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Purpose: The purpose of the study was to evaluate the efficacy and safety of pre-emptive transcatheter arterial embolization (P-TAE) of aortic side branches to prevent type II endoleak in patients with abdominal aortic aneurysm after endovascular abdominal aneurysm repair (EVAR)., Materials and Methods: This multicenter, prospective, single-arm trial enrolled 100 patients with abdominal aortic aneurysm from nine hospitals between 2018 and 2021. There were 85 men and 15 women, with a mean age of 79.6 ± 6.0 (standard deviation) years (range: 65-97 years). P-TAE was attempted for patent aortic side branches, including the inferior mesenteric artery, lumbar arteries, and other branches. The primary endpoint was late type II endoleak incidence at 6 months post-repair. Secondary endpoints included changes in aneurysmal sac diameter at 6- and 12 months, complications, re-intervention, and aneurysm-related mortality. Aneurysm sac changes at 6- and 12 months was compared between the late and no-late type II endoleak groups., Results: Coil embolization was successful in 80.9% (321/397) of patent aortic side branches, including 86.3% of the inferior mesenteric arteries, 80.3% of lumbar arteries, and 55.6% of other branches without severe adverse events. Late type II endoleak incidence at 6 months was 8.9% (8/90; 95% confidence interval: 3.9-16.8%). Aneurysm sac shrinkage > 5 mm was observed in 41.1% (37/90) and 55.3% (47/85) of the patients at 6- and 12-months post-EVAR, respectively. Patients with late type II endoleak had less aneurysm sac shrinkage than those without type II endoleak at 12 months (-0.2 mm vs. -6.0 mm; P = 0.040). No patients required re-intervention for type II endoleak, and no aneurysm-related mortalities occurred., Conclusion: P-TAE is safe and effective in preventing type II endoleak, leading to early sac shrinkage at 12 months following EVAR., Competing Interests: Declaration of competing interests The authors declare no actual or potential conflict of interest related to this study., (Copyright © 2024 Société française de radiologie. Published by Elsevier Masson SAS. All rights reserved.)

Background: Although endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA) is widely used worldwide, the fact that it is associated with increased rates of reintervention has been considered a problem. This study aimed to analyze the outcomes of primary open AAA repair and open conversion with explantation of stent grafts after EVAR., Methods: In this retrospective study, we enrolled 1,120 patients (open repair, n = 664; EVAR, n = 456) who underwent AAA repair at Kobe University from 1999 to 2019. Of the 664 patients who underwent open repair, 121 (patients who underwent primary open repair (POR) as a concomitant procedure and patients with ruptured AAA) were excluded from the study. The outcomes of POR were compared with those of open conversion with explantation of stent grafts., Results: Of the 543 patients who underwent open repair, 513 underwent POR and 30 underwent open conversion with explantation of stent grafts. The operation time for POR was significantly less than that for open conversion with explantation. During surgery, patients who underwent open conversion with explantation required significantly more transfusions of red cell concentrate, fresh frozen plasma, and platelet concentrate than those who underwent POR. Overall, 30 patients who underwent open conversion with explantation required a total of 48 reinterventions before surgery. Hospital mortality rates were 0.7% and 0% in the POR and open conversion with explantation groups, respectively (P = 0.62). Although overall survival at 5 years in the POR group was significantly better than that in the open conversion with explantation group (89.3 ± 1.7% vs. 79.5 ± 9.6%; P = 0.01), there were no significant differences between the 2 groups regarding the freedom from aortic event (hospital death, reintervention, and aortic death). According to the multivariate analysis, open conversion with explantation was not an independent risk factor for late death. There were 20 patients who were hesitant to undergo OCE, although we recommended OCE. In a subgroup analysis, the overall mean cost borne by patients who underwent EVAR was approximately 2.3 times higher compared with that borne by patients who underwent POR., Conclusions: Although demanding, both early and long-term outcomes of OCE have been favorable in our present study. OCE is highly recommended in patients with persistent sac enlargement after EVAR., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Purpose: To evaluate the effectiveness and safety of pre-emptive transcatheter arterial embolization (P-TAE) for