Search

Aims: Abdominal aortic aneurysm (AAA) represents a life-threatening condition characterized by medial layer degeneration of the abdominal aorta. Nevertheless, knowledge regarding changes in regulators associated with aortic status remains incomplete. A thorough understanding of cell types and signalling pathways involved in the development and progression of AAAs is essential for the development of medical therapy., Methods and Results: We harvested specimens of the abdominal aorta with different pathological features in Angiotensin II (AngII)-infused ApoE-/- mice, conducted scRNA-seq, and identified a unique population of interferon-inducible monocytes/macrophages (IFNICs), which were amply found in the AAAs. Gene set variation analysis revealed that activation of the cytosolic DNA sensing cGAS-STING and JAK-STAT pathways promoted the secretion of type I interferons in monocytes/macrophages and differentiated them into IFNICs. We generated myeloid cell-specific deletion of Sting1 (Lyz2-Cre+/-; Sting1flox/flox) mice and performed bone marrow transplantation and found that myeloid cell-specific deletion of Sting1 or Ifnar1 significantly reduced the incidence of AAA, aortic rupture rate, and diameter of the abdominal aorta. Mechanistically, the activated pyroptosis- and inflammation-related signalling pathways, regulated by IRF7 in IFNICs, play critical roles in the developing AAAs., Conclusion: IFNICs are a unique monocyte/macrophage subset implicated in the development of AAAs and aortic rupture., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Objective: Whether angiotensin II blockade is an effective medical treatment for abdominal aortic aneurysms (AAAs) has not been established. This systematic review and meta-analysis aimed to determine the association between angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) prescription and AAA growth and events., Data Sources: MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library databases were searched from their inception to 4 January 2024, with no language restrictions., Review Methods: The five databases were searched for randomised controlled trials (RCTs) and observational studies reporting the association between ACEi or ARB prescription and AAA growth, repair, or rupture. The primary outcome was AAA growth, with secondary outcomes of AAA rupture, AAA repair, and AAA related events (rupture and repair combined). Risk of bias was assessed using the Risk of Bias 2 tool for RCTs and with a modified Newcastle-Ottawa scale for observational studies. Certainty of evidence was assessed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE). Random effects models were used for meta-analyses., Results: Eleven studies (two RCTs, eight observational studies, and one meta-analysis of individual patient data from seven populations) involving 58 022 patients were included. ACEi prescription was not associated with a statistically significant reduction in AAA growth (standard mean difference 0.01 mm/year, 95% confidence interval [CI] -0.26 - 0.28; p = .93; I 2  = 98%) or AAA repair (odds ratio [OR] 0.73, 95% CI 0.50 - 1.09; p = .65; I 2  = 61%), but was associated with a statistically significantly lower risk of AAA rupture (OR 0.87, 95% CI 0.81 - 0.93; p < .001; I 2  = 26%) and AAA related events (OR 0.82, 95% CI 0.72 - 0.95; p = .006; I 2  = 80%). ARB prescription was not associated with significantly reduced AAA growth or a lower risk of AAA related events. The two RCTs had a low risk of bias, with one observational study having low, seven moderate, and one high risk of bias. All of the findings had a very low certainty of evidence based on the GRADE analysis., Conclusion: There was no association between ACEi or ARB prescription and AAA growth, but ACEi prescription was associated with a reduced risk of AAA rupture and AAA related events with very low certainty of evidence., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Clinical Problem: Most abdominal aortic aneurysms (AAAs) are small with low rupture risk (<1%/y) when diagnosed but slowly expand to ≥55 mm and undergo surgical repair. Patients and clinicians require medications to limit AAA growth and rupture, but drugs effective in animal models have not translated to patients., Recommendations for Increasing Translation From Mouse Models: Use models that simulate human AAA tissue pathology, growth patterns, and rupture; focus on the clinically relevant outcomes of growth and rupture; design studies with the rigor required of human clinical trials; monitor AAA growth using reproducible ultrasound; and perform studies in both males and females., Summary of Strengths and Weaknesses of Mouse Models: The aortic adventitial elastase oral β-aminopropionitrile model has many strengths including simulating human AAA pathology and modeling prolonged aneurysm growth. The Ang II (angiotensin II) model performed less well as it better simulates acute aortic syndrome than AAA. The elastase plus TGFβ (transforming growth factor-β) blocking antibody model displays a high rupture rate, making prolonged monitoring of AAA growth not feasible. The elastase perfusion and calcium chloride models both display limited AAA growth., Competing Interests: Disclosures None.

Background: β-aminopropionitrile (BAPN) is a pharmacological inhibitor of LOX (lysyl oxidase) and LOXLs (LOX-like proteins). Administration of BAPN promotes aortopathies, although there is a paucity of data on experimental conditions to generate pathology. The objective of this study was to define experimental parameters and determine whether equivalent or variable aortopathies were generated throughout the aortic tree during BAPN administration in mice., Methods: BAPN was administered in drinking water for a period ranging from 1 to 12 weeks. The impacts of BAPN were first assessed with regard to BAPN dose, and mouse strain, age, and sex. BAPN-induced aortic pathological characterization was conducted using histology and immunostaining. To investigate the mechanistic basis of regional heterogeneity, the ascending and descending thoracic aortas were harvested after 1 week of BAPN administration before the appearance of overt pathology., Results: BAPN-induced aortic rupture predominantly occurred or originated in the descending thoracic aorta in young C57BL/6J or N mice. No apparent differences were found between male and female mice. For mice surviving 12 weeks of BAPN administration, profound dilatation was consistently observed in the ascending region, while there were more heterogeneous changes in the descending thoracic region. Pathological features were distinct between the ascending and descending thoracic regions. Aortic pathology in the ascending region was characterized by luminal dilatation and elastic fiber disruption throughout the media. The descending thoracic region frequently had dissections with false lumen formation, collagen deposition, and remodeling of the wall surrounding the false lumen. Cells surrounding the false lumen were predominantly positive for α-SMA (α-smooth muscle actin). One week of BAPN administration compromised contractile properties in both regions equivalently, and RNA sequencing did not show obvious differences between the 2 aortic regions in smooth muscle cell markers, cell proliferation markers, and extracellular components., Conclusions: BAPN-induced pathologies show distinct, heterogeneous features within and between ascending and descending aortic regions in mice., Competing Interests: Disclosures None.

