcode. Primary outcome was overall survival by Kaplan-Meier. Secondary outcomes included comparison of pre-operative fitness assessments, and comorbidity. Clinical outcomes included length of hospital stay (LOS) and complications. Cox-proportional hazard analyses were conducted. Results Patients (n=472) were divided into two groups (IMD 1-3 (n=171) and IMD 4-10 (n=301)). Gender ratios were comparable, with similar AAA size, other co-morbidities and CPET assessment results. IMD 1-3 participants were younger (72.4(8.1) vs 74.6 (7.8), p=0.011), had higher smoking rates (61.4% vs 19.6%, P=0.03) and more frequent history of stroke (18.1% vs 11.3%, P=0.036). There was no difference in survival based upon IMD but patients from IMD 1-3 spent longer in level 2/3 care (2(2-3) vs 1(1-2), P=0.022) and experienced more re-admissions (14% vs. 6%. P=0.003). In addition, cox-regression indicated that patients without COPD were twice as likely to survive (HR 0.54 (0.31-0.94 P=0.03). Conclusion IMD was not associated with poor outcome. Smoking was more prevalent in lower IMD groups. As COPD was associated with increased likelihood of death, pre-operative optimisation can be targeted towards higher risk groups.

Elective Endovascular Aneurysm Repair (EVAR) for the Treatment of Infrarenal Abdominal Aortic Aneurysms of 5.0–5.5 cm: Differences between Men and Women

Background: There is significant debate regarding the existence of sex-related differences in the presentation, treatment, and outcomes of men versus women affected by abdominal aortic aneurysm (AAA). The purpose of this study is to compare endovascular aneurysm repair (EVAR) of infrarenal AAAs with the current sex-neutral 5.0–5.5 cm-diameter threshold for intervention between the two sexes. Methods: Retrospective review of consecutive cases from a single teaching institution over a period of five years of patients who had undergone elective EVAR for AAAs between 5.0 and 5.5 cm in diameter. Outcomes of interest were compared according to sex. Results: Ninety-four patients were included in the analysis, with a higher prevalence of men (53%). Females were older at the time of repair, 78 ± 5.1 years, versus 71.7 ± 7 years (p &lt; 0.01), and had higher incidence of underlying comorbidities, namely, arrhythmia, chronic kidney disease, and previous carotid revascularization. Women had higher incidence of immediate systemic complications (p = 0.021), post-operative AMI (p = 0.001), arrhythmia (p = 0.006), pulmonary oedema (p &lt; 0.001), and persistent renal dysfunction (p = 0.029). Multivariate analysis for post-operative factors associated to mortality and adjusted for sex confirmed that AMI (p = 0.015), arrhythmia (p = 0.049), pulmonary oedema (p = 0.015), persistent renal dysfunction (p &lt; 0.001), cerebral ischemia (p &lt; 0.001), arterial embolism of lower limbs (p &lt; 0.001), and deep-vein thrombosis of lower limbs (p &lt; 0.001) were associated to higher EVAR-related mortality; a higher incidence of post-operative AMI (p = 0.014), pulmonary edema (p = 0.034), and arterial embolism of lower limbs (p = 0.046) were associated to higher 30-days mortality. In females there was also a higher rate of suprarenal fixation (p = 0.026), insertion outside the instruction for use (p = 0.035), and a more hostile neck anatomy with different proximal aortic diameter (p &lt; 0.001) and angle (p = 0.003). Conclusions: A similar threshold of size of AAA for elective surgery for both males and females might not be appropriate for surgical intervention, as females tend to have worse outcomes. Further population-based studies are needed to guide on sex-related differences and intervention on AAA.

Factors associated with all-cause mortality following endovascular abdominal aortic aneurysm repair.

