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Objectives: This study aimed to derive a novel classification of blood flow pattern in abdominal aortic aneurysms (AAA) based on computational fluid dynamics (CFDs), and to determine the predictive value of flow patterns in AAA rupture., Methods: This was an age and sex matched case control study. Cases were identified as patients who underwent emergency endovascular or open repair due to ruptured or AAA at risk of impending rupture. Controls were age and sex matched with patients with an AAA who were asymptomatic and had a confirmed unruptured AAA from computed tomography angiography images from the same period. Classification of blood flow pattern (type I: non-helical main flow channel with multiple vortices; type II: non-helical main flow channel with single vortices; and type III, helical main flow channel with helical vortices) and haemodynamic parameters (areas of low wall shear stress [A lowWSS ], aneurysm pressure drop [Δ pressure], etc) were derived from CFD analyses. Multivariable regression was used to determine independent AAA rupture risk factors. The incremental discriminant and reclassification abilities for AAA rupture were compared among different models., Results: Fifty-three ruptured and 53 intact AAA patients were included. Ruptured AAA showed a higher prevalence of type III flow pattern than intact AAA (60.4% vs. 15.1%; p < .001). Type III flow pattern was associated with a significantly increased risk of aneurysm rupture (odds ratio 10.22, 95% confidence interval 3.43 - 30.49). Among all predicting models, the combination of AAA diameter, haemodynamic parameters (A lowWSS or Δ pressure), and flow pattern showed highest discriminant abilities in both the overall population (c-index = 0.862) and subgroup patients with AAAs < 55 mm (c-index = 0.972). Compared with AAA diameter, adding the flow pattern could significantly improve the reclassification abilities in both the overall population (net reclassification index [NRI] = 0.321; p < .001) and the subgroup of AAAs < 55 mm (NRI = 0.732; p < .001)., Conclusion: Type III flow pattern was associated with a significantly increased risk of AAA rupture. The integration of blood flow pattern may improve the identification of high risk aneurysms in both overall population and in those with AAAs < 55 mm., (Copyright © 2022 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

Several observational studies and randomized trials have compared open surgery (OS) and endovascular aortic repair (EVAR) for ruptured abdominal aortic aneurysm (rAAA). However, none of these studies addressed optimal management of hemodynamically (hd) unstable patients. Our objective was to compare perioperative outcomes in patients undergoing OS vs EVAR for hd-stable and hd-unstable rAAAs.This retrospective study was conducted in West China Hospital from January 2005 to December 2015. Unstable patients were defined as those who have at least 1 of the following: preoperative shock, preoperative transfusion >4 units, preoperative intubation, cardiac arrest, or unconsciousness. Univariable and multivariable logistic regression analyses were performed.Of the 102 patients, 70.6% underwent OS and 29.4% EVAR. About 46.1% were unstable, and for these patients, OS was performed in 70.2% and EVAR in 29.8%. The 30-day mortality was 23.6% (OS, 25.6%; EVAR, 18.8%; P = .585) for hd-stable patients and was 42.6% (OS, 45.5%; EVAR, 35.7%; P = .537) for hd-unstable patients. Patients with OS had longer operative time and more transfusion. Amongst hd-stable patients, OS subgroup had a higher rate of pneumonia (33.3% vs 6.3%, P = .045), longer intensive care unit (ICU) stay (43.2 vs 15.2 hours, P = .02), and length of stay (11.6 vs 8.6 days, P = .041). Among hd-unstable patients, OS subgroup had a longer ICU stay (134.3 vs 63.8 hours, P = .047). Hospitalization costs of OS group were significantly lower than those of EVAR group, regardless of hemodynamic stability.Approximately one-third of patients with rAAA were treated by EVAR at our institution. EVAR may be the preferred approach for anatomically suitable rAAAs. However, patients treated by EVAR had a similar mortality compared with those treated by OS. In addition, OS is not an independent factor for a higher 30-day mortality, and the costs of OS were much cheaper than those of EVAR. Therefore, OS is difficult to replace, especially in developing countries.

Consideration for oversizing the proximal stent graft is suggested in endovascular aortic repair. However, a special recommendation for the proximal oversizing ratio (OSR) in patients with ruptured abdominal aortic aneurysm (rAAA) is ambiguous. This study aims to evaluate the effect of different degrees of the proximal oversizing ratio (OSR) on risk of type IA endoleak (TIAEL) in hemodynamically stable and unstable patients with rAAA undergoing emergency endovascular aortic repair (EVAR). Our study included 134 rAAA patients undergoing emergent EVAR, and we did not observe a significant association between hemodynamic instability and risk of T1AEL (HR 3.89, 95%CI 0.40–37.75, p = 0.24). All three T1AELs in the hemodynamically unstable subgroup were observed in patients with OSR ≤ 30%, but no significant difference was found regarding T1AEL between patients with OSR > 30% and OSR ≤ 30% (0.00% vs. 11.11%, p = 0.19). As for hemodynamically stable patients, OSR > 20% was associated with a significantly decreased risk of T1AEL (HR 0.03, 95%CI 0.01–0.53, p = 0.016). In conclusion, a proximal OSR > 20% is associated with a decreased risk of T1AEL in hemodynamically stable patients, while an OSR > 30% did not add an additional advantage of lowering the risk of T1AEL in hemodynamically unstable patients. [ABSTRACT FROM AUTHOR]

Adaptive immunity and innate immunity have been implicated in the pathogenesis of abdominal aortic aneurysm (AAA), and damage and remodelling in the tunica media are a focus of the aneurysm development. Thus, identification of key immune cells or molecules that might be targets for the treatment of AAA is critical. We characterized the innate immune cells in human AAA tissue specimens by flow cytometry and found that apart from other lymphocytes, many invariant natural killer T (iNKT) cells marked as CD3 and Va24Ja18 had invaded the aortic tissues and were numerous, especially in the tunica media. These infiltrating iNKT cells have a high expression of CD69, indicating a highly active function. We were interested in whether iNKT cells could be the drivers of media damage in AAA. To answer this question, we used an AAA mouse model induced by angiotensin II (Ang II) infusion, which can reproduce the inflammatory response of AAA in mouse, which was confirmed by RNAseq. The results showed that the incidence of AAA was significantly higher after administration of α‐galactosylceramide (α‐GalCer), a synthetic glycolipid that activates iNKT cells via CD1d, compared with the Ang II‐induced AAA alone (61·54% vs 31·82%) in mice. Histopathological and immunofluorescent staining results showed significantly more severe inflammatory infiltration and pathological lesions in the Ang II+α‐GalCer treatment group. These results are highly suggestive that activated iNKT cells greatly contribute to AAA development and that the control of the activation state in iNKT cells may represent an important therapeutic strategy for AAA. [ABSTRACT FROM AUTHOR]