Background: The 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., Methods: We 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., Results: The 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., Conclusions: The 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., (Copyright © 2024 Society for Vascular Surgery. All rights reserved.)

Objective: Large abdominal aortic aneurysms (AAAs) present a significant mortality risk. While numerous medical interventions have been proposed, no drugs have convincingly reduced AAA progression, rupture rates, or repair risk. This systematic review and meta-analysis aimed to assess the impact of re-purposed drugs or dietary supplements on slowing expansion rates, reducing the risk of rupture, or minimising the risk of repair for individuals with AAA., Methods: A systematic search was conducted in five databases. Both observational studies and randomised controlled trials were included. Unpublished data from two screening trials were incorporated. Risk of bias was assessed using the Newcastle-Ottawa scale and revised Cochrane risk of bias tool. Meta-analyses were performed for each identified drug subclass and were stratified by overall risk of bias. Results were reported following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines., Results: Of 7 484 screened studies, 39 met the inclusion criteria. No studies on dietary supplements were included. A total of 84 cohorts were derived from the included studies, and twelve distinct drug groups underwent meta-analyses. Two drug groups, metformin and statins, were statistically significant in slowing AAA growth. No low risk of bias studies were included for these two drug groups, and the results had very high heterogeneity (I 2 > 80%). Both groups had a GRADE certainty of very low. Metformin, excluding high risk of bias studies, presented an estimated mean growth difference of AAA diameter between users and non-users of -0.73 mm/year, whilst statins had an overall estimated mean difference of -0.84 mm/year., Conclusion: This systematic review and meta-analysis suggests that metformin and statins may provide some effect in slowing AAA progression. However, no definitive evidence was found for any of the investigated drugs included in this study. Further research is needed to identify effective medical treatments for AAA progression with more robust methodology., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Objectives: For a long time, the association of the false lumen status and the outcomes of patients suffering from aortic dissection has been unclear, so this review article aims to study whether the unobstructed of the false lumen is related to the outcome of patients suffering from aortic dissection., Methods: We performed this systematic review and meta-analysis according to the Preferred Reporting Items for Systematic Reviews and Meta Analyzes Protocols (PRISMA) statement 2009 and registered with PROSPERO (CRD42022381869). We searched PubMed, the Cochrane library, Web of Science and Embase to collect potential studies. The Newcastle-Ottawa Scale was used to assess the quality of the included studies. The main outcome is long-term survival. Data included in the study were summarized using the risk ratio or mean difference and 95% confidence interval., Results: There were 16 trials, 2829 patients in total, with a mean age of 62.1 years. Compared with completely thrombosed false lumen, patent group has better long-term survival (risk ratio (RR), 0.88; 95% CI, 0.79 to 0.97; p = 0.01; I2 = 58%) and smaller yearly aortic growth rate (mean difference (MD), 1.03; 95% CI, 0.23 to 1.82; p = 0.01; I2 = 98%). In addition, patients with a patent false lumen had a lower risk of aortic event (RR, 0.81; 95% CI, 0.68 to 0.97; p = 0.02; I2 = 37%), but higher risk of aortic rupture (RR, 7.02; 95% CI, 2.55 to 19.3; p = 0.0002; I2 = 0) and hospital death (RR, 2.72; 95% CI, 1.45 to 5.08; p = 0.002; I2 = 0)., Conclusion: Completely thrombosed of the false lumen is more beneficial to the long-term survival of patients with aortic dissection. And the risk of aortic rupture and hospital death in patients with patent false lumen is 7 times and 3 times that of patients with complete thrombosed false lumen. It is expected to provide individualized medical care for different types of patients according to different false lumen status to minimize death and related complications.

Abdominal aortic aneurysm (AAA) is a severe vascular disease and a major public health issue with an unmet medical need for therapy. This disease is featured by a progressive dilation of the abdominal aorta, boosted by atherosclerosis, ageing, and smoking as major risk factors. Aneurysm growth increases the risk of aortic rupture, a life-threatening emergency with high mortality rates. Despite the increasing progress in our knowledge about the etiopathology of AAA, an effective pharmacological treatment against this disorder remains elusive and surgical repair is still the unique available therapeutic approach for high-risk patients. Meanwhile, there is no medical alternative for patients with small aneurysms but close surveillance. Clinical trials assessing the efficacy of antihypertensive agents, statins, doxycycline, or anti-platelet drugs, among others, failed to demonstrate a clear benefit limiting AAA growth, while data from ongoing clinical trials addressing the benefit of metformin on aneurysm progression are eagerly awaited. Recent preclinical studies have postulated new therapeutic targets and pharmacological strategies paving the way for the implementation of future clinical studies exploring these novel therapeutic strategies. This review summarises some of the most relevant clinical and preclinical studies in search of new therapeutic approaches for AAA., (© 2023 The Author(s).)

