Combining Volumetric and Wall Shear Stress Analysis from CT to Assess Risk of Abdominal Aortic Aneurysm Progression.

Background Despite known limitations, the decision to operate on abdominal aortic aneurysm (AAA) is primarily on the basis of measurement of maximal aneurysm diameter. Purpose To identify volumetric and computational fluid dynamics parameters to predict AAAs that are likely to progress in size. Materials and Methods This study, part of a multicenter prospective registry (NCT01599533), included 126 patients with AAA. Patients were sorted into stable (≤10-mL increase in aneurysm volume) and progression (>10-mL increase in aneurysm volume) groups. Initial AAA characteristics of the derivation cohort were analyzed (maximal diameter and surface, thrombus and lumen volumes, maximal wall pressure, and wall shear stress [WSS]) to identify relevant parameters for a logistic regression model. Model and maximal diameter diagnostic performances were assessed in both cohorts and for AAAs smaller than 50 mm by using area under the receiver operating characteristic curve (AUC). Results Eighty-one patients were included (mean age, 73 years ± 7 years [standard deviation]; 78 men). The derivation and validation cohorts included, respectively, 50 and 31 participants. In the derivation cohort, there was higher mean lumen volume and lower mean WSS in the progression group compared with the stable group (60 mL ± 14 vs 46 mL ± 18 [P = .005] and 66% ± 6 vs 53% ± 9 [P = .02], respectively). Mean lumen volume and mean WSS at baseline were correlated to total volume growth (r = 0.47 [P = .002] and -0.42 [P = .006], respectively). In the derivation cohort, a regression model including lumen volume and WSS to predict aneurysm enlargement was superior to maximal diameter alone (AUC, 0.78 vs 0.52, respectively; P = .003); although no difference was found in the validation cohort (AUC, 0.79 vs 0.71, respectively; P = .51). For AAAs smaller than 50 mm, a regression model that included both baseline WSS and lumen volume performed better than maximal diameter (AUC, 0.79 vs 0.53, respectively; P = .01). Conclusion Combined analysis of lumen volume and wall shear stress was associated with enlargement of abdominal aortic aneurysms at 1 year, particularly in aneurysms smaller than 50 mm in diameter. © RSNA, 2020 Online supplemental material is available for this article. See also the editorial by Mitsouras and Leach in this issue.

Incidence, etiology, and management of type III endoleak after endovascular aortic repair.

OBJECTIVE: The objective of this study was to retrospectively assess the incidence, etiology, and management of type III endoleaks in a large cohort of patients treated with endovascular aneurysm repair (EVAR) in two European university centers. METHODS: From 1995 until 2014, 965 EVAR procedures were performed with use of first- and second-generation (n = 79) or third-generation (n = 886) endografts. Radiologic follow-up was performed with computed tomography and abdominal plain film examinations in accordance with the European Collaborators on Stent/graft Techniques for aortic Aneurysm Repair (EUROSTAR) scheme. The potential relationship between the type of endograft and the incidence of type III endoleak and the time interval between initial EVAR and diagnosis of type III endoleak were calculated. RESULTS: Twenty patients (2.1%) were identified with 25 type III endoleaks (n = 10/79 [12.7%] for first- and second-generation endografts and n = 10/886 [1.2%] for third-generation endografts; P < .001). Disconnection was found in 14 of 25 endoleaks (56%) and a fabric defect in 11 of 25 (44%) endoleaks, both without any difference between first- and second- vs third-generation endografts (P = .216). The time interval between initial EVAR and type III endoleak was 3.87 and 5.92 years, respectively, for first- or second-generation and third-generation endografts (P = .148). Twenty-five type III endoleaks were treated using endovascular techniques (n = 22 [88%]) or by open surgical conversion (n = 3 [12%]). CONCLUSIONS: Type III endoleak rarely (2.1%) occurs after EVAR, with a higher incidence in first- and second-generation endografts. In the majority of cases, the underlying mechanism is disconnection of the stent graft components. Type III endoleaks may occur early or late after initial EVAR and can, in most cases, be managed endovascularly, although type III endoleak may recur.

