The potential involvement of glycocalyx disruption in abdominal aortic aneurysm pathogenesis.

BACKGROUND: Abdominal aortic aneurysm is a weakening and expansion of the abdominal aorta. Currently, there is no drug treatment to limit abdominal aortic aneurysm growth. The glycocalyx is the outermost layer of the cell surface, mainly composed of glycosaminoglycans and proteoglycans. OBJECTIVE: The aim of this review was to identify a potential relationship between glycocalyx disruption and abdominal aortic aneurysm pathogenesis. METHODS: A narrative review of relevant published research was conducted. RESULTS: Glycocalyx disruption has been reported to enhance vascular permeability, impair immune responses, dysregulate endothelial function, promote extracellular matrix remodeling and modulate mechanotransduction. All these effects are implicated in abdominal aortic aneurysm pathogenesis. Glycocalyx disruption promotes inflammation through exposure of adhesion molecules and release of proinflammatory mediators. Glycocalyx disruption affects how the endothelium responds to shear stress by reducing nitric oxide availabilty and adversely affecting the storage and release of several antioxidants, growth factors, and antithromotic proteins. These changes exacerbate oxidative stress, stimulate vascular smooth muscle cell dysfunction, and promote thrombosis, all effects implicated in abdominal aortic aneurysm pathogenesis. Deficiency of key component of the glycocalyx, such as syndecan-4, were reported to promote aneurysm formation and rupture in the angiotensin-II and calcium chloride induced mouse models of abdominal aortic aneurysm. CONCLUSION: This review provides a summary of past research which suggests that glycocalyx disruption may play a role in abdominal aortic aneurysm pathogenesis. Further research is needed to establish a causal link between glycocalyx disruption and abdominal aortic aneurysm development.

A stable aneurysm sac after endovascular aneurysm repair as a predictor for mortality: An in-depth analysis.

OBJECTIVE: The aim of the present study was to compare the long-term survival of patients with a stable aneurysm sac vs those with aneurysm sac regression after endovascular aneurysm repair (EVAR) and to identify the independent risk factors for aneurysm sac regression and mortality after EVAR. METHODS: We reviewed all the patients who had undergone EVAR from 2005 to 2018 with computed tomography angiography available at 1 year of follow-up. Aneurysm sac regression was defined as a diameter decrease of >10%. We used multivariable regression to identify the independent risk factors for sac regression. Kaplan-Meier analysis and Cox regression were performed to test the differences in 5-year mortality between a stable sac diameter and sac regression. RESULTS: The inclusion criteria were met by 325 patients, with 185 in the sac regression group and 140 in the stable sac group. Multivariable logistic regression analysis showed that treatment of a ruptured aneurysm was an independent risk factor for aneurysm sac regression (hazard ratio [HR], 0.26; 95% confidence interval [CI], 0.07-0.96). Age (HR, 1.05; 95% CI, 1.01-1.09), ischemic heart disease (HR, 1.94; 95% CI, 1.13-3.31), neck thrombus (HR, 2.72; 95% CI, 1.07-6.95), and a type II endoleak (HR, 19.21; 95% CI, 7.32-50.40) were independent risk factors for a stable aneurysm sac diameter. Multivariable Cox regression showed a significantly increased risk of mortality for patients with a stable aneurysm sac after EVAR (odds ratio, 2.25; 95% CI, 1.36-3.72). No significant differences were found in cause of death between the two groups. CONCLUSIONS: A stable aneurysm sac after EVAR was associated with increased mortality. Age, ischemic heart disease, neck thrombus, and a type II endoleak were independent risk factors for a stable aneurysm sac. However, a well-founded explanation for this finding is still lacking. Future research should focus on aggressive treatment of type II endoleaks and inflammatory processes as potential pathophysiologic mechanisms.

Emergency Repair of a Ruptured Para-Renal Abdominal Aortic Aneurysm in a Patient with a Functional Renal Graft: A Case Report and Review of the Literature.