Background: Thoracic aortic aneurysms (TAAs) are abnormal aortic dilatations and a major cardiovascular complication of Marfan syndrome. We previously demonstrated a critical role for vascular smooth muscle (VSM) SirT1 (sirtuin-1), a lysine deacetylase, against maladaptive aortic remodeling associated with chronic oxidative stress and aberrant activation of MMPs (matrix metalloproteinases)., Methods: In this study, we investigated whether redox dysregulation of SirT1 contributed to the pathogenesis of TAA using fibrillin-1 hypomorphic mice (Fbn1 mgR/mgR ), an established model of Marfan syndrome prone to aortic dissection/rupture., Results: Oxidative stress markers 3-nitrotyrosine and 4-hydroxynonenal were significantly elevated in aortas of patients with Marfan syndrome. Moreover, reversible oxidative post-translational modifications (rOPTM) of protein cysteines, particularly S-glutathionylation, were dramatically increased in aortas of Fbn1 mgR/mgR mice, before induction of severe oxidative stress markers. Fbn1 mgR/mgR aortas and VSM cells exhibited an increase in rOPTM of SirT1, coinciding with the upregulation of acetylated proteins, an index of decreased SirT1 activity, and increased MMP2/9 activity. Mechanistically, we demonstrated that TGFβ (transforming growth factor beta), which was increased in Fbn1 mgR/mgR aortas, stimulated rOPTM of SirT1, decreasing its deacetylase activity in VSM cells. VSM cell-specific deletion of SirT1 in Fbn1 mgR/mgR mice (SMKO-Fbn1 mgR/mgR ) caused a dramatic increase in aortic MMP2 expression and worsened TAA progression, leading to aortic rupture in 50% of SMKO-Fbn1 mgR/mgR mice, compared with 25% of Fbn1 mgR/mgR mice. rOPTM of SirT1, rOPTM-mediated inhibition of SirT1 activity, and increased MMP2/9 activity were all exacerbated by the deletion of Glrx (glutaredoxin-1), a specific deglutathionylation enzyme, while being corrected by overexpression of Glrx or of an oxidation-resistant SirT1 mutant in VSM cells., Conclusions: Our novel findings strongly suggest a causal role of S-glutathionylation of SirT1 in the pathogenesis of TAA. Prevention or reversal of SirT1 rOPTM may be a novel therapeutic strategy to prevent TAA and TAA dissection/ruptures in individuals with Marfan syndrome, for which, thus far, no targeted therapy has been developed., Competing Interests: Disclosures None.

Background The best medical therapy to control hypertension following abdominal aortic aneurysm repair is yet to be determined. We therefore examined whether treatment with renin-angiotensin-aldosterone system inhibitors (RAASIs) versus beta blockers influenced postoperative and 1-year clinical end points following abdominal aortic aneurysm repair in a Medicare-linked database. Methods and Results All patients with hypertension undergoing endovascular aneurysm repair and open aneurysm repair in the Vascular Quality Initiative Vascular Implant Surveillance and Interventional Outcomes Network database between 2003 and 2018 were included. Patients were divided into 2 groups based on their preoperative and discharge medications, either RAASIs or beta blockers. Our cohort included 8789 patients, of whom 3523 (40.1%) were on RAASIs, and 5266 (59.9%) were on beta blockers. After propensity score matching, there were 3053 matched pairs of patients in each group. After matching, RAASI use was associated with lower risk of postoperative mortality (odds ratio [OR], 0.3 [95% CI, 0.1-0.6]), myocardial infarction (OR, 0.1 [95% CI, 0.03-0.6]), and nonhome discharge (OR, 0.6 [95% CI, 0.5-0.7]). Before propensity score matching, RAASI use was associated with lower 1-year mortality (hazard ratio [HR], 0.4 [95% CI, 0.4-0.5]) and lower risk of aneurysmal rupture (HR, 0.7 [95% CI, 0.5-0.9]). These results persisted after propensity score matching for mortality (HR, 0.4 [95% CI, 0.4-0.5]) and aneurysmal rupture (HR, 0.7 [95% CI, 0.5-0.9]). Conclusions In this large contemporary retrospective cohort study, RAASI use was associated with favorable postoperative outcomes compared with beta blockers. It was also associated with lower mortality and aneurysmal rupture at 1 year of follow-up.

Background The biological mechanism of action for osteoprotegerin, a soluble decoy receptor for the receptor activator of nuclear factor-kappa B ligand in the vascular structure, has not been elucidated. The study aim was to determine if osteoprotegerin affects aortic structural integrity in angiotensin II (Ang II)-induced hypertension. Methods and Results Mortality was higher ( P <0.0001 by log-rank test) in 8-week-old male homozygotes of osteoprotegerin gene-knockout mice given subcutaneous administration of Ang II for 28 days, with an incidence of 21% fatal aortic rupture and 23% aortic dissection, than in age-matched wild-type mice. Ang II-infused aorta of wild-type mice showed that osteoprotegerin immunoreactivity was present with proteoglycan. The absence of osteoprotegerin was associated with decreased medial and adventitial thickness and increased numbers of elastin breaks as well as with increased periostin expression and soluble receptor activator of nuclear factor-kappa B ligand concentrations. PEGylated human recombinant osteoprotegerin administration decreased all-cause mortality ( P <0.001 by log-rank test), the incidence of fatal aortic rupture ( P =0.08), and aortic dissection ( P <0.001) with decreasing numbers of elastin breaks, periostin expressions, and soluble receptor activator of nuclear factor-kappa B ligand concentrations in Ang II-infused osteoprotegerin gene-knockout mice. Conclusions These data suggest that osteoprotegerin protects against aortic rupture and dissection in Ang II-induced hypertension by inhibiting receptor activator of nuclear factor-kappa B ligand activity and periostin expression.

Purpose of Review: Abdominal aortic aneurysms (AAA) can carry extremely high mortality rates and most will only present with symptoms with impending rupture. We present an overview of management of this disease process starting with screening, to medical management, surveillance and treatment options currently available, as well as those being studied for future use., Recent Findings: Screening has been proven to reduce the mortality rate. There still remains a paucity of data to support medical therapies to help mitigate the rate of aneurysm growth and prevent rupture. However, on the topic of repair, there have been advancements in endovascular devices which have broadened the scope of treatment for patients with anatomy not amenable to standard endovascular repair or those who are not suitable candidates for open surgical repair. Appropriate surveillance, risk factor modification, and operative repair, when indicated, are the cornerstones of contemporary management of AAAs. Advancements in endovascular technologies have allowed us to treat more patients. Further research is warranted on non-operative medical therapies., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: The goal of this study was to determine whether boosting mitochondrial respiration prevents the development of fatal aortic ruptures triggered by atherosclerosis and hypertension., Methods: Ang-II (angiotensin-II) was infused in ApoE (Apolipoprotein E)-deficient mice fed with a western diet to induce acute aortic aneurysms and lethal ruptures., Results: We found decreased mitochondrial respiration and mitochondrial proteins in vascular smooth muscle cells from murine and human aortic aneurysms. Boosting NAD levels with nicotinamide riboside reduced the development of aortic aneurysms and sudden death by aortic ruptures., Conclusions: Targetable vascular metabolism is a new clinical strategy to prevent fatal aortic ruptures and sudden death in patients with aortic aneurysms.