aortic side branches (ASBs) to prevent Type 2 endoleaks (EL2) before endovascular aneurysm repair (EVAR) using the Excluder stent-graft system (Excluder)., Materials and Methods: In this prospective, multicenter study, 80 patients (mean age, 79.1 years [SD ± 6.7]; 85.0% were men; mean aneurysmal sac diameter, 48.4 mm [SD ± 7.4]) meeting the eligibility criteria were prospectively enrolled from 9 hospitals. Before EVAR, P-TAE was performed to embolize the patent ASBs originating from the abdominal aortic aneurysm. Contrast-enhanced computed tomography (CT) was performed at 1 month and 6 months after EVAR. The primary endpoint was EL2 incidence at 6 months, and the secondary endpoints were aneurysmal sac diameter changes at 6 and 12 months, P-TAE outcomes, adverse events related to P-TAE, reintervention, and aneurysm-related mortality., Results: All patients successfully underwent P-TAE without serious. Coil embolization was successful in 81.6% of ASBs. EL2 incidence at 6 months was identified in 18 of 70 (25.7%) patients. Aneurysmal sac diameter shrinkage (≥5 mm) was observed in 30.0% of patients at 6 months and in 40.9% at 12 months. Only 1 patient required reintervention for EL2 within 1 year of EVAR; aneurysm-related deaths were not observed., Conclusions: P-TAE for ASBs before EVAR using Excluder is a safe and effective strategy. It aids in achieving early aneurysmal sac shrinkage and reduces EL2 reintervention at 1 year after EVAR., (Copyright © 2024 SIR. Published by Elsevier Inc. All rights reserved.)

Purpose: The present study analyzed the outcomes of our experience with abdominal aortic aneurysm (AAA) repair over 20 years using endovascular aortic repair (EVAR) with commercially available devices or open aortic repair (OAR) and reviewed our surgical strategy for AAA., Methods: From 1999 to 2019, 1077 patients (659 OAR, 418 EVAR) underwent AAA repair. The OAR and EVAR groups were compared retrospectively, and a propensity matching analysis was performed., Results: EVAR was first introduced in 2008. Our strategy was changed to an EVAR-first strategy in 2010. Beginning in 2018, this EVAR-first strategy was changed to an OAR-first strategy. After propensity matching, the overall survival in the OAR group was significantly better than that in the EVAR group at 10 years (p = 0.006). Two late deaths due to AAA rupture were identified in the EVAR group, although there were no significant differences between the OAR and EVAR groups with regard to the freedom from AAA-related death at 10 years. The rate of freedom from aortic events at 10 years was significantly higher in the OAR group than in the EVAR group (p < 0.0001)., Conclusion: The rates of freedom from AAA-related death in both the OAR and EVAR groups were favorable, and the rate of freedom from aortic events was significantly lower in the EVAR group than in the OAR group. Close long-term follow-up after EVAR is mandatory., (© 2023. The Author(s).)

Background: Abdominal aortic aneurysm (AAA) is a life-threatening cardiovascular disease characterized by dilated abdominal aorta. Immune cells have been shown to contribute to the development of AAA, and that the gut microbiota is associated with numerous diseases, including cardiovascular diseases, by regulating immune systems or metabolic pathways of the host. However, the interaction between the gut microbiota and AAA remains unknown., Methods: Apolipoprotein E-deficient male mice were fed a high-cholesterol diet and divided into three groups: the control group was maintained under normal water (control group), the oral AVNM group was maintained under drinking water supplemented with ampicillin, vancomycin, neomycin, and metronidazole, and the i.p. AVNM group was injected AVNM intraperitoneally. After 1 week of pretreatment with antibiotics, these mice were administrated Ang II via subcutaneous osmotic pumps for 4 weeks and euthanized to evaluate AAA formation., Results: Depletion of gut microbiota by oral AVNM ameliorated the incidence of AAAs (control group: 58.9% versus oral AVNM group: 28.6% versus i.p. AVNM group: 75.0%, P = 0.0005) and prevented death due to ruptured aneurysms (control group: 11% versus oral AVNM group: 0% versus i.p. AVNM group: 15%). Oral AVNM suppressed monocyte storage in the spleen, but not in other organs. Despite possessing a higher level of cholesterol, recruitment of monocytes into the suprarenal aorta was suppressed in the oral AVNM group. In AVNM drinking mice, NOD1 ligand, a kind of PRR ligands, increased the development of AAAs and accumulation of macrophages in the aortae., Conclusions: The gut microbiota plays a critical role in AAA formation. Therefore, regulation of the microbiota or the immune system can be a therapeutic approach for AAA.