INDRODUCTION: Rupture of and abdominal aortic aneurysm (AAA) in a kidney transplant patient is a rare and rarely reported event. Emergent treatment can be challenging and should achieve effective aortic repair while minimizing ischemic damage to the renal graft during aortic cross-clamping. Several renal protective measures have been proposed such as permanent or temporary shunts, renal cold perfusion and general hypothermia. CASE REPORT: We report the effective treatment of a para-renal AAA in a patient with a functional renal allograft. A temporary extra-corporeal axillofemoral shunt was constructed to maintain graft's perfusion during open surgical repair. EVAR was not an option due to a short aortic neck. The postoperative period was complicated by colon ischemia and aortic graft infection. At 3 years follow-up the patient was well and graft's function was unchanged. CONCLUSION: This case is a reminder that renal graft protection must be accounted for when AAA rupture occurs in kidney transplant patients. We reviewed the literature to find previously reported cases and how they were managed.

Degeneration and Regeneration of Smooth Muscle Cells in Two Different Abdominal Aortic Aneurysm Models in Rabbits.

BACKGROUND: We aimed to investigate the formation and self-healing process of rabbit abdominal aortic aneurysm (AAA) by focus on the degeneration and regeneration of smooth muscle cells (SMCs) in elastase-induced AAA model and enlarging AAA model in rabbits. METHODS: Sixty rabbits were equally divided into 2 aneurysm groups (Group A and Group B). Rabbits received a 10-min incubation of elastase in Group A (10 units/µL) and Group B (1 unit/µL). Rabbits underwent aortic stenosis above the incubated segment in Group B. Aortic diameter was measured and rabbits were sacrificed for histopathological and immunohistochemical studies. RESULTS: The incubated aorta dilated immediately and ran up to maxima by day 21 in Group A. All aneurysms formed by day 21 and enlarged progressively in Group B. SMCs content, elastin content and intima-media thickness decreased significantly by day 0 in Group A. SMCs and elastic fibers were destroyed gradually in Group B, however, SMCs content was significantly lower than Group A by day 70. Intimal thickness increased significantly by day 70 in the Aneurysm groups. MMP2 maintained moderate expression in Group A, which decreased significantly by day 3 in Group B. MMP9 and RAM11 expressions were higher by day 1, but decreased significantly by day 3 in Group B. CONCLUSIONS: Irreversible degeneration of SMCs is critical to a rapid formation of elastase-induced rabbit AAA model, and SMCs excessive regeneration accounts for the selfhealing process. SMCs degradation and regeneration remain relatively stable in an enlarging AAA model. SMCs should be the key target for studying the mechanism of AAA and intervention therapy.

Stress Analysis in AAA does not Predict Rupture Location Correctly in Patients with Intraluminal Thrombus.

BACKGROUND: A biomechanical approach to the rupture risk of an abdominal aortic aneurysm could be a solution to ensure a personalized estimate of this risk. It is still difficult to know in what conditions, the assumptions made by biomechanics, are valid. The objective of this work was to determine the individual biomechanical rupture threshold and to assess the correlation between their rupture sites and the locations of their maximum stress comparing two computed tomography scan (CT) before and at time of rupture. METHODS: We included 5 patients who had undergone two CT; one within the last 6 months period before rupture and a second CT scan just before the surgical procedure for the rupture. All DICOM data, both pre- and rupture, were processed following the same following steps: generation of a 3D geometry of the abdominal aortic aneurysm, meshing and computational stress analysis using the finite element method. We used two different modelling scenarios to study the distribution of the stresses, a "wall" model without intraluminal thrombus (ILT) and a "thrombus" model with ILT. RESULTS: The average time between the pre-rupture and rupture CT scans was 44 days (22-97). The median of the maximum stresses applied to the wall between the pre-rupture and rupture states were 0.817 MPa (0.555-1.295) and 1.160 MPa (0.633-1.625) for the "wall" model; and 0.365 MPa (0.291-0.753) and 0.390 MPa (0.343-0.819) for the "thrombus" model. There was an agreement between the site of rupture and the location of maximum stress for only 1 patient, who was the only patient without ILT. CONCLUSIONS: We observed a large variability of stress values at rupture sites between patients. The rupture threshold strongly varied between individuals depending on the intraluminal thrombus. The site of rupture did not correlate with the maximum stress except for 1 patient.