Vascular Ehlers-Danlos syndrome is a rare inherited disorder caused by genetic variants in type III collagen. Its prognosis is especially hampered by unpredictable arterial ruptures and there is no therapeutic consensus. We created a knock-in Col3a1+/G182R mouse model and performed a complete genetic, molecular and biochemical characterization. Several therapeutic strategies were also tested. Col3a1+/G182R mice showed a spontaneous mortality caused by thoracic aortic rupture that recapitulates the vascular Ehlers-Danlos syndrome with a lower survival rate in males, thin non-inflammatory arteries and an altered arterial collagen. Transcriptomic analysis of aortas showed upregulation of genes related to inflammation and cell stress response. Compared to water, survival rate of Col3a1+/G182R mice was not affected by beta-blockers (propranolol or celiprolol). Two other vasodilating anti-hypertensive agents (hydralazine, amlodipine) gave opposite results on aortic rupture and mortality rate. There was a spectacular beneficial effect of losartan, reversed by the cessation of its administration, and a marked deleterious effect of exogenous angiotensin II. These results suggest that blockade of the renin angiotensin system should be tested as a first-line medical therapy in patients with vascular Ehlers-Danlos syndrome., Competing Interests: The authors have declared that no competing interests exist.

Aortic dissection and rupture are triggered by decreased vascular wall strength and/or increased mechanical loads. We investigated the role of mTOR signaling in aortopathy using a well-described model of angiotensin II-induced dissection, aneurysm, or rupture of the suprarenal abdominal aorta in Apoe-deficient mice. Although not widely appreciated, nonlethal hemorrhagic lesions present as pseudoaneurysms without significant dissection in this model. Angiotensin II-induced aortic tears result in free rupture, contained rupture with subadventitial hematoma (forming pseudoaneurysms), dilatation, or healing, while the media invariably thickens regardless of mural tears. Medial thickening results from smooth muscle cell hypertrophy and extracellular matrix accumulation, including matricellular proteins. Angiotensin II activates mTOR signaling in vascular wall cells, and inhibition of mTOR signaling by rapamycin prevents aortic rupture but promotes dissection. Decreased aortic rupture correlates with decreased inflammation and metalloproteinase expression, whereas extensive dissection correlates with induction of matricellular proteins that modulate adhesion of vascular cells. Thus, mTOR activation in vascular wall cells determines whether aortic tears progress to dissection or rupture. Previous mechanistic studies of aortic aneurysm and dissection by angiotensin II in Apoe-deficient mice should be reinterpreted as clinically relevant to pseudoaneurysms, and mTOR inhibition for aortic disease should be explored with caution.

Objective: Contemporary data on the natural history of large abdominal aortic aneurysms (AAAs) in patients undergoing delayed or no repair are lacking. In this study, we examine the impact of large AAA size on the incidence of rupture and mortality., Methods: From a prospectively maintained aneurysm surveillance registry, patients with an unrepaired, large AAA (≥5.5 cm in men and ≥5.0 cm in women) at baseline (ie, index imaging) or who progressed to a large size from 2003 to 2017 were included, with follow-up through March 2020. Outcomes of interest obtained by manual chart review included rupture (confirmed by imaging/autopsy), probable rupture (timing/findings consistent with rupture without more likely cause of death), repair, reasons for either no or delayed (>1 year after diagnosis of large AAA) repair and total mortality. Cumulative incidence of rupture was calculated using a nonparametric cumulative incidence function, accounting for the competing events of death and aneurysm repair and was stratified by patient sex., Results: Of the 3248 eligible patients (mean age, 83.6 ± 9.1 years; 71.2% male; 78.1% white; and 32.0% current smokers), 1423 (43.8%) had large AAAs at index imaging, and 1825 progressed to large AAAs during the follow-up period, with a mean time to qualifying size of 4.3 ± 3.4 years. In total, 2215 (68%) patients underwent repair, of which 332 were delayed >1 year; 1033 (32%) did not undergo repair. The most common reasons for delayed repair were discrepancy in AAA measurement between surgeon and radiologist (34%) and comorbidity (20%), whereas the most common reasons for no repair were patient preference (48%) and comorbidity (30%). Among patients with delayed repair (mean time to repair, 2.6 ± 1.8 years), nine (2.7%) developed symptomatic aneurysms, and an additional 11 (3.3%) ruptured. Of patients with no repair, 94 (9.1%) ruptured. The 3-year cumulative incidence of rupture was 3.4% for initial AAA size 5.0 to 5.4 cm (women only), 2.2% for 5.5 to 6.0 cm, 6.0% for 6.1 to 7.0 cm, and 18.4% for >7.0 cm. Women with AAA size 6.1 to 7.0 cm had a 3-year cumulative incidence of rupture of 12.8% (95% confidence interval, 7.5%-19.6%) compared with 4.5% (95% confidence interval, 3.0%-6.5%) in men (P = .002)., Conclusions: In this large cohort of AAA registry patients over 17 years, annual rupture rates for large AAAs were lower than previously reported, with possible increased risk in women. Further analyses are ongoing to identify those at increased risk for aneurysm rupture and may provide targeted surveillance regimens and improve patient counseling., (Copyright © 2021 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Objective: To evaluate the efficacy of thoracic endovascular aortic repair (TEVAR) in the treatment of patients with complicated type B aortic intramural haematoma (IMH)., Methods: A retrospective observational study of patients treated between January 2002 and December 2017 was performed. Complicated type B IMH was defined as persistent pain, rapid dilatation, presence of ulcer-like projections (ULPs), haemothorax, and other signs of (impending) rupture. Thirty day results and long term follow up outcomes were reported., Results: Thirty-nine patients were included for analysis (mean age 68 ± 8 years, 36% male). The thirty day mortality rate was 5%, stroke rate 10%, and re-intervention rate 3%. The median follow up duration was 49 months (25th - 75th percentile: 2 - 96 months). At 10 years, estimated freedom from all cause mortality was 66 ± 9%. During follow up, nine re-interventions were performed, leading to a 10 year estimated freedom from re-intervention rate of 72 ± 8%. Estimated freedom from aortic growth at 10 years was 85 ± 9%., Conclusion: Complicated type B IMH can be treated effectively by TEVAR, thus preventing death from aortic rupture. However, severe early post-operative complications, most importantly stroke, are of concern. Long term outcomes are excellent, although re-interventions are not uncommon, either for progression of proximal or distal aortic disease or due to stent graft related complications., Competing Interests: Conflict of interest statement and funding None., (Copyright © 2021. Published by Elsevier B.V.)