Background: Knowledge of factors that influence all-cause mortality after endovascular abdominal aortic aneurysm repair (EVAR) could improve therapeutic strategies post-EVAR and thus patient prognosis. Our study aimed to evaluate the association between sociodemographic information, comorbidities, laboratory parameters, treatment, selected anatomical and genetic factors and all-cause mortality post-EVAR. Patients and methods: We reviewed all patients who had undergone elective EVAR for non-ruptured abdominal aortic aneurysm (AAA) between January 2010 and December 2019. AAA size (maximum diameter and volume) was measured using CT-angiography. Sac expansion was defined as at least 5 mm increase, sac regression as at least 5 mm decrease in the sac diameter determined at 36±3 months post-EVAR in relation to pre-EVAR AAA diameter. Adjustments were performed for age, hypertension, diabetes mellitus, dyslipidaemia, sex, smoking, number of lumbar arteries, patency of inferior mesenteric artery and number of reinterventions post-EVAR. Results: One hundred and sixty-two patients (150 men, 12 women) with a mean age of 72.6±7.3 years were included in the analysis. Pre-EVAR AAA diameter (HR 1.07; 95% CI 1.03 - 1.12; p=0.001), pre-EVAR AAA volume (HR 1.01; 95% CI 1.002 - 1.011; p=0.008), post-EVAR sac diameter (HR 1.06; 95% CI 1.03 - 1.10; p=0.000), post-EVAR sac volume (HR 1.01; 95% CI 1.002 - 1.011; p=0.006) and anticoagulation therapy (HR 2.46; 95% CI 1.18 - 5.14; p=0.019) were associated with higher mortality in multivariate analysis. Sac regression (HR 0.42; 95% CI 0.22 - 0.82; p=0.011), and treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) (HR 0.71; 95% CI 0.36 - 0.97; p=0.047) were associated with lower mortality. Conclusions: Greater pre- and post-EVAR diameter and volume, failure of sac regression and anticoagulation were associated with higher mortality post-EVAR. Reduced mortality was observed in patients treated with ACE inhibitors or ARBs, and in patients with AAA sac regression.

Plasma Lipidomics Analysis Reveals the Potential Role of Lysophosphatidylcholines in Abdominal Aortic Aneurysm Progression and Formation.

Abdominal aortic aneurysm (AAA) is hallmarked by irreversible dilation of the infrarenal aorta. Lipid deposition in the aortic wall and the potential importance of a lipid disorder in AAA etiology highlight the need to explore lipid variation during AAA development. This study aimed to systematically characterize the lipidomics associated with AAA size and progression. Plasma lipids from 106 subjects (36 non-AAA controls and 70 AAA patients) were comprehensively analyzed using untargeted lipidomics. An AAA animal model was established by embedding angiotensin-II pump in ApoE-/- mice for four weeks and blood was collected at 0, 2 and 4 weeks for lipidomic analysis. Using a false-discovery rate (FDR) < 0.05, a group of lysophosphatidylcholines (lysoPCs) were specifically decreased in AAA patients and mice. LysoPCs were principally lower in the AAA patients with larger diameter (diameter > 50 mm) than those with a smaller size (30 mm < diameter < 50 mm), and levels of lysoPCs were also found to be decreased with modelling time and aneurysm formation in AAA mice. Correlation matrices between lipids and clinical characteristics identified that the positive correlation between lysoPCs and HDL-c was reduced and negative correlations between lysoPCs and CAD rate, lysoPCs and hsCRP were converted to positive correlations in AAA compared to control. Weakened positive correlations between plasma lysoPCs and circulating HDL-c in AAA suggested that HDL-lysoPCs may elicit instinctive physiological effects in AAA. This study provides evidence that reduced lysoPCs essentially underlie the pathogenesis of AAA and that lysoPCs are promising biomarkers for AAA development.