The effect of acute kidney injury (AKI) on mid-term outcomes following thoracoabdominal aortic aneurysm (TAAA) repair is not well known. We hypothesized that postoperative AKI would reduce mid-term survival and aimed to analyze the effect of AKI on mid-term outcomes after TAAA repair. This retrospective study identified 294 consecutive TAAA repairs at Kobe University Hospital from October 1999 to March 2019. Patients with preexisting end-stage renal disease that required hemodialysis (n = 11) and patients who died intraoperatively (n = 2) were excluded. Finally, 281 patients were analyzed. AKI was defined according to Kidney Disease: Improving Global Outcomes guidelines (KDIGO) classification. Of the 281 patients, 178 (63.3%) developed AKI, of which 98 (34.9%) had mild, 34 (12.1%) had moderate, and 46 (16.4%) had severe AKI. Twenty-six patients (12.8%) required renal replacement therapy after surgery. Twenty-three in-hospital deaths (8.2%) were recorded, including 2 (0.7%) without AKI, 0 (0%) with mild AKI, 1 (0.4%) with moderate AKI, and 20 (7.1%) with severe AKI (p < .001). The 4-year survival was 91.9 ± 3.0% for no AKI, 91.3 ± 3.2% for mild AKI, 72.4 ± 8.5% for moderate AKI and 32.6 ± 7.4% for severe AKI (p < .001). Multivariable Cox-hazard regression analysis demonstrated that moderate and severe AKI, older age and emergency surgery were significant risk factors for mid-term survival. In patients undergoing TAAA repair, severe AKI was associated with an increase in in-hospital mortality and both moderate and severe AKI were negatively associated with mid-term survival. Preventing moderate/severe AKI may improve mid-term survival after TAAA repair., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Purpose: To evaluate the mid-term outcomes of transarterial embolization (TAE) for type II endoleak after endovascular abdominal aortic aneurysm repair (EVAR) and investigate the predictors of sac enlargement after embolization., Materials and Methods: We conducted a retrospective analysis of 55 patients [48 men and 7 women, median age 79.0 (interquartile ranges 74-82) years] who underwent TAE for type II endoleak from 2010 to 2018. The aneurysmal sac enlargement, endoleaks, aneurysm-related adverse event rate, and reintervention rate were evaluated. Patients' characteristics and clinical factors were evaluated for their association with sac enlargement., Results: Fifty-five patients underwent TAE with technical success and were subsequently followed for a median of 636 (interquartile ranges 446-1292) days. The freedom from sac enlargement rates at 1, 3, and 5 years was 73.2%, 32.0%, and 26.7%, respectively. After initial TAE, the recurrent type II, delayed type I, and occult type III endoleak were identified in 39 (71%), 5 (9%), and 3 (5%) patients, respectively. Although a patient had aorto-duodenal fistula, there was no aneurysm-related death. The freedom from reintervention rates was 84.6%, 35.7%, and 17.0%, respectively. In the multivariate analysis, sac diameter > 55 mm at initial TAE (hazard ratios, 3.23; 95% confidence intervals, 1.22-8.58; P < 0.05) was a significant predictor of sac enlargement., Conclusion: TAE for type II endoleak was not effective in preventing sac enlargement, and reinterventions were required among the mid-term follow-up. The sac diameter > 55 mm at initial TAE was a significant predictor of sac enlargement.