Objectives: This study aimed to construct a risk prediction model for distal aortic enlargement in patients with type B aortic dissection (TBAD) treated with proximal thoracic endovascular aortic repair (TEVAR)., Methods: From June 2010 to June 2016, patients with TBAD who underwent proximal TEVAR were retrospectively analyzed. A total of 38 clinical and imaging variables were collected. Univariable logistic regression was conducted to explore potential risk factors associated with distal aortic enlargement. Elastic net regression was employed to select significantly influential variables. Then, machine learning algorithms (logistic regression (LR), artificial neutral network (ANN), random forest and support vector machine) were applied to build risk prediction models. The area under the receiver operating characteristic curve (AUC), sensitivity and specificity were used to evaluate the performance of these models., Results: A total of 503 patients were enrolled in this study. During the follow-up, 105 (20.9%) patients were identified as having distal aortic enlargement, and 69 (13.7%) patients were found to have distal aortic aneurysm formation. Five patients were identified with aortic rupture. True lumen collapse and multi-false lumens were two potential risk factors for distal aortic enlargement after proximal repair of TBAD. The LR model performed the best in predicting distal aortic enlargement, with the highest sensitivity (96.7%) and an AUC of 0.773. The best model for predicting distal aneurysm formation was the ANN model, which yielded the highest AUC (0.876) and a specificity of 79.1%., Conclusions: Machine learning approaches can produce accurate predictions of distal aortic enlargement after proximal repair of TBAD, which potentially benefits subsequent management., (Copyright © 2021. Published by Elsevier Inc.)

Objective: Greater population life expectancy and consistent improvement in diagnostic techniques have increased the diagnosis of abdominal aortic aneurysms (AAAs) in the elderly population. The aim was to study the natural history of small (< 55 mm) incidental AAAs in octogenarian and nonagenarian patients to assess the need for follow up and/or invasive treatment., Methods: This was a retrospective analysis of a prospective registry. Patients ≥ 80 years old at the time of diagnosis of a < 55 mm AAA in 1988-2018 were selected. Clinical and anatomical characteristics were registered. Patients were divided in three groups: 30 - 39 mm, 40 - 49 mm, and 50 - 54 mm AAA. The outcome variables were aorto-iliac rupture, AAA reaching a surgical threshold (≥ 55 mm), and death. A descriptive statistical analysis was performed and life tables, Kaplan-Meier curves, and uni- and multivariable Cox regression were used., Results: Three hundred and ten patients were included, 256 (82.6%) men, with mean index age of 84.5 years (standard deviation [SD] 3.5), and median follow up of 37.9 months (interquartile range [IQR] 18.2 - 65.4). Eighteen (5.8%) AAAs ruptured; four of these patients were operated on and only one survived. Sixty-two (20%) AAA reached a surgical size; eight were repaired electively, with 0% early mortality. The survival rates were 81%, 70%, and 38% at one, two, and five years. The rupture rates were 1%, 2%, and 6% and the AAAs reaching surgical threshold were 1%, 4%, and 19% for the same time periods. AAA size < 40 mm was an independent protective factor from rupture (0.13; 95% confidence interval [CI] 0.03 - 0.48), reaching surgical threshold (0.08; 95% CI 0.04 - 0.16) and death (0.63; 95% CI 0.42 - 0.95)., Conclusion: The risk of late rupture of small incidental AAA diagnosed in octogenarian and nonagenarian patients is very small, especially when the AAA is < 40 mm in diameter. In contrast, global mortality is high. Conservative management seems sensible, with strict selection of the patients who would benefit from follow up and eventual repair., (Copyright © 2021 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

Background: The National Health Service (NHS) abdominal aortic aneurysm (AAA) screening programme (NAAASP) in England screens 65-year-old men. The programme monitors those with an aneurysm, and early intervention for large aneurysms reduces ruptures and AAA-related mortality. AAA screening services have been disrupted following COVID-19 but it is not known how this may impact AAA-related mortality, or where efforts should be focussed as services resume., Methods: We repurposed a previously validated discrete event simulation model to investigate the impact of COVID-19-related service disruption on key outcomes. This model was used to explore the impact of delayed invitation and reduced attendance in men invited to screening. Additionally, we investigated the impact of temporarily suspending scans, increasing the threshold for elective surgery to 7cm and increasing drop-out in the AAA cohort under surveillance, using data from NAAASP to inform the population., Findings: Delaying invitation to primary screening up to two years had little impact on key outcomes whereas a 10% reduction in attendance could lead to a 2% lifetime increase in AAA-related deaths. In surveillance patients, a 1-year suspension of surveillance or increase in the elective threshold resulted in a 0.4% increase in excess AAA-related deaths (8% in those 5-5.4cm at the start). Longer suspensions or a doubling of drop-out from surveillance would have a pronounced impact on outcomes., Interpretation: Efforts should be directed towards encouraging men to attend AAA screening service appointments post-COVID-19. Those with AAAs on surveillance should be prioritised as the screening programme resumes, as changes to these services beyond one year are likely to have a larger impact on surgical burden and AAA-related mortality., Competing Interests: No authors have competing interests.