Women Have a Lower Rate of Abdominal Aortic Aneurysm Repair and Higher Long-term Aortic-related Mortality Compared With Men in a Population-based Study

Increased mortality has been reported after open or endovascular repair of abdominal aortic aneurysms (AAAs) in women. Our aim was to evaluate the natural history and outcomes of AAAs in women at a population level. A population-based cohort study was conducted (1980-2017) of all patients with AAA based on identification using International Classification of Diseases, 9th or 10th Revision and Current Procedural Terminology codes. The gender-specific incidences of AAAs were initially calculated. Medical records were reviewed to confirm diagnosis and identify late events and clinical reasons for opting against repair. Survival analysis for overall and aortic mortality was performed and stratified based on gender and repair status. There were 1537 patients with AAAs; 381 (25%) were female. The incidence of AAA in women was 4.5 times lower than men (23 vs 105 per 100,000 person-years). Compared with men, women were diagnosed at an older age (80 vs 73 years, P < .001), with smaller initial aneurysm size (4 vs 4.3 cm, P < .001). In 99 of 1537 patients, the initial presentation was with rupture (male:female; 79:20); 14 ruptured AAAs were <5.5 cm, 10 of 14 in women. Median follow-up was 18 years. AAA repair was less frequent in women (26% vs 41%, P < .001); with no change after availability of endovascular repair (16% vs 20%, P = .2), women had similar 30-day mortality from AAA repair (4% vs 5%, P = .5). However, on Kaplan-Meier analysis, aortic and all-cause mortality at 10 and 20 years were highest in women who did not undergo repair of their AAA (NRF, hazard ratio: 3, 95% confidence interval: 1.8-4.5, P < .001) as compared with all men and women who underwent repair (Table). This cumulative incidence of aortic-related death remained significantly higher in NRF when analyzed with non-aortic-related deaths as a competing risk, 15% vs 5%-8% in the other groups. All patients with aortic-related death (both women and men) had refused repair because of older age and risk from comorbidities, except in 2 females with rupture of 4.8 and 5.5 cm AAAs while awaiting repair. AAAs are diagnosed in women almost a decade later than men. In this study, mortality after AAA repair was not inferior in women compared with men; however, the incidence of repair was significantly lower in women. Based on the findings of threefold greater long-term aortic-related mortality in women not undergoing AAA repair, it may be advisable to consider repair in women earlier at a smaller AAA size.

Tributyrin Intake Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm in LDLR-/- Mice.

Abdominal aortic aneurysm (AAA) is a multifactorial cardiovascular disease with a high risk of death, and it occurs in the infrarenal aorta with vascular dilatation. High blood pressure acts on the aortic wall, resulting in rupture and causing life-threatening intra-abdominal hemorrhage. Vascular smooth muscle cell (VSMC) dysregulation and extracellular matrix (ECM) degradation, especially elastin breaks, contribute to structural changes in the aortic wall. The pathogenesis of AAA includes the occurrence of oxidative stress, inflammatory cell infiltration, elastic fiber fragmentation, VSMC apoptosis, and phenotypic transformation. Tributyrin (TB) is decomposed by intestinal lipase and has a function similar to that of butyrate. Whether TB has a protective effect against AAA remains uncertain. In the present study, we established an AAA murine model by angiotensin II (AngII) induction in low-density lipoprotein receptor knockout (LDLR-/-) mice and investigated the effects of orally administered TB on the AAA size, ratio of macrophage infiltration, levels of matrix metalloproteinase (MMP) expression, and epigenetic regulation. TB attenuates AngII-induced AAA size and decreases elastin fragmentation, macrophage infiltration, and MMP expression in the medial layer of the aorta and reduces the levels of SBP (systolic blood pressure, p < 0.001) and MMP-2 (p < 0.02) in the serum. TB reduces the AngII-stimulated expression levels of MMP2 (p < 0.05), MMP9 (p < 0.05), MMP12, and MMP14 in human aortic smooth muscle cells (HASMCs). Moreover, TB and valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, suppress AngII receptor type 1 (AT1R, p < 0.05) activation and increase the expression of acetyl histone H3 by HDAC activity inhibition (p < 0.05). Our findings suggest that TB exerts its protective effect by suppressing the activation of HDAC to attenuate the AngII-induced AT1R signaling cascade.