French multicenter experience with the GORE TIGRIS Vascular Stent in superficial femoral and popliteal arteries.

BACKGROUND: Preliminary results in small single-center studies after stenting with the GORE TIGRIS Vascular Stent (W. L. Gore & Associates, Flagstaff, Ariz) show promising short-term primary patency rates, but larger, multicenter studies are needed. This study therefore investigated the performance of the GORE TIGRIS Vascular Stent at three different centers in France in patients with symptomatic peripheral artery disease. METHODS: This retrospective, single-arm, multicenter cohort study included 215 patients with peripheral artery disease (Rutherford-Becker category 2-6) who were treated with the GORE TIGRIS Vascular Stent, a dual-component stent consisting of a nitinol wire frame combined with a fluoropolymer-interconnecting structure. The efficacy end point was primary patency defined by freedom from binary restenosis as derived by duplex ultrasound imaging until 2 years after the intervention. Primary, secondary, and primary assisted patency rates at 3, 6, 12, 18, and 24 months were estimated by Kaplan-Meier analysis. RESULTS: The GORE TIGRIS Vascular Stent was used to successfully treat 239 lesions, of which 141 lesions were located in the superficial femoral artery and 98 in the popliteal artery. Patients were a mean age of 74 ± 12 years. Mean lesion length was 86.8 ± 44.7 mm. After 12 and 24 months, the overall primary patency rates were 81.5% and 67.2%, respectively, and primary assisted patency was 94.9% and 84.8%. Secondary patency was achieved in 99.1% at 24 months. CONCLUSIONS: Our multicenter experience with the GORE TIGRIS Vascular Stent demonstrates continued good results at 2 years for endovascular treatment of challenging obstructive superficial femoral artery and popliteal artery disease.

Results of endovascular aortic arch repair using the Relay Branch system.

OBJECTIVES: Our goal was to evaluate results of endovascular aortic arch repair using the Relay Branch system. METHODS: Forty-three patients with thoracic aortic pathology involving the aortic arch have been treated with the Relay Branch system (Terumo Aortic, Sunrise, FL, USA) in 10 centres. We assessed in-hospital mortality, neurological injury, treatment success according to current reporting standards and the need for secondary interventions. In addition, outcome was analysed according to the underlying pathology: non-dissective disease versus residual aortic dissection (RAD) (defined as remaining dissection after previous type A repair, chronic type B aortic dissections). RESULTS: In-hospital mortality was 9% (0% in patients with RAD). Disabling stroke occurred in 7% (0% in patients with RAD); non-disabling stroke occurred in 19% (7% in patients with RAD). Early type IA and B endoleak formation occurred in 4%. Median follow-up was 16 ± 18 months. During the follow-up period, 23% of the patients died. Aortic-related deaths were low (3% in patients with RAD). CONCLUSIONS: The results of endovascular aortic arch repair using the Relay Branch system in a selected patient population with regard to technical success are good. In-hospital mortality is acceptable, the number of disabling strokes is low and technical success is high. Non-disabling stroke is a major concern, and every effort has to be taken to reduce this to a minimum. The best outcome is seen in patients with underlying RAD. Finally, more data are needed.

Single aortic branch device: the Mona LSA experience.

Endovascular treatment of aortic arch pathologies is challenging due to its complex anatomical architecture and the presence of vital collateral branches. This paper aims to provide an overview of the currently available and future endovascular options for these diseases, particularly regarding branched stent-grafts and the Mona LSA device. After discussing the indications for revascularization of supra-aortic trunks in endovascular aortic repair, we present the principles, benefits and drawbacks of the main modern methods to overcome an insufficient proximal landing zone, i.e. hybrid repair with associated surgical bypass, chimney or snorkel grafts, fenestrated stent-grafts and branched stent-grafts. Subsequently, we detail the technical specifications of the two main branched stent-graft devices under study: the Valiant Mona LSA (Medtronic, Santa Rosa, CA, USA) and the W.L. Gore (Flafstaff, AZ, USA) arch branch device. The steps of the deployment procedure are described from examples of branched stent-graft aortic repair of aortic dissection and aneurysm of the left subclavian artery. Finally, available results of the premarket trial on the Mona LSA branched stent-graft device are recalled. Branched stent grafts represent a promising therapeutic option for pathologies of the aortic arch with insufficient proximal landing zone or mandatory revascularization of supra-aortic trunks. Further studies are needed to specify their indications, long-term effectiveness and safety.