[Figure: see text].

Thoracic aortic aneurysm and dissection (TAAD) is a deadly disease characterized by intimal disruption induced by hemodynamic forces of the circulation. The effect of exercise in patients with TAAD is largely unknown. β-Aminopropionitrile (BAPN) is an irreversible inhibitor of lysyl oxidase that induces TAAD in mice. The objective of this study was to investigate the effect of aerobic exercise on BAPN-induced TAAD. Upon weaning, mice were given either BAPN-containing water or standard drinking water and subjected to either conventional cage activity (BAPN-CONV) or forced treadmill exercise (BAPN-EX) for up to 26 wk. Mortality was 23.5% (20/85) for BAPN-CONV mice versus 0% (0/22) for BAPN-EX mice (hazard ratio 3.8; P = 0.01). BAPN induced significant elastic lamina fragmentation and intimal-medial thickening compared with BAPN-untreated controls, and aneurysms were identified in 50% (5/10) of mice that underwent contrast-enhanced CT scanning. Exercise significantly decreased BAPN-induced wall thickening, calculated circumferential wall tension, and lumen diameter, with 0% (0/5) of BAPN-EX demonstrating chronic aortic aneurysm formation on CT scan. Expression of selected genes relevant to vascular diseases was analyzed by qRT-PCR. Notably, exercise normalized BAPN-induced increases in TGF-β pathway-related genes Cd109 , Smad4 , and Tgfβr1 ; inflammation-related genes Vcam1 , Bcl2a1 , Ccr2 , Pparg , Il1r1 , Il1r1 , Itgb2 , and Itgax ; and vascular injury- and response-related genes Mmp3 , Fn1 , and Vwf . Additionally, exercise significantly increased elastin expression in BAPN-treated animals compared with controls. This study suggests that moderate aerobic exercise may be safe and effective in preventing the most devastating outcomes in TAAD. NEW & NOTEWORTHY Moderate aerobic exercise was shown to significantly reduce mortality, extracellular matrix degradation, and thoracic aortic aneurysm and dissection formation associated with lysyl oxidase inhibition in a mouse model. Gene expression suggested a reversal of TGF-β, inflammation, and extracellular matrix remodeling pathway dysregulation, along with augmented elastogenesis with exercise.

Objective: The aims of the present study were to examine the impact of type 2 endoleaks (T2EL) on overall survival and to determine the need for secondary intervention after endovascular aneurysm repair (EVAR)., Methods: A multicentre retrospective cohort study in the Netherlands was conducted among patients with an infrarenal abdominal aortic aneurysm (AAA) who underwent EVAR between 2007 and 2012. The primary endpoint was overall survival for patients with (T2EL+) or without (T2EL-) a T2EL. Secondary endpoints were sac growth, AAA rupture, and secondary intervention. Kaplan-Meier survival and multivariable Cox regression analysis were used., Results: A total of 2 018 patients were included. The median follow up was 62.1 (range 0.1 - 146.2) months. No difference in overall survival was found between T2EL+ (n = 388) and T2EL- patients (n = 1630) (p = .54). The overall survival estimates at five and 10 years were 73.3%/69.4% and 45.9%/44.1% for T2EL+/T2EL- patients, respectively. Eighty-five of 388 (21.9%) T2EL+ patients underwent a secondary intervention. There was no difference in overall survival between T2EL+ patients who underwent a secondary intervention and those who were treated conservatively (p = .081). Sac growth was observed in 89 T2EL+ patients and 44/89 patients (49.4%) underwent a secondary intervention. In 41/44 cases (93.1%), sac growth was still observed after the intervention, but was left untreated. Aneurysm rupture occurred in 4/388 T2EL patients. In Cox regression analysis, higher age, ASA classification, and maximum iliac diameter were significantly associated with worse overall survival., Conclusion: No difference in overall survival was found between T2EL+ and T2EL- patients. Also, patients who underwent a secondary intervention did not have better survival compared with those who did not undergo a secondary intervention. This study reinforces the need for conservative treatment of an isolated T2EL and the importance of a prospective study to determine possible advantages of the intervention., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Abdominal aortic aneurysm (AAA) is a potentially fatal condition predominantly affecting older adult men (60 years or over). Based on evidence, preventative health-care guidelines recommend screening older males for AAA using ultrasound. In attempts to reduce AAA mortality among men, screening has been utilized for early detection in some Western countries including the UK and Sweden. The current scoping review includes 19 empirical studies focusing on AAA screening in men. The findings from these studies highlight benefits and potential harms of male AAA screening. The benefits of AAA screening for men include decreased incidence of AAA rupture, decreased AAA mortality, increased effectiveness of elective AAA repair surgery, and cost-effectiveness. The potential harms of AAA screening included lack of AAA mortality reduction, negative impacts on quality of life, and inconsistent screening eligibility criteria being applied by primary care practitioners. The current scoping review findings are discussed to suggest changes to AAA screening guidelines and improve policy and practice.

Aortic annulus rupture is a dangerous complication of transcatheter aortic valve implantation, with an overall incidence of around 1%. Ruptures can be distinguished into supra-annular, involving injuries of the sinus of Valsalva and the sinotubular junction, annular, involving the fibrous portion of the aortic annulus, and sub-annular, located in the left ventricular outflow tract below the aortic valve cusp insertion. Annular rupture can be "contained", which usually evolves in aortic hematoma or pseudoaneurysm and rarely requires emergent cardiac surgery; or "non-contained", acutely evolving in hemopericardium with cardiac tamponade, often requiring emergent cardiac surgery and with an in-hospital mortality of 75%. Balloon-expandable oversizing and severe left ventricular outflow tract calcifications, especially under the left coronary cusp, are the most important risk factors for annular rupture. A careful computed tomography scan-based procedural planning is of paramount importance to reduce the risk of this complication. The presence and extension of left ventricular outflow tract calcifications, together with precise measurement of the virtual basal ring, should drive the operator to the right choice of prosthesis type and size in order to prevent this terrible complication.