A systematic review and case presentation: Giant abdominal aortic aneurysm.

An abdominal aortic aneurysm is considered giant when its transverse diameter is greater than 10-13cm in diameter. A giant abdominal aortic aneurysm is rare but with a significant risk of rupture if it is not diagnosed or left untreated. The authors have performed a systematic review of the evidence that has looked into the clinical presentations, and management methods employed and have presented a 14cm giant abdominal aortic aneurysm patient. The systematic review has been based on level-IV evidence due to the rarity of the condition. The final analysis included 61 relevant reported cases. The mean age was 72.4years, the male to female ratio was 52: 8, and the average size of a giant abdominal aortic aneurysm was 14.7cm. These were mostly infra renal (72.58%). Rupture of these aneurysms was found in 23 (37.1%) patients, and was treated by laparotomy in 51 (82.25%) cases. There were 11 (17.74%) mortalities. The size of an abdominal aortic aneurysm is known to be the biggest factor in the rupture of an aneurysm. The reason abdominal aortic aneurysms can reach such size without rupturing is unclear but needs further exploring. Early diagnosis with effective screening programmes is essential to diagnose in a timely manner to avoid life-threatening consequences.

Abdominal aortic aneurysm monitoring via arterial waveform analysis: towards a convenient point-of-care device

Abdominal aortic aneurysms (AAAs) are lethal but treatable yet substantially under-diagnosed and under-monitored. Hence, new AAA monitoring devices that are convenient in use and cost are needed. Our hypothesis is that analysis of arterial waveforms, which could be obtained with such a device, can provide information about AAA size. We aim to initially test this hypothesis via tonometric waveforms. We study noninvasive carotid and femoral blood pressure (BP) waveforms and reference image-based maximal aortic diameter measurements from 50 AAA patients as well as the two noninvasive BP waveforms from these patients after endovascular repair (EVAR) and from 50 comparable control patients. We develop linear regression models for predicting the maximal aortic diameter from waveform or non-waveform features. We evaluate the models in out-of-training data in terms of predicting the maximal aortic diameter value and changes induced by EVAR. The best model includes the carotid area ratio (diastolic area divided by systolic area) and normalized carotid-femoral pulse transit time ((age·diastolic BP)/(height/PTT)) as input features with positive model coefficients. This model is explainable based on the early, negative wave reflection in AAA and the Moens-Korteweg equation for relating PTT to vessel diameter. The predicted maximal aortic diameters yield receiver operating characteristic area under the curves of 0.83 ± 0.04 in classifying AAA versus control patients and 0.72 ± 0.04 in classifying AAA patients before versus after EVAR. These results are significantly better than a baseline model excluding waveform features as input. Our findings could potentially translate to convenient devices that serve as an adjunct to imaging.

Effects of abdominal aortic aneurysm appropriateness dashboard on clinical practice