Mid-Term Outcomes of Chimney Endovascular Aortic Aneurysm Repair: A Systematic Review and Meta-analysis.

BACKGROUND: To provide an overview of the literature on the mid-term outcomes of chimney EVAR (ChEVAR) for the treatment of juxtarenal abdominal aortic aneurysms (JAAA). METHODS: Different electronic databases were searched for published articles up to January 2020. The eligibility criteria were studies describing mid- or long-term outcomes of chimney EVAR (mean follow-up at least 1 year) for treatment of JAAA, including more than 10 cases, published in English, and with full text available. The outcomes measure were overall survival rate, target vessel patency, and freedom from reintervention at 3 years. Quality of the included studies was analyzed using the MINORS criteria. Pooled effect estimates were analyzed using random-effect models and heterogeneity was tested using I2 statistics. RESULTS: Thirteen articles met the inclusion criteria. The included studies described 1,019 patients. According to the quality assessment, methodological quality was moderate to poor. The pooled overall survival, freedom from reintervention, and target vessel patency at 3 year was 81.4 % (95%CI 73.8-87.9), 85.7% (95%CI 75.6-93.5), and 95.1% (95%CI 89.3-98.7) respectively. CONCLUSIONS: The results of this review show good to acceptable short and mid-term survival and good mid-term durability, which supports that ChEVAR as a suitable alternative in high-risk JAAA. However, proper patient selection for ChEVAR seems essential to attain good mid-term outcomes, and further large prospective and good quality studies are required to demonstrate its long-term results and enable conclusions on specific determinants for outcome.

Midterm Outcomes of Endovascular Abdominal Aortic Aneurysm Repair with Prevention of type 2 Endoleak by Intraoperative Aortic Side Branch Coil Embolization.

OBJECTIVE: The midterm results of endovascular abdominal aortic aneurysm repair (EVAR) with aortic side branch coil embolization during EVAR was evaluated. METHODS: Our center began coil embolization for all patent inferior mesenteric artery (IMA) and lumbar artery (LA) with an inner diameter more than 2.0 mm during EVAR since June 2015. When four or more LA were patent, coil embolization for LA with inner diameter 2.0 mm or less was done. EVAR without aortic side branches coil embolization was performed for 59 patients prior to June 2015 (control group) and 79 patients underwent EVAR with coil embolization during EVAR (coil group). The success rate of coil embolization for IMA and LA was evaluated in coil group. The frequency of type 2 endoleak (T2EL), freedom from aneurysm sac expansion (5 mm or more) rate and the rate of the aneurysm sac shrinkage (10 mm or more) were compared between the coil and control groups. Additionally, multiple logistic regression analysis for all patients was conducted to analyze whether IMA patency and the number of patent lumbar artery at the end of EVAR were the risk factors of the aneurysm sac expansion of 5 mm or more. RESULTS: The success rate of IMA coil embolization was 96.4% and that of LA was 74.5%. Compared to the control group, the frequency of T2EL was significantly lower in coil group at 7 days (1.3% vs. 60.4%, P <0.0001) and at 6 months (2.1% vs 38.2%, P <0.0001) after EVAR. The freedom from aneurysm sac expansion rate was significantly better in the coil group at 5 years (100% in coil group and 65.2% in control group, P = 0.002). The rate of aneurysm sac shrinkage was significantly better in coil group (15.5% vs. 2.0% at 1 year, 42.8% vs. 6.3% at 2 years and 53.4% vs. 17.8% at 3 years, p = 0.0007). The risk of aneurysm sac expansion of 5 mm or more was estimated to be 11 times greater when the IMA was patent, and 4.9 times greater when 3 or more LAs were patent at the end of EVAR. CONCLUSION: When IMA was occluded and the number of patent LA became 2 or less by aortic side branch coil embolization during EVAR, favorable mid-term results were safely obtained and good long-term result could be expected with EVAR.

The Femoral Venoarterial Perfusion During Open Abdominal Aortic Aneurysm Repair in Patient With Renal Transplant.