The proper management of small abdominal aortic aneurysms (AAAs), namely those under the threshold of 5.5 cm in diameter, has been under investigation for years. Risk of rupture for this group of AAAs is higher than the general population, although it remains low enough not to require a repair. However, specific factors have been associated with increased expansion or rupture rate, and these factors could identify potential candidates for earlier intervention. This review aims to collect and present all available data on the development and progress of small AAAs. Moreover, recommendations on proper management are discussed as well., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Abdominal aortic aneurysm (AAA) is a permanent and irreversible dilation of the lower region of the aorta. It is typically an asymptomatic condition that if left untreated can expand to the point of rupture. In simple mechanical terms, rupture of an artery occurs when the local wall stress exceeds the local wall strength. It is therefore understandable that numerous studies have attempted to estimate the AAA wall stress and investigate the relationship between the AAA wall stress and AAA symptoms., Materials and Methods: We conducted computational biomechanics analysis for 19 patients with AAA (a proportion of these patients were classified as symptomatic) to investigate whether the AAA wall stress fields (both the patterns and magnitude) correlate with the clinical definition of symptomatic and asymptomatic AAAs. For computation of AAA wall stress, we used a very efficient method recently presented by the Intelligent Systems for Medicine Laboratory. The Intelligent Systems for Medicine Laboratory's method uses geometry from computed tomography images and mean arterial pressure as the applied load. The method is embedded in the software platform BioPARR-Biomechanics based Prediction of Aneurysm Rupture Risk, freely available from http://bioparr.mech.uwa.edu.au/. The uniqueness of our stress computation approach is three-fold: i) the results are insensitive to unknown patient-specific mechanical properties of arterial wall tissue; ii) the residual stress is accounted for, according to Y.C. Fung's Uniform Stress Hypothesis; and iii) the analysis is automated and quick, making our approach compatible with clinical workflows., Results: Symptomatic patients could not be identified from the plots (pattern) of AAA wall stress and stress magnitude. Although the largest stress was predicted for a patient who suffered from AAA symptoms, the three patients with the smallest stress were also symptomatic., Conclusions: The results demonstrate, contrary to the common view, that neither the wall stress magnitude nor the stress distribution appears to be associated with the presence of clinical symptoms., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Abdominal aortic aneurysm (AAA) rupture is a common cause of death in adults. Current AAA treatment is by open surgical or endovascular aneurysm repair. Rodent model and human epidemiology, and genetic and observational studies over the last few decades have highlighted the potential of a number of drug therapies, including medications that lower blood pressure, correct dyslipidaemia, or inhibit thrombosis, inflammation or matrix remodelling, as approaches to managing small AAA. This review summarizes prior AAA pathogenesis data from animal and human studies aimed at identifying targets for the development of drug therapies. The review also systematically assesses past randomized placebo-controlled drug trials in patients with small AAAs. Eleven previously published randomized-controlled clinical trials testing different drug therapies aimed at slowing AAA progression were identified. Five of the trials tested antibiotics and three trials assessed medications that lower blood pressure. Meta-analyses of these trials suggested that neither of these approaches limit AAA growth. Allocation to blood pressure-lowering medication was associated with a small reduction in AAA rupture or repair, compared to placebo (relative risk 0.94, 95% confidence intervals 0.89, 1.00, P = 0.047). Three further trials assessed the effect of a mast cell inhibitor, fibrate or platelet aggregation inhibition and reported no effect on AAA growth or clinical events. Past trials were noted to have a number of design issues, particularly small sample sizes and limited follow-up. Much larger trials are needed to properly test potential therapeutic approaches if a convincingly effective medical therapy for AAA is to be identified., (© 2019 The Association for the Publication of the Journal of Internal Medicine.)

Gradual dilatation of the ascending aorta is a common phenomenon in patients with Marfan's disease, which often leads to dissection and rupture. It is estimated that around two-thirds of the patients either die or require major surgery before the age of 42 years. In the mirror of the experience of 40 years with aortic wall reinforcement, the author forward the postulate that whenever the ascending aorta of an individual with proven Marfan's disease reaches adult size, that is, approximately 3.5 cm in diameter, the wall of his/her ascending aorta should be reinforced to prevent further expansion., Competing Interests: None declared., (Georg Thieme Verlag KG Stuttgart · New York.)