ObjectiveThe Society for Vascular Surgery published abdominal aortic aneurysm (AAA) practice guidelines in 2003, 2009, and 2018 to improve the management and treatment of AAAs. In 2014, our vascular surgery department implemented a quarterly AAA dashboard (AAAdb) to record the perioperative outcomes and guideline compliance with a focus on intervention appropriateness and procedural follow-up, which supplemented our Vascular Quality Initiative data. From the available reported evidence and expert consensus opinions, nine additional criteria for the appropriate treatment of AAAs <5 cm in women and <5.5 cm in men were noted, when applicable. The purpose of our study was to assess the effects of AAAdb implementation on adherence to society and institutional guidelines, documentation of treatment rationale, and the quality of follow-up. MethodsWe performed a retrospective review of elective open and endovascular AAA repair at a single institution from 2010 to 2018. The AAAdb was implemented in the middle of this period in 2014. The patient demographics, aortic size, repair indication, repair type, 30-day mortality, and postoperative and 1-year follow-up imaging findings were analyzed. The primary outcome was adherence to intervention appropriateness and the follow-up guidelines. The categorical factors were summarized using frequencies and percentages and compared using the Pearson χ2 test or Fisher exact test. Continuous measures were summarized using the mean ± standard deviation and compared between study periods using two-sample t tests. ResultsFrom 2010 to 2018, 1549 patients had undergone elective AAA repair: 657 before and 892 after AAAdb implementation. No differences were found in AAA size after AAAdb (5.6 ± 1.2 cm vs 5.6 ± 1.1 cm; P = .88). However, the proportion of size-appropriate repairs increased (64.1% vs 71.3%; P = .003). The proportion of small AAA repairs with a documented rationale had increased (64.4% vs 80.5%; P < .001), with rapid disease progression cited most often. No difference was found in 30-day mortality (1.2% vs 1.5%; P = .69). Follow-up imaging after endovascular abdominal aortic aneurysm repair increased at <60 days postoperatively (76% vs 84%; P = .004) and at 1 year of follow-up (78% vs 86%; P = .0005). The proportion of patients with endoleak at <60 days postoperatively had increased in the post-AAAdb cohort (21% vs 29%; P = .012). ConclusionsThe AAAdb served as a centerpiece for improving the appropriateness of care and compliance with national and institutional guidelines, including treatment of small AAAs in special circumstances. Its implementation was associated with higher quality follow-up and surveillance in a high-volume, regional aortic center. Consideration should be given to adding additional criteria to the Society for Vascular Surgery guidelines and Vascular Quality Initiative reporting.

S3427 Implicit Bias Contributing to Delayed Diagnosis in a Rare Case of Endoscopic Biopsy Proven Gastrointestinal Amyloidosis

Introduction: Gastrointestinal amyloidosis often requires extensive workup to diagnose, but early diagnosis and initiation of treatment improves mortality.1 Implicit bias leads to narrow workups which can misdiagnose rare diseases. We present a case of gastrointestinal amyloidosis ultimately diagnosed by endoscopic biopsy. The rarity of this disease as well as bias that led to anchoring on more common diagnoses resulted in months of misdiagnosis. Case Description/Methods: A 67 year old woman with a history of abdominal aortic aneurysm (AAA), substance use disorder in remission, and chronic malnutrition presented with worsening of chronic abdominal pain. Workup over the course of eight prior ED visits for abdominal pain was unremarkable. Her pain was attributed to functional pain or opioid use and withdrawal despite a lack of documented opioid relapse. On this presentation, expanding AAA size prompted surgical consult. The surgical team expressed concern that she would not tolerate an open repair with a BMI of 13.9; TPN was started. GI recommended endoscopy to assess for a malabsorptive process. Unfortunately the procedure was delayed 22 days as the patient felt her uncontrolled pain was not validated by the care team. After many care conferences, she agreed to upper endoscopy which showed flattening of the villi of the duodenum. Microscopic testing from biopsies showed extensive amyloidosis (Figure). Amyloidosis resulting in intestinal ischemia was thought to be the cause of her pain and malnutrition. Discussion: Implicit bias associated with the patient’s history of addiction led to anchoring bias and initial narrow workup and misdiagnosis. Implicit bias amongst physicians regarding substance use disorders has been associated with suboptimal care.2 The severity of the patient’s abdominal pain and malnutrition should have prompted earlier referral to GI and may have led to expedited diagnosis of intestinal amyloidosis. Additionally, the frequent misdiagnosis and dismissal of symptoms resulted in mistrust leading the patient to decline further workup. Recognizing implicit bias can allow clinicians to provide more equitable workup and care.Figure 1.: DUODENUM, BIOPSY Amyloidosis, extensive, involving mucosa and submucosa, perivascular and diffuse.

Relationship between the Levels of Calprotectin and Soluble Receptor for Advanced Glycation End Products with Abdominal Aortic Aneurysm Diameter: A Preliminary Clinical Trial.