Objective: Vitamin B2 (riboflavin) reportedly has an antioxidant effect through superoxide dismutase (SOD) activation. However, the effect of riboflavin on abdominal aortic aneurysm (AAA) has never been investigated. In the present study, we examined the hypothesis that riboflavin has a protective effect on AAA formation in an experimental rat model., Methods: The AAA model, which was induced with intraluminal elastase and extraluminal calcium chloride, was created in 36 rats. The 36 rats were divided into a riboflavin group (group R; 25 mg/kg/d), and control group (carboxymethyl cellulose). Riboflavin administration by gastric gavage once per day was started at 3 days before aneurysm preparation. On day 3, SOD activity in aneurysm walls was assayed. On day 7, reactive oxygen species (ROS) levels were semiquantified by dihydroethidium staining, and the oxidation product of DNA produced by ROS, 8-hydroxydeoxyguanosine (8-OHdG), was measured by immunohistochemical staining. Histopathologic examination (hematoxylin/eosin and elastica Van Gieson staining) was performed on day 28, and the AAA dilatation ratio was calculated to evaluate the protective effect of riboflavin., Results: On day 3, SOD activity was significantly increased in aneurysm walls by riboflavin administration (370 ± 204 U/mL in normal, 334 ± 86 U/mL in control, 546 ± 143 U/mL in group R; P = .021). On day 7, ROS levels and 8-OHdG-positive cells in aneurysm walls were significantly decreased by riboflavin treatment (ROS levels: 1.0 ± 0.1 in normal, 4.5 ± 0.4 in control, 3.1 ± 0.5 in group R, P < .01; 8-OHdG-positive cells: 30 ± 2 cells in normal, 148 ± 20 cells in control, 109 ± 15 cells in group R, P < .01). Riboflavin treatment significantly reduced matrix metalloproteinase (MMP)-9 messenger RNA expression in aneurysm walls (relative expression: MMP-9: 0.4 ± 0.7 in normal, 2.6 ± 1.3 in control, 0.5 ± 0.3 in group R, P < .01). On day 28, the aortic walls were less dilated and had higher elastin content in group R than in control (dilatation ratio: 194.9% ± 10.9% in control, 158.6% ± 2.5% in group R; P <.01)., Conclusions: Riboflavin treatment prevents AAA formation in a rat model through an antioxidant effect and might be a potent pharmacologic agent for AAA treatment in clinical practice., (Copyright © 2016 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Purpose: To demonstrate the protective effect of glucagon-like peptide 1 (GLP-1) signaling on the cardiovascular system, we conducted this study to show that the GLP-1 receptor analog (lixisenatide) could inhibit abdominal aortic aneurysm (AAA) development in rats., Methods: Lixisenatide was injected subcutaneously 7 days after aneurysm preparation. We evaluated reactive oxygen species (ROS) expression by dihydroethidium staining and 8-hydroxydeoxyguanosine (8-OHdG; the oxidation product of DNA) by immunohistochemical staining. We also analyzed the effect of GLP-1 signaling on the inflammatory response. Histopathological examination was done on day 28, and the AAA dilatation ratio was calculated., Results: On day 14, ROS expression and 8-OHdG-positive cells in the aneurysm walls were seen to have been significantly decreased by lixisenatide treatment. Western blot analysis showed decreased ERK expression. There was significantly reduced tumor necrosis factor-α mRNA expression in the aneurysm walls and CD68-positive cell infiltration in the aneurysm walls. On day 28, it was evident that the lixisenatide had dramatically reduced aneurysm development in the rats., Conclusion: GLP-1 elevation inhibits AAA development in rats through its anti-oxidant and anti-inflammatory effects. Thus, GLP-1 could be a potent pharmacological target for AAA treatment.

Objective: Abdominal aortic aneurysms (AAAs) are associated with oxidative stress and inflammatory response. We investigated the hypothesis that the known antioxidant ascorbic acid, which can also promote elastin and collagen production by smooth muscle cells, would prevent AAA formation in a rat model., Methods: An intraluminal elastase and extraluminal calcium chloride-induced rat AAA model was used, and the animals were divided into three groups: control (group C, n = 18), the aorta wrapped with a saline-impregnated gelatin hydrogel sheet (group G, n = 18), and the aorta wrapped with a gelatin hydrogel sheet incorporating ascorbic acid (group A, n = 18). Wrapping of the sheet was completed