Background: Effectiveness and optimal timing of endovascular treatment for type B aortic dissection (AD) remain controversial., Method: An extensive search of literature (January 1999-December 2017) was conducted using PubMed, Cochrane Library and Science-Direct databases for studies on endovascular repair for acute/chronic type B AD; ≥10 patients; not reviews; and reporting predefined baseline data and ≥50% of predefined study outcomes, which were extracted and analysed according to Preferred Reporting Items for Systematic reviews and Meta-Analyses. Primary outcomes were in-hospital all-cause mortality and aorta-related mortality., Result: Based on 92 publications (5956 patients), pooled estimate for overall in-hospital mortality was 7.0% [95% CI, 6.2%-7.8%]. Major perioperative complications included stroke (4.2% [3.6%-4.9%]), spinal cord ischemia (3.3% [2.8%-3.9%]), retrograde type A AD (3.2% [2.7%-3.9%]), type I endoleak (4.9% [3.8%-6.2%]), visceral ischemia (3.1% [2.5%-3.8%]) and acute renal failure requiring haemodialysis (5.1% [4.3%-5.9%]). Mid-term mortality incidence was 8.9% [7.2%-10.9%], and secondary intervention rate was 12.5% [10.5%-15.0%] with 6.1% [5.3%-7.2%] conversion to open surgery. Institutions with ≥40 endovascular treatment caseload had significantly lower rates of in-hospital and aorta-related mortality, stroke, type I endoleak, renal failure and retrograde type A AD. Patients treated in the acute phase had significantly higher incidence of in-hospital or aorta-related mortality and renal failure. Patients with chronic dissection required significantly more often secondary intervention during follow-up., Conclusion: Endovascular stent-graft for type B AD therefore appeared feasible and safe with a low incidence of mortality and perioperative complications, particularly for delayed intervention and centres with ≥40 caseload. Standardized and long-term follow-up data are warranted., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Aims: Antihypertensive drugs are included in the medical therapy of vascular Ehlers-Danlos syndrome (vEDS). The β-blocker celiprolol has been suggested to prevent arterial damage in vEDS, but the underlying mechanism remains unclear. It is also unknown whether the widely used angiotensin II receptor type 1 antagonist losartan has a therapeutic effect in vEDS. Here, we evaluated the impact of celiprolol and losartan on the biomechanical integrity of the vEDS thoracic aorta., Methods and Results: We established a new approach to measure the maximum tensile force at rupture of uniaxially stretched murine thoracic aortic rings. In a vEDS model, which we (re-)characterized here at molecular level, heterozygous mice showed a significant reduction in the rupture force compared to wild-type mice, reflecting the increased mortality due to aortic rupture. For the assessment of treatment effects, heterozygous mice at 4 weeks of age underwent a 4-week treatment with celiprolol, losartan, and, as a proof-of-concept drug, the matrix metalloproteinase inhibitor doxycycline. Compared to age- and sex-matched untreated heterozygous mice, treatment with doxycycline or celiprolol resulted in a significant increase of rupture force, whereas no significant change was detected upon losartan treatment., Conclusions: In a vEDS model, celiprolol or doxycycline, but not losartan, can improve the biomechanical integrity of the aortic wall, thereby potentially reducing the risk of dissection and rupture. As doxycycline is a broad-spectrum antibiotic with considerable side effects, celiprolol may be more suitable for a long-term therapy and thus rather indicated for the medication of patients with vEDS., (© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Current clinical guidelines for surgical repair of abdominal aortic aneurysms (AAAs) are primarily based on maximum diameter assessment. From a biomechanical point of view, not only the diameter but also peak wall stresses will play an important role in rupture risk assessment. These methods require patient specific geometry which typically uses computed tomography (CT) or magnetic resonance imaging. Recently, wall stress analysis based on 3D ultrasound (US) has been proposed, and shows promising results. However, the major limitations in these studies were the use of manual segmentation and the limiting field of view of US. Therefore in this study, the AAA is imaged with multiperspective 3D ultrasound, merged to obtain a large field of view, and afterwards automatically segmented. Geometry and wall stress results were validated using CT imaging., Methods: Three dimensional US and CT data were available for 40 AAA patients (maximum diameter 34-61 mm). The full US based AAA geometry was determined using automatic segmentation, and when the aneurysm exceeded a single 3D volume, automatic fusion of multiple 3D US volumes was used. Wall stress analysis was performed for all AAA patients and percentile wall stresses were derived. The accuracy of the US based geometry and wall stress prediction was measured by comparison with CT data., Results: Estimated geometries derived from 3D US and CT data showed good similarity, with an overall median similarity index (SI) of 0.89 and interquartile range of 0.87-0.92, whereas the median Hausdorff distances (HD), a measure for the maximum local mismatch, was 4.6 (4.0-5.9) mm for all AAA geometries. Thereby, the wall stress results based on merged multiperspective 3D US data revealed a greater similarity to CT than single 3D US data., Conclusion: This study showed that large volume geometry assessment of AAAs using multiperspective 3D ultrasound, segmentation and fusion, and wall stress analysis is feasible in a robust and labour efficient manner., (Copyright © 2019 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

Transcatheter aortic valve (TAVI) is the treatment of choice in patients with severe symptomatic aortic stenosis at high surgical risk. Recent data have also shown favorable results in patients considered to have an intermediate operative risk, which broadens the application of this new technology. Despite its success, the TAVI procedure has been associated with life-threatening complications. Advances in preoperative screening and patient selection have reduced the incidence of these complications. When these complications occur, early recognition and rapid management are essential. The purpose of this review is to describe non-rhythmic mechanical complications attributable to TAVI procedures with their predictive factors, how to prevent and manage them., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)

Objective: The relationship between dietary patterns and development of abdominal aortic aneurysm (AAA) is not well understood. Thus, we prospectively evaluated the association between the anti-inflammatory potential of diet and risk of AAA., Methods: The study population included the Cohort of Swedish Men (45 072 men) and the Swedish Mammography Cohort (36 633 women), aged 45-83 years at baseline. The anti-inflammatory potential of diet was estimated using Anti-inflammatory Diet Index (AIDI) based on 11 foods with anti-inflammatory potential and 5 with proinflammatory potential (maximum 16 points) that was validated againsthigh sensitivity C reactive protein (hsCRP). Cox proportional hazard regression models were used to estimate HRs and 95% CIs. During the 14.9 years of follow-up (1 217 263 person-years), 1528 AAA cases (277 (18%) ruptured, 1251 non-ruptured) were ascertained via the Swedish Inpatient Register, the National Cause of Death Register and the Register for Vascular Surgery (Swedvasc)., Results: We observed an inverse association between the AIDI and AAA risk in women and men; HRs between extreme quartiles of the AIDI (≥8 vs ≤5 points) were 0.55 (95% CI 0.36 to 0.83) in women and 0.81 (95% CI 0.68 to 0.98) in men. The AIDI was inversely associated with both ruptured and non-ruptured AAA incidence; the HR of participants in the highest quartile of AIDI compared with those in the lowest quartile was 0.61 (95% CI 0.41 to 0.90) for ruptured AAA and 0.79 (95% CI 0.65 to 0.95) for non-ruptured AAA., Conclusion: Adherence to diet with a high anti-inflammatory potential was associated with a reduced AAA risk, an association that was even more pronounced for AAA rupture., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)