We report of a patient with abdominal aortic aneurysm and renal transplant who underwent aneurysm repair. These patients can be treated by eather open or endovascular approach, depending on several factors, including aneurysm morphologic suitability for endovascular tretament, age of patient, and comorbidities.The main challange with open repair approach is to maintain renal transplant perfusion during the aortic cross clamping. Several methods of renal transplant perfusion during aneurysm repair have been described. In this case, we opted for open aneurysm repair beacuse of the age of the patient. The femoral venoarterial perfusion technique using extracorporal circulation machine was employed. We found this technique safe and easy in treating such patients.

Real-Time Evaluation of Blood Flow Patterns Using AneurysmFlow for an in vivo Abdominal Aortic Aneurysm Model.

BACKGROUND: Many new tools for abdominal aortic aneurysm (AAA) rupture risk evaluation have been developed. These new tools need detailed hemodynamic information in AAA. However, hemodynamic data obtained from in vivo research are lacking. Thus, the objective of this study was to analyze blood flow patterns in an in vivo AAA model to acquire real-time hemodynamic information using AneurysmFlow, a novel flow evaluation system. METHODS: Digital subtraction angiography images of patients who underwent endovascular aneurysm repair were analyzed using the visualization function of the AneurysmFlow to classify blood flow patterns as laminar or turbulent flow. The presence of boundary layer separation was also evaluated. The time taken for contrast medium to travel from the infrarenal aortic neck to aortic bifurcation was acquired to calculate the flow velocity. Associations between characteristics of aneurysm including lumen occupying ratio of intraluminal thrombus (ILT) and the hemodynamic flow pattern were evaluated. RESULTS: A total of 37 AAA patients was enrolled. Their blood flow patterns were evaluated using the AneurysmFlow. Logistic regression analyses with lumen occupying ratio of ILT as an independent variable showed that the larger the lumen occupying ratio of ILT, the more likely the aneurysm was to show a laminar pattern (P = 0.03), and the more likely the boundary layer separation would not exist (P = 0.04). The flow velocity from the infrarenal aortic neck to the aortic bifurcation showed a positive association with the lumen occupying ratio of the ILT in linear regression analysis (P < 0.001). CONCLUSIONS: Hemodynamic analysis of AAA with the AneurysmFlow using real-time individual patient models showed different flow patterns and flow velocities depending on ILT. This novel analytic approach using AneurysmFlow has potential to play an important role in obtaining clinically meaningful hemodynamic information of AAA.

Chronic Intermittent Hypoxia Regulates CaMKII-Dependent MAPK Signaling to Promote the Initiation of Abdominal Aortic Aneurysm.

Obstructive sleep apnea (OSA) is highly prevalent in patients with abdominal aortic aneurysm (AAA). However, the effects of OSA on AAA initiation in a murine model of sleep apnea have not been completely studied. In this paper, Apoe-/- C57BL/6 mice infused with angiotensin II (Ang II) were placed in chronic intermittent hypoxia (CIH) condition for inducing OSA-related AAA. CIH significantly promoted the incidence of AAA and inhibited the survival of mice. By performing ultrasonography and elastic Van Gieson staining, CIH was found to be effective in promoting aortic dilation and elastin degradation. Immunohistochemical and zymography results show that CIH upregulated the expression and activity of MMP2 and MMP9 and upregulated MCP1 expression while downregulating α-SMA expression. Also, CIH exposure promoted ROS generation, apoptosis, and mitochondria damage in vascular smooth muscle cells (VSMCs), which were measured by ROS assay, TUNEL staining, and transmission electron microscopy. The result of RNA sequencing of mouse aortas displayed that 232 mRNAs were differently expressed between Ang II and Ang II+CIH groups, and CaMKII-dependent p38/Jnk was confirmed as one downstream signaling of CIH. CaMKII-IN-1, an inhibitor of CaMKII, eliminated the effects of CIH on the loss of primary VSMCs. To conclude, a mouse model of OSA-related AAA, which contains the phenotypes of both AAA and OSA, was established in this study. We suggested CIH as a risk factor of AAA initiation through CaMKII-dependent MAPK signaling.

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

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

A reduction in the vascular smooth muscle cell focal adhesion component syndecan-4 is associated with abdominal aortic aneurysm formation.