at the end of treatment for AAA creation. The aortic dilatation ratio was measured, and aortic tissues were further examined for oxidative stress and oxidative DNA damage using biochemical and histologic techniques., Results: Aortic dilatation at both 4 and 8 weeks was inhibited in group A (dilatation ratio [%] at 4 weeks: 186.2 ± 21.8 in group C, 152.3 ± 10.2 in group G, 126.8 ± 11.6 in group A; P < .0001; dilatation ratio [%] at 8 weeks: 219.3 ± 37.5 in group C, 194.0 ± 11.6 in group G, 145.7 ± 8.3 in group A; P = .0002). Elastin and collagen content were significantly preserved in group A (elastin, P = .0015; collagen, P < .0001). The messenger RNA expressions of matrix metalloproteinase (MMP)-9, monocyte chemotactic protein-1, interleukin-1β, and tissue necrosis factor-α (P = .0024, P < .0001, P < .0001, and P < .0001, respectively) were downregulated in group A (P = .0024), whereas tissue inhibitors of metalloproteinase (TIMP)-1 and TIMP-2 were both upregulated in group A (TIMP-1, P = .0014; TIMP-2, P < .0001). Gelatin zymography showed activities of pro-MMP-2, MMP-2, and MMP-9 were significantly suppressed in group C (P < .0001 for each). Reactive oxygen species expression and 8-hydroxydeoxyguanosine and cluster of differentiation 68 staining were significantly suppressed in group A (reactive oxygen species expression, P < .0001; 8-hydroxydeoxyguanosine-positive cells, P < .0001; cluster of differentiation 68 positive cells, P < .0001)., Conclusions: Controlled release of ascorbic acid using gelatin hydrogel sheet-attenuated AAA formation through antioxidant and anti-inflammatory effect, regulation of MMP-2, TIMP-1, and TIMP-2, and preserving elastin and collagen in this animal model., (Copyright © 2014 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: Dipeptidyl peptidase-4 (DPP-4) inhibitor, a novel antidiabetic drug, has a cardioprotective effect on ischemia-reperfusion injury through an antioxidant effect. However, the effect of DPP-4 inhibitor on aneurysm formation has not been investigated. We aimed to test the hypothesis that the DPP-4 inhibitor, alogliptin, attenuates vascular oxidative stress and thus inhibits abdominal aortic aneurysm (AAA) formation., Methods: AAAs were created with intraluminal elastase and extraluminal calcium chloride in 36 male rats. Rats were divided into three groups: a low dose of alogliptin group (group LD; 1 mg/kg/d), a high-dose group (group HD; 3 mg/kg/d), and a control group (group C, water). Alogliptin was administered by gastric gavage once daily beginning 3 days before surgery. On day 7 after aneurysm preparation, reactive oxygen species (ROS) expression was semiquantified by dihydroethidium staining, and the oxidation product of DNA produced by ROS, 8-hydroxydeoxyguanosine (8-OHdG), was measured by immunohistochemical staining. Blood glucose concentrations were measured. Hematoxylin and eosin and elastica Van Gieson stainings were performed on day 28, and the AAA dilatation ratio was calculated., Results: On day 7 (six in each group), dihydroethidium staining of the aneurysm wall showed a reduced level of ROS expression (4.6 ± 0.6 in group C, 2.7 ± 0.3 in group LD, and 1.7 ± 0.5 in group HD; P < .0001) and showed fewer 8-OHdG-positive cells in alogliptin-treated samples (138.1 ± 7.4 cells in group C, 102.5 ± 4.5 cells in group LD, and 66.1 ± 4.5 cells in group HD; P < .0001) The treatment significantly reduced messenger RNA expression of matrix metalloproteinases (MMPs) in aneurysm walls (relative expression: MMP-2: 2.1 ± 0.4 in group C, 1.3 ± 0.3 in group LD, and 0.9 ± 0.2 in group HD; P < .001; MMP-9: 2.0 ± 0.5 in group C, 0.3 ± 0.3 in group LD, and 0.3 ± 0.2 in group HD; P < .001). On day 28 (six in each group), the aortic wall in groups LD and HD was less dilated (dilatation ratio: 199.2% ± 11.8% in group C, 159.6% ± 2.8% in group LD, and 147.1% ± 1.9% in group HD; P < .02 group C vs HD) and had higher elastin content than in group C. The difference in blood glucose levels among the three groups was not significant., Conclusions: The DPP-4 inhibitor, alogliptin, attenuates aneurysm formation and expansion dose-dependently in a rat AAA model via an antioxidative action., (Copyright © 2014 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: An ideal pharmaceutical treatment for abdominal aortic aneurysm (AAA) is to prevent aneurysm formation and development (further dilatation of pre-existing