An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta greater than 50% of the diameter of a healthy aorta. Previous experimental studies confirm the effect of calprotectin (CAL) on the onset of arterial pathology. It has been suggested that low levels of soluble receptors for advanced glycation end products (RAGEs) increase levels of cytokines that lead to the inhibition of matrix metalloproteinases (MMPs), affecting AAA formation. This study aimed to analyze the correlation of levels of RAGE and CAL with AAA diameter. A group of 32 patients aged 50–75 with diagnosed AAA was enrolled in the study. This group of patients was further divided into three subgroups based on AAA diameter: (1) <4.5 cm, (2) 4.5–5.5 cm, (3) >5.5 cm. Peripheral blood was drawn from all participants on admission to measure the serum CAL and RAGE levels. An enumeration survey was performed three months after AAA surgical treatment. CAL and RAGE plasma levels were measured with the enzyme-linked immunosorbent assay (ELISA). The median CAL levels were 2273.0 ng/mL before and 1217.0 ng/mL after treatment. There was a statistically significant decrease in CAL levels following the surgical treatment (p = 0.003). The correlation analysis between CAL levels and RAGE levels before and after surgical treatment showed no statistically significant correlations. In addition, there were no statistically significant correlations between CAL and RAGE levels with AAA size. In conclusion, CAL levels appear to be a significant marker in patients with AAA. There is an almost twofold decrease in CAL levels after AAA excision.

Genetic and Pharmacological Disruption of Interleukin-1α Leads to Augmented Murine Aortic Aneurysm

Interleukin-1 (IL-1) signaling has an established role as a cytokine signaling pathway important for progression of abdominal aortic aneurysms (AAAs). While the IL-1β ligand and IL-1R1 have been previously investigated, the role of the IL-1α ligand in AAAs remains unknown. In this study, we sought to examine the role of IL-1α in AAAs using genetic and pharmacologic approaches. Eight-week-old wild-type (WT) or IL-1α knock-out (KO) male and female mice (n=10-16/group) underwent experimental AAA and were harvested 14days following surgery to assess AAA size and characteristics. In separate studies, 8-week-old WT mice were treated with an inhibitor to IL-1α during AAA formation and harvested 14days following surgery. Finally, WT and IL-1α KO mice were administered Anakinra, an IL-R1 inhibitor, during AAA formation to determine the effect of inhibiting IL-1R1 when IL-1α is knocked out. Male and female IL-1α KO mice had larger AAAs compared to WT AAAs (male: 153% vs. 89.2%, P=0.0001; female: 86.6% vs. 63.5%, P=0.02). IL-1α KO mice had greater elastin breakage (P=0.01), increased levels of macrophage staining (P=0.0045), and greater pro-metallo proteinase 2 (P=0.02). Pharmacologic inhibition of WT male mice with an IL-1α neutralizing antibody resulted in larger AAAs (133.1% vs. 77.0%, P<0.001). Finally, treatment of IL-1α KO male mice with Anakinra decreased AAA formation compared with vehicle control AAAs (Anakinra+IL-1α KO: 47.7% vs. WT: 147.1%; P=0.0001). IL-1α disruption using either genetic or pharmacologic approaches worsens AAAs.