Orthotopic branched endovascular aortic arch repair in patients who cannot undergo classical surgery.

OBJECTIVES: Our goal was to assess the results after orthotopic branched endovascular aortic arch repair using a new double-branch endoprosthesis in patients with thoracic aortic disease affecting the aortic arch who cannot undergo classical surgery. METHODS: Within a 4-year period, 15 patients with thoracic aortic disease affecting the aortic arch were treated with the Bolton Relay plus double-branch endoprosthesis (Bolton Medical, Sunrise, FL, USA). We assessed clinical outcome, occurrence of endoleaks and the need for secondary interventions. The median logistic EuroSCORE I level was 13.6 (4.2; 22.8). RESULTS: The in-hospital mortality rate was 6.7%. A disabling stroke was observed in 1 (6.7%) patient, whereas non-disabling strokes occurred in 2 (13.3%) patients. Type I and III endoleaks occurred in 6.7%. The median follow-up period was 263 (1st quartile 84; 2nd quartile 564) days. Four patients died during the follow-up period. Aortic-related survival was 100%. CONCLUSIONS: Orthotopic branched endovascular aortic arch repair using the Bolton Relay Plus double-branch endoprosthesis is a safe and feasible technique enriching the armamentarium to treat patients with thoracic aortic disease who cannot undergo classical surgery. Aortic-related survival is excellent, and the occurrence of disabling stroke and endoleaks warranting treatment is low. Further studies are needed to assess the long-term durability of this new method.

The neutral sphingomyelinase-2 is involved in angiogenic signaling triggered by oxidized LDL.

Capillaries of the external part of the normal arterial wall constitute the vasa vasorum network. In atherosclerotic lesions, neovascularization occurs in areas of intimal hyperplasia where it may promote plaque expansion, and intraplaque hemorrhage. Oxidized LDL that are present in atherosclerotic areas activate various angiogenic signaling pathways, including reactive oxygen species and the sphingosine kinase/sphingosine-1-phosphate pathway. We aimed to investigate whether oxidized LDL-induced angiogenesis requires neutral sphingomyelinase-2 activation and the neutral sphingomyelinase-2/sphingosine kinase-1 pathway. The role of neutral sphingomyelinase-2 in angiogenic signaling was investigated in Human Microvascular Endothelial Cells (HMEC-1) forming capillary tube on Matrigel and in vivo in the Matrigel plug assay in C57BL/6 mice and in the chicken chorioallantoic membrane model. Low concentration of human oxidized LDL elicits HMEC-1 capillary tube formation and neutral sphingomyelinase-2 activation, which were blocked by neutral sphingomyelinase-2 inhibitors, GW4869 and specific siRNA. This angiogenic effect was mimicked by low concentration of C6-Ceramide and was inhibited by sphingosine kinase-1 inhibitors. Upstream of neutral sphingomyelinase-2, oxidized LDL-induced activation required LOX-1, reactive oxygen species generation by NADPH oxidase and p38-MAPK activation. Inhibition of sphingosine kinase-1 blocked the angiogenic response and triggered HMEC-1 apoptosis. Low concentration of oxidized LDL was angiogenic in vivo, both in the Matrigel plug assay in mice and in the chorioallantoic membrane model, and was blocked by GW4869. In conclusion, low oxLDL concentration triggers sprouting angiogenesis that involves ROS-induced activation of the neutral sphingomyelinase-2/sphingosine kinase-1 pathway, and is effectively inhibited by GW4869.