aneurysm). Recent studies have reported that oxidative stress with reactive oxygen species (ROS) is crucial in aneurysm formation. We hypothesized that edaravone, a free-radical scavenger, would attenuate vascular oxidative stress and inhibit AAA formation and development., Methods: An AAA model induced with intraluminal elastase and extraluminal calcium chloride was created in 42 rats. Thirty-six rats were divided three groups: a low-dose (group LD; 1 mg/kg/d), high-dose (group HD; 5 mg/kg/d), and control (group C, saline). Edaravone or saline was intraperitoneally injected twice daily, starting 30 minutes before aneurysm preparation. The remaining six rats (group DA) received a delayed edaravone injection (5 mg/kg/d) intraperitoneally, starting 7 days after aneurysm preparation to 28 days. AAA dilatation ratio was calculated. Pathologic examination was performed. ROS expression was semi-quantified by dihydroethidium staining and the oxidative product of DNA induced by ROS, 8-hydroxydeoxyguanosine (8-OHdG), by immunohistochemical staining., Results: At day 7, ROS expression and 8-OHdG-positive cells in aneurysm walls were decreased by edaravone treatment (ROS expression: 3.0 ± 0.5 in group LD, 1.7 ± 0.3 in group HD, and 4.8 ± 0.7 in group C; 8-OHdG-positive cells: 106.2 ± 7.8 cells in group LD, 64.5 ± 7.7 cells in group HD, and 136.6 ± 7.4 cells in group C; P < .0001), compared with group C. Edaravone treatment significantly reduced messenger RNA expressions of cytokines and matrix metalloproteinases (MMPs) in aneurysm walls (MMP-2: 1.1 ± 0.5 in group LD, 0.6 ± 0.1 in group HD, and 2.3 ± 0.4 in group C; P < .001; MMP-9: 1.2 ± 0.1 in group LD, 0.2 ± 0.6 in group HD, and 2.4 ± 0.2 in group C; P < .001). At day 28, aortic walls in groups LD and HD were less dilated, with increased wall thickness and elastin content than those in group C (dilatation ratio: 204.7% ± 16.0% in group C, 156.5% ± 6.6% in group LD, 136.7% ± 2.0% in group HD; P < .0001). Delayed edaravone administration significantly prevented further aneurysm dilatation, with increased elastin content (155.2% ± 2.9% at day 7, 153.1% ± 11.6% at day 28; not significant)., Conclusions: Edaravone inhibition of ROS can prevent aneurysm formation and expansion in the rat AAA model. Free-radical scavenger edaravone might be an effective pharmaceutical agent for AAA in clinical practice., (Copyright © 2012 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: The altered structure and composition of the vascular extracellular matrix (ECM) influences the formation of abdominal aortic aneurysms (AAA). Transglutaminase type 2 (TG2), which is a Ca(2+)-dependent cross-linking enzyme, has been proven the importance for ECM homeostasis, but there is no evidence of TG2 in AAA formation. The hypothesis was investigated that TG2 contributes to protect aortic walls during remodeling of the AAAs., Methods: In a rat abdominal aortic aneurysm model using a combination of intraluminal elastase infusion and extraluminal calcium chloride, TG2 expression and activity were evaluated at 1 and 8 weeks after the AAA preparation (n = 6 at each endpoint), compared with those of the non-prepared aorta (n = 6). Additionally, ex vivo experiments of isolated AAA tissue culture with recombinant human TG2, TG2 inhibitor cystamine, or tissue necrosis factor (TNF)-α were performed., Results: TG2 mRNA expression in the AAAs was significantly upregulated at both 1 and 8 weeks (22.4-fold and 5.4-fold increases of the non-prepared aorta, P = .0022 and P = .0048, respectively). TG2 protein expression and activity were also enhanced by fluorescent staining of the AAAs. Similar mRNA upregulation of TNF-α, interleukin-1β, matrix metalloproteinases (MMP)-2, MMP-9, and tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2 was observed in the AAAs, and TG2 and TNF-α were colocalized in the aortic walls at 1 week. Ex vivo experiments showed that mRNA expressions of TNF-α, MMP-2, and MMP-9 in the cultured AAA tissue were decreased by exogenous TG2, whereas were increased by cystamine. TNF-α exposure to the AAA tissues was significantly upregulated TG2 mRNA expression (P = .0333)., Conclusion: TG2 expression and activity in AAA formation were enhanced, possibly due to compensatory reaction. TG2 has a potential role of ECM protector in aortic walls during remodeling of the AAAs., (Copyright © 2010 Society for Vascular Surgery. All rights reserved.)