“Large Diameter” Aortic Endografts are Associated With Aneurysm Sac Expansion

The purpose of this study was to evaluate the association between aortic endograft diameter and long-term outcomes following endovascular aneurysm repair (EVAR) performed in accordance with manufacturer instructions for use (IFU). A retrospective review of consecutive patients undergoing on-IFU EVAR (2000-2018) was performed to facilitate a comparative analysis of long-term patient outcomes based on device diameter. "Large diameter" devices were defined as >34mm. The primary outcome of interest was freedom from sac expansion throughout long-term follow-up. Analyses included standard bivariate analyses, Kaplan-Meier with log-rank comparison, and Cox proportional hazards multivariate analysis. A total of 1,099 underwent on-IFU EVAR from 2000-2018. Follow-up data were available for 980 patients. Of these, 75 patients (7.6%) were treated with >34-mm devices. There were no significant differences in demographics or comorbidities between the 2 groups, although preoperative abdominal aortic aneurysm size was greater in patients undergoing implantation of >34-mm devices (58±8.5mm vs. 56±17.4mm; P=0.05). Median follow-up was 10.3years. Patients with grafts >34mm had reduced freedom from sac expansion throughout follow-up (P=0.038). There were no significant differences in reintervention rates, open conversion, or rupture when stratified by graft diameter. A multivariate Cox regression identified patient age, preoperative abdominal aortic aneurysm size, need for reintervention, and use of >34-mm endografts as independent factors associated with expansion. The use of large diameter aortic endografts is associated with higher rates of sac expansion during long-term follow-up. Although there is undoubtedly a role for large diameter graft use in selected patients, it is important to recognize that these devices were typically approved post hoc without the same regulatory scrutiny of smaller endografts. These findings underscore the importance of ongoing surveillance for patients treated with >34-mm grafts, irrespective of compliance with manufacturer IFU.

Abstract 298: Ketosis Prevents Abdominal Aortic Aneurysm Progression And Rupture In Male Rats

Abdominal aortic aneurysms (AAA) are common in aging populations, and its rupture is associated with high mortality. There is no effective medical therapy for the prevention of AAA expansion and rupture. Ketone bodies (KB) are argued to produce novel responses against injury. Serum KB are elevated through a ketogenic diet (KD) or the intake of exogenous KB (EKB). We hypothesize that ketosis can reduce AAA expansion and risk of rupture. Male Sprague-Dawley rats underwent intraluminal exposure to porcine pancreatic elastase (PPE) to induce AAA formation. Rats were also administered daily β-aminopropionitrile (BAPN) to promote AAA rupture. Control rats (N=12) were fed a standard diet (SD). Treated rats were given either a KD (N=9) or EKB (N=10) starting 3 days post AAA induction. Ketosis was verified by blood BHB level &gt;0.5mmol/L. In vivo aortic diameter was evaluated by USG. After 2 weeks, survival animals were harvested, and AAA tissue analysis was performed. Rupture AAA was determined by necropsy. Rats treated with KD consistently remained in ketosis, while rats treated with EKB remained in ketosis for only 8-hour per day. AAA size was significantly reduced (p&lt;0.01 and p&lt;0.05) in both, KD and EKB groups at week 1 and 2 respectively. Rupture rate was also reduced in the KD and EKB groups (22% and 40%, respectively) compared to 67% in the SD group (p=0.03 and 0.12, respectively). AAA trichrome staining demonstrated greater content of collagen in KD and EKB groups when compared to SD group (p=0.08 and 0.02, respectively). AAA gelatin zymography demonstrated significantly decreased active MMP 9 levels in KD and EKB groups (p&lt;0.05) while total MMP 2 was attenuated in the KD group (p&lt;0.01). Ketosis appears to reduce AAA expansion and risk of rupture. This may have resulted from AAA increased collagen deposition as well as decreased MMP activity. These findings provide initial impetus to investigate whether ketosis in patients with small AAAs can prevent expansion and risk of rupture.

Understanding who benefits from endovascular aortic repair in those deemed unfit for open repair