BACKGROUND: Abdominal aortic aneurysm (AAA) is a serious vascular disease for which there is no effective drug treatment. The incidence of AAA increases significantly as a subject ages, and the molecular mechanism of AAA formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), an important component of focal adhesions, in AAA formation and its association with phenotypic changes in vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: The protein expression levels of SDC4 were significantly decreased in human AAA tissue and those of an AAA mouse model. Moreover, SDC4 knockout (KO) in mice accelerated the formation and rupture of AAAs induced by angiotensin II (Ang II) and calcium chloride (CaCl2 ) Mechanistically, the decrease in SDC4 led to the transformation of cultured VSMCs from a contractile to a secretory phenotype. The RhoA-F/G-actin-myocardin-related transcription factor-A (MRTF-A) signalling pathway was shown to be involved in SDC4-dependent VSMC alteration. Sphingosine-1-phosphate (S1P), a G-protein-coupled receptor, attenuated the AAA formation in SDC4-KO and wild-type (WT) mice in response to Ang II and CaCl2 stimulation. CONCLUSION: We herein demonstrated that silencing SDC4 was associated with increased AAA formation and phenotypic changes in VSMCs via the RhoA-F/G-actin-MRTF-A pathway. These findings indicated that a reduction in SDC4 expression was an important pathological alteration and potential therapeutic target for AAA formation.

Low Shear Stress at Baseline Predicts Expansion and Aneurysm-Related Events in Patients With Abdominal Aortic Aneurysm.

BACKGROUND: Low shear stress has been implicated in abdominal aortic aneurysm (AAA) expansion and clinical events. We tested the hypothesis that low shear stress in AAA at baseline is a marker of expansion rate and future aneurysm-related events. METHODS: Patients were imaged with computed tomography angiography at baseline and followed up every 6 months >24 months with ultrasound measurements of maximum diameter. From baseline computed tomography angiography, we reconstructed 3-dimensional models for automated computational fluid dynamics simulations and computed luminal shear stress. The primary composite end point was aneurysm repair and/or rupture, and the secondary end point was aneurysm expansion rate. RESULTS: We included 295 patients with median AAA diameter of 49 mm (interquartile range, 43-54 mm) and median follow-up of 914 (interquartile range, 670-1112) days. There were 114 (39%) aneurysm-related events, with 13 AAA ruptures and 98 repairs (one rupture was repaired). Patients with low shear stress (<0.4 Pa) experienced a higher number of aneurysm-related events (44%) compared with medium (0.4-0.6 Pa; 27%) and high (>0.6 Pa; 29%) shear stress groups (P=0.010). This association was independent of known risk factors (adjusted hazard ratio, 1.72 [95% CI, 1.08-2.73]; P=0.023). Low shear stress was also independently associated with AAA expansion rate (ß=+0.28 mm/y [95% CI, 0.02-0.53]; P=0.037). CONCLUSIONS: We show for the first time that low shear stress (<0.4 Pa) at baseline is associated with both AAA expansion and future aneurysm-related events. Aneurysms within the lowest tertile of shear stress, versus those with higher shear stress, were more likely to rupture or reach thresholds for elective repair. Larger prospective validation trials are needed to confirm these findings and translate them into clinical management.

Comparison of small symptomatic and asymptomatic abdominal aortic aneurysms based on computational fluid dynamics analysis.

BACKGROUND: The purpose of this study was to compare the hemodynamic parameters of symptomatic and asymptomatic abdominal aortic aneurysms (AAAs) to explore the risk factors for AAA rupture. METHODS: We conducted a retrospective analysis of 26 patients with symptomatic small AAAs and 60 patients with asymptomatic small AAAs. Computational fluid dynamics methods were used to compare hemodynamic characteristics between the symptomatic and asymptomatic groups and to evaluate risk factors for the occurrence of symptomatic AAAs. RESULTS: The maximum diameters in the symptomatic and asymptomatic groups were 49.7 ±â€Š4.94 mm and 48.4 ±â€Š4.55 mm, respectively. Wall shear stress values at turbulent flow regions in the symptomatic and asymptomatic groups were 0.0098 ±â€Š0.0084 Pa versus 0.0174 ±â€Š0.0068 Pa, respectively. Shear stress values at the site with maximal blood flow impact force in the symptomatic and asymptomatic groups were 1.13 ±â€Š0.466 Pa and 2.04 ±â€Š0.42 Pa, respectively. The areas of the intra-luminal thrombus in the section with the maximum diameter in the symptomatic and asymptomatic groups were 952.19 ±â€Š413.53 mm2 versus 646.63 ±â€Š296.88 mm2, respectively. CONCLUSION: The wall shear stress in the symptomatic group was lower than that in the asymptomatic group.