Objective: An ideal animal model of abdominal aortic aneurysm (AAA) is of great importance for clarifying unknown complex mechanisms of the pathogenesis. We introduce a new, simple technique to create reliable AAAs that simulate human aneurysms., Methods: Experimental models of AAAs were created in 71 rats by means of a 20-minute application of intraluminal elastase (30 U) and extraluminal calcium chloride (0.5M) in the 1-cm segment of infrarenal abdominal aorta (group EC, n = 26). A single application of elastase (group E, n = 24) or calcium chloride (group C, n = 21) was used as control. The treated aorta in each group was measured under physiologic conditions and harvested at 1 and 4 weeks. Successful AAA formation was defined as a dilation ratio >50%. Inflammatory response, elastolytic activity, and histology in the treated aorta were evaluated among the three groups., Results: The surgical procedure in each group was similarly completed for approximate 30 minutes and performed without any technical failure or operative death. At 4 weeks, the dilation ratio and wall thickness were 94.8% +/- 9.9% and 125.4 +/- 5.6 microm in group EC, 43.3% +/- 6.3% and 149.6 +/- 6.5 microm in group E, and 10.9% +/- 4.2% and 152.9 +/- 7.2 microm in group C. The success rate of AAA formation in group EC (92.7%) was significantly higher than that in group E (25.0%) and group C (0.0%). Less elastin content in the aortic wall was observed in group EC. At 1 week, tumor necrosis factor-alpha and interleukin-1beta messenger RNA (mRNA) expressions were significantly upregulated, and CD3+ and CD11b+ cells were significantly infiltrated into the treated aorta of group EC, compared with groups E or C. Gelatinolytic activities and mRNA expressions of matrix metalloproteinase (MMP)-2 and MMP-9 were also significantly activated in group EC., Conclusion: The rat AAA model using a combination of intraluminal elastase infusion and extraluminal calcium chloride exposure is simple and easy to perform and is highly reliable and reproducible to create a saccular aneurysm similar to human AAAs. This model could be more useful to clarify AAA pathogenesis, mechanisms, and treatment interventions in experimental researches.

The optimal approach to abdominal aortic aneurysm with horseshoe kidney is still debated. We describe a successful abdominal aortic aneurysm repair through a left retroperitoneal approach in a 77-year-old woman with a horseshoe kidney.

Background: The purpose of this study is to investigate the influence of perioperative circulation on spinal cord during the repair of descending thoracic or thoracoabdominal aortic aneurysms., Methods: From October 1999, 92 patients (aged 66 +/- 13 years; 65 men) underwent the repair of descending thoracic (n = 30) or thoracoabdominal aortic aneurysm (Crawford I, 9; II, 14; III, 35; IV, 4). We measured the time duration of hypotension, defined as follows, and evaluated the relationship between the incidence of paraplegia and each duration: T1, systolic arterial pressure less than 80 mm Hg, or mean pressure less than 60 mm Hg during aortic cross-clamping; T2, distal aortic pressure less than 60 mm Hg during aortic cross-clamping; T3, systolic arterial pressure less than 80 mm Hg after coming off bypass; T4, systolic arterial pressure less than 80 mm Hg in the intensive care unit., Results: Hospital mortality was 8% (7 patients). Neurologic deficits occurred in 10 patients (10.9%). The T1 and T2 periods showed no difference between paraplegia cases (group P) and normal cases (group N). The T3 periods in both groups were 54 +/- 52 and 6.6 +/- 18, and the T4 periods were 62 +/- 89 and 2.3 +/- 14, respectively. The T3 and T4 periods in group P were significantly longer than in group N (p < 0.0001). Multivariate analysis demonstrated that T3 was an independent risk factor for paraplegia. When divided according to body temperature, the T2 period under mild hypothermia was significantly longer in group P than in group N, as well as the T3 and T4 periods., Conclusions: Perioperative hemodynamics stability is of vital importance for spinal cord protection during thoracoabdominal aortic surgery. In particular, the duration of hypotension after coming off bypass was an independent risk factor for paraplegia.

Background: The purpose of this study was to evaluate the efficacy of myogenic transcranial motor evoked potentials (tc-MEPs) for spinal cord ischemia in the repair of descending thoracic or thoracoabdominal aortic aneurysms., Methods: Intraoperative tc-MEPs was used in 72 patients who underwent the repair of descending thoracic (n = 24) or thoracoabdominal aortic aneurysms (n = 49) classed as Crawford I in 10 patients, II in 12, III in 23, and IV in 3. There were 52 men and 20 women, and their mean age was 64.9 +/- 12.8 years. Tc-MEPs were recorded by transcranial electrical stimulation and compound muscle action potentials., Results: The hospital mortality rate was 5.6% (n = 4), and the incidence of neurologic deficits was 11.1% (n = 8). All patients whose MEP amplitude recovered to more than 75% of the baseline showed normal spinal function, and 8 of 9 patients whose MEP amplitude decreased to below 75% of the baseline at the end of the procedure showed neurologic deficits postoperatively. The sensitivity of tc-MEPs was 100% and specificity was 98.4%. Latency in patients with postoperative paraplegia was 123% +/- 9% and was significantly prolonged at the end of the procedure., Conclusions: Tc-MEPs were very sensitive and specific to spinal cord ischemia with reduced amplitude and prolongation of the latency period. Tc-MEPs are considered a useful monitor of spinal cord ischemia during descending thoracic or thoracoabdominal aortic surgery.