IntroductionPatients with abdominal aortic aneurysms (AAAs) who are deemed unacceptable candidates for open repair (UNFIT) pose a clinical challenge. The EVAR2 Trial randomized UNFIT patients to endovascular aortic repair (EVAR) vs no intervention from 1999 to 2003, concluding that survival was not improved by EVAR. However, outcomes after EVAR over the last 2 decades have dramatically changed. Thus, the purpose of this study was to evaluate outcomes after EVAR in UNFIT patients using more contemporary data and to determine which subsets of UNFIT patients may potentially benefit from EVAR. MethodsThe Vascular Quality Initiative database (2003-2020) was used to identify elective EVARs for AAAs. Patients were categorized as UNFIT or suitable (SUITABLE) for open repair by the operative surgeon. Predicted 1-year mortality of untreated AAAs was calculated via a modified Gagne Index adjusted for AAA size. The primary outcome for the study was 30-day mortality. Secondary outcomes included perioperative major adverse cardiac events (a composite of clinically significant arrhythmia, congestive heart failure, and myocardial infarction), length of stay, and 1-year mortality. ResultsA total of 31,471 patients met study criteria with 27,036 (85.9%) deemed SUITABLE and 4435 (14.1%) UNFIT. UNFIT patients were more likely to experience a perioperative major adverse cardiac event (5.1% vs 2.2%, P < .001) and had longer lengths of stay (1 day [interquartile range, 1-3 days] vs 1 day [interquartile range, 1-2 days], P < .001). The 30-day mortality was significantly higher for UNFIT patients (0.8% vs 0.4%, P < .001). UNFIT patients had worse 1-year survival compared with SUITABLE patients. However, UNFIT and SUITABLE patients had significantly improved actual 1-year mortality with EVAR compared with predicted 1-year mortality without EVAR: 9.5% vs 15.6% (P < .001) and 4.0% vs 11.7% (P < .001), respectively. The mortality benefit after EVAR in UNFIT patients was primarily restricted to those with smaller Gagne Indices and larger aneurysm diameters. Patients deemed unsuitable for open repair due to frailty or multiple reasons had significantly higher 30-day mortality rates after EVAR when compared with SUITABLE patients (1.3% vs 1.6% vs 0.4%, P < .001). Those deemed unsuitable for open repair due to frailty or multiple reasons had worse 1-year cumulative survival compared with all other UNFIT patients. ConclusionsDespite being high risk with higher perioperative morbidity and mortality, UNFIT patients have lower actual 1-year mortality with EVAR than predicted 1-year mortality without EVAR. However, this potential benefit is reserved to those with small Gagne Indices, larger AAA diameters, and lack of frailty.

Pharmacological Inhibition of Factor XIIa Attenuates Abdominal Aortic Aneurysm, Reduces Atherosclerosis, and Stabilizes Atherosclerotic Plaques.

Background 3F7 is a monoclonal antibody targeting the enzymatic pocket of activated factor XII (FXIIa), thereby inhibiting its catalytic activity. Given the emerging role of FXIIa in promoting thromboinflammation, along with its apparent redundancy for hemostasis, the selective inhibition of FXIIa represents a novel and highly attractive approach targeting pathogenic processes that cause thromboinflammation-driven cardiovascular diseases. Methods The effects of FXIIa inhibition were investigated using three distinct mouse models of cardiovascular disease—angiotensin II-induced abdominal aortic aneurysm (AAA), an ApoE −/− model of atherosclerosis, and a tandem stenosis model of atherosclerotic plaque instability. 3F7 or its isotype control, BM4, was administered to mice (10 mg/kg) on alternate days for 4 to 8 weeks, depending on the experimental model. Mice were examined for the development and size of AAAs, or the burden and instability of atherosclerosis and associated markers of inflammation. Results Inhibition of FXIIa resulted in a reduced incidence of larger AAAs, with less acute aortic ruptures and an associated fibro-protective phenotype. FXIIa inhibition also decreased stable atherosclerotic plaque burden and achieved plaque stabilization associated with increased deposition of fibrous structures, a >2-fold thicker fibrous cap, increased cap-to-core ratio, and reduction in localized and systemic inflammatory markers. Conclusion Inhibition of FXIIa attenuates disease severity across three mouse models of thromboinflammation-driven cardiovascular diseases. Specifically, the FXIIa-inhibiting monoclonal antibody 3F7 reduces AAA severity, inhibits the development of atherosclerosis, and stabilizes vulnerable plaques. Ultimately, clinical trials in patients with cardiovascular diseases such as AAA and atherosclerosis are warranted to demonstrate the therapeutic potential of FXIIa inhibition.