Endograft apposition and infrarenal neck enlargement after endovascular aortic aneurysm repair.

BACKGROUND: Sufficient apposition and oversizing of the endograft in the aortic neck are both essential for durable endovascular aneurysm repair (EVAR). These measures are however not regularly stated on post-EVAR computed tomography angiography (CTA) scan reports. In this study endograft apposition and neck enlargement (NE) after EVAR with an Endurant II(s) endograft were analyzed and associated with supra- and infrarenal aortic neck morphology. METHODS: In 97 consecutive elective patients, the aortic neck morphology was measured on the pre-EVAR CTA scan on a 3mensio vascular workstation. The distance between the lowest renal artery and the proximal edge of the fabric (shortest fabric distance, SFD), and the shortest length of circumferential apposition between endograft and aortic wall (shortest apposition length, SAL) were determined on the early post-EVAR CTA scan. NE, defined as the aortic diameter change between pre- and post-EVAR CTA scan, was determined at eight levels: +40, +30, +20, +15, +10, 0, -5 and -10 mm relative to the lowest renal artery baseline. The aortic neck diameter and preoperative oversizing were correlated to NE with the Pearson correlation coefficient. The effective post-EVAR endograft oversizing is calculated from the nominal endograft diameter and the post-EVAR neck diameter where the endograft is circumferentially apposed. RESULTS: The median time (interquartile range, IQR) between the EVAR procedure and the pre- and post-EVAR CTA scan was 40 (25, 71) days and 36 (30, 46) days, respectively. The Endurant II(s) endograft was deployed with a median (IQR) SFD of 1.0 (0.0, 3.0) mm. The SAL was <10 mm in 9% of patients and significantly influenced by the pre-EVAR aortic neck length (P=0.001), hostile neck shape (P=0.017), and maximum curvature at the suprarenal aorta (P=0.039). The median (interquartile range) SAL was 21.0 (15.0, 27.0) mm with a median (IQR) pre-EVAR infrarenal neck length of 23.5 (13.0, 34.8) mm. The median (IQR) difference between the SAL and neck length was -5.0 (-12.0, 2.8) mm. Significant (P<0.001) NE of 1.7 (0.9, 2.5) mm was observed 5 mm below the renal artery baseline, which resulted in an effective post-EVAR endograft oversizing <10% in 43% of the patients. No correlation was found between NE and aortic neck diameter or preoperative oversizing. CONCLUSIONS: Circumferential apposition between an endograft and the infrarenal aortic neck, SAL, and NE can be derived from standard postoperative CT scans. These variables provide essential information about the post-procedural endograft and aortic neck morphology regardless of the preoperative measurements. Patients with SAL<10 mm or effective oversizing <10% due to NE may benefit from intensified follow-up, but clinical consequences of SAL and NE should be evaluated in future longitudinal studies with longer term follow-up.

Evaluation of physician-modified endografts for the treatment of thoraco-abdominal and pararenal aortic pathologies at a single institution.