A 52-year-old man underwent a replacement of the thoracoabdominal aorta. The aorta was severely calcified, and was replaced by a 24-mm woven Dacron (Vascutek, Renfrewshire, Scotland) graft wrapped with the calcificated aneurysmal wall. His postoperative course was uneventful; however, he collapsed on the 18th postoperative day. He underwent an emergent thoracotomy and the wrapped aneurysmal wall was taken down. The prosthesis graft had a 1-mm disruption in the middle portion, which did not relate to the anastomoses. Experimental study ex vivo showed that disruption of the prosthesis could have occurred after a 3-week pulsatile force caused by a seashell simulating aortic calcification.

A 75-year-old woman presented with superior mesenteric artery and celiac artery occlusion associated with acute type B dissection. Emergent bypass grafting by using the right gastroepiploic artery and the left radial artery for the superior mesenteric artery and the celiac artery was performed without bowel resection.

Background: Aortic dissection after femoral arterial perfusion has been reported as a dreadful complication. Apart from such a drastic event, using intraoperative transesophageal echocardiography we detected aortic dissection confined to the abdominal aorta that was associated with visceral malperfusion., Methods: We examined 11 consecutive patients with aortic dissection in whom the abdominal aorta was intact, and surgeries were performed with femoral perfusion. The abdominal aorta and visceral branches were examined for new development of dissection or malperfusion by means of transesophageal echocardiography before, during, and after cardiopulmonary bypass. These echocardiographic findings were then related to the postoperative assessment and midterm results., Results: Aortic dissection was found in 3 of 11 cases (27.2%). Unusual progression of metabolic acidosis (base excess < or =10 mEq/L) occurred, possibly as a result of malperfusion of visceral arteries, in 2 of these 3 cases, whereas none of the 8 cases presented with such findings. The presence of dissection was later confirmed by postoperative computed tomography in all but 1 case. In the midterm follow-up period, aneurysm formation was found in the infrarenal aorta and iliac arteries in 2 of the 3 cases with new aortic dissection but not in any of the remaining 8 cases., Conclusions: New development of aortic dissection after femoral arterial perfusion was found in 27% of the cases in this series. Although these occurred without dramatic symptoms, this event may be related to unusual metabolic acidosis during cardiopulmonary bypass or to subsequent aneurysmal formation of the infrarenal aorta or iliac arteries, or both.

Objective: Of 125 surgical patients with abdominal aortic aneurysm (AAA) treated from 1999, 11 patients with deep shock from ruptured AAAs who underwent aortic occlusion balloon catheter (AOBC) insertion before laparotomy were studied., Methods: With the patients under local anesthesia, the brachial artery was exposed and the balloon catheter was inserted into the thoracic aorta. The balloon was inflated halfway and pulled back gently to the orifice of the left subclavian artery, and was advanced with the aid of blood flow down to the abdominal aorta. After full inflation of the balloon, the catheter was pulled until the balloon was fixed at the proximal shoulder of the AAA., Results: AOBC insertion was completed within 16.1 +/- 5.1 minutes. Systolic blood pressure at presentation was 84.1 +/- 31.7 mm Hg, deteriorated to 60.9 +/- 15.4 mm Hg on arrival in the operating room, and increased significantly (P <.0001) to 123.4 +/- 25.3 mm Hg after AOBC insertion. The balloon burst in three patients. Embolic complications were observed in two patients. There were three deaths, two associated with the balloon bursting. In nine patients whose shock was successfully controlled by AOBC, operative mortality was 11%., Conclusion: Transbrachial arterial insertion of an AOBC may be useful to ameliorate hemorrhagic shock in patients with ruptured AAAs.