BACKGROUND: This study aimed to describe the outcomes of high-risk patients with symptomatic or impending ruptured pararenal aneurysm and thoraco-abdominal aortic aneurysm with comorbidities unsuitable for conventional open surgery, using physician-modified endografts (PMEGs). METHODS: A single-center retrospective analysis was conducted on 59 patients (mean age: 75 years; 47 males) treated with PMEGs between 2017 and 2020. Data on baseline characteristics, procedures, and clinical follow-up were collected to retrospectively analyze early (technical success, perioperative mortality, and major adverse events) and late (patency, endoleak, intervention, aneurysm thrombosis, and survival) outcomes. RESULTS: Technical success was achieved in 96.6% (57/59) of cases. The 30-day mortality rate was 5.1% (3/59). Five patients suffered renal failure and required temporary or permanent dialysis, one developed respiratory failure, and one suffered bowel ischemia. The major stroke rate was 3.4%, the spinal cord injury rate was 0%, and the myocardial infarction rate was 3.4%. During a mean follow-up period of 18.8±9.2 months, one patient suffered upper gastrointestinal bleeding and died after 7 postoperative months. Primary branch patency was observed in 97.2% of target vessels. Estimated freedom from reintervention was 88.1% and 87.5% at 6 months and 1 year, respectively. Five cases of endoleak (one type I, one type II, and three type III) were detected, and 7.1% required reintervention. The aneurysmal lumen thrombosis rate at 1 year was 89.6%. The estimated overall survival rate was 94.9% and 92.9% at 6 and 12 months, respectively. CONCLUSIONS: When used by experienced teams under appropriate anatomical conditions, PMEGs are a safe and effective alternative to open surgery. However, further technical advancement and larger studies with long-term follow-up periods are warranted.

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

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

Aberrant Mitochondrial Dynamics: An Emerging Pathogenic Driver of Abdominal Aortic Aneurysm.

Abdominal aortic aneurysm (AAA) is defined as a progressive segmental dilation of the abdominal aorta and is associated with high mortality. The characterized features of AAA indicate several underlying mechanisms of AAA formation and progression, including reactive oxygen species production, inflammation, and atherosclerosis. Mitochondrial functions are critical for determining cell fate, and mitochondrial dynamics, especially selective mitochondrial autophagy, which is termed as mitophagy, has emerged as an important player in the pathogenesis of several cardiovascular diseases. The PARKIN/PARIS/PGC1α pathway is associated with AAA formation and has been proposed to play a role in mitochondrial dynamics mediated by the PINK/PARKIN pathway in the pathogenesis underlying AAA. This review is aimed at deepening our understanding of AAA formation and progression, which is vital for the development of potential medical therapies for AAA.

Limb Graft Occlusion Following Endovascular Aneurysm Repair for Infrarenal Abdominal Aortic Aneurysm with the Zenith Alpha, Excluder, and Endurant Devices: a Multicentre Cohort Study.

OBJECTIVE: Limb graft occlusion (LGO) is a serious complication after endovascular aneurysm repair (EVAR) and while device development enables treatment of increasingly complex aortic anatomy, little is known about how endograft type affects the risk of occlusion. This observational study aimed to explore the incidence of LGO after EVAR for three major endograft systems. METHODS: All patients with standard EVAR as the primary intervention for infrarenal abdominal aortic aneurysm (AAA), between January 2012 and December 2018, at five Swedish vascular surgery centres, were included in this multicentre retrospective cohort study. LGO was defined as a total limb occlusion regardless of symptoms, or a treated significant stenosis. A nested case control (NCC) design with incidence density sampling of 1:3 was used for analysis of potential per-operative and morphological risk factors. Conditional logistic regression was used to estimate multivariable odds ratios (OR) with 95% confidence intervals (CI) RESULTS: A total of 924 patients were included. The majority were male (84%), the mean age was 76 years (± 7.5 SD), and median AAA diameter was 59 mm (IQR 55, 67). Patients were treated with Zenith Alpha (n = 315, ZISL limbs), Excluder (n = 152, PLC/PXC limbs), and Endurant (n = 457, ETLW/ ETEW limbs). During median follow up of 37 months (IQR 21, 62), 55 occlusions occurred (5.9%); 39 with Zenith Alpha (12.4%), one with Excluder (0.7%), and 15 with Endurant (3.3%). In the NCC analysis, the Zenith Alpha device (OR 5.31, 95% CI 1.97 - 14.3), external iliac artery (EIA) landing (OR 5.91, 95% CI 1.30 - 26.7), and EIA diameter < 10 mm (OR 4.99, 95% CI 1.46 - 16.9) were associated with an increased risk of LGO. CONCLUSION: Endograft device type is an independent risk factor for LGO after EVAR. Specifically, the Zenith Alpha demonstrated an increased risk of LGO compared with the Endurant and Excluder devices. In addition, a narrow EIA and landing zone in EIA are also risk factors for LGO.