[Bio-Bentall Procedure in Patients Over 65 Years of Age].

OBJECTIVE: This study aimed to review the results of the bio-Bentall procedure in patients over 65 years of age at our hospital. MATERIALS AND METHODS: Of the 65 aortic root replacement procedures performed at our hospital from October 2015 to January 2024, we reviewed 45 bio-Bentall procedures performed on patients 65 years of age or older. These patients consisted of 39 men and 6 women, with a mean age of 72 years. There were 5 patients with aortic dissection and 40 patients with non-dissection, and 6 patients had reoperation. There were 19 concomitant surgeries, including coronary artery bypass grafting, valve surgery, and aortic procedure. The bioprosthetic valves used were Magna EASE in 17 patients, Inspiris in 25 patients, Trifecta in 2 patients, and Avalus in 1 patient. All Valsalva grafts used were J Graft Valsalva. RESULTS: The mean intubation time was 19 hours, and the mean intensive care unit( ICU) stay was 6 days. The number of in-hospital deaths was 3 patients, and the mean length of hospital stay was 18 days. The remote mortality rate was 4( 1 heart failure, 2 lung cancer, and 1 pancreatic cancer). There have been no case of reoperation, structural valve deterioration (SVD), or thromboembolism to date, and the rates of freedom of reoperation, SVD, and thromboembolism were all 100%. The 1-, 3-, 5-, and 7-year survival rates were 91.1%, 86.4%, 83.6%, and 83.6%, respectively. CONCLUSION: The surgical and long-term outcomes of the bio-Bentall procedure in patients over 65 years of age were stable. In patients who may outlive the bioprosthetic valve life, it is important to perform an appropriate and durable Bentall procedure, including valve-in-valve, prioritizing the future of each patient.

[Acute Aortic Dissection Complicated by Lower Limb Ischemia:Evaluation of Ischemic Severity and Appropriate Surgical Technique].

The International Registry of Aortic Dissection (IRAD) reported that the incidence of limb ischemia in Stanford type A aortic dissection( TAAD) was 17%. The incidence of lower limb ischemia in Stanford type B aortic dissection( TBAD) ranged from 5.7% to 30.0%, and in-hospital mortality was high in patients with lower limb ischemia complications. The reasons for this are:ischemia of other organs, especially intestinal ischemia, often coexists in patients with lower limb ischemia, resulting in a high incidence of myonephropathic metabolic syndrome (MNMS);thoracic aortic open surgery is often prioritized under the concept of central repair, and prolonged lower limb ischemia time results in compartmentalization due to ischemia-reperfusion injury. The prolonged ischemic time in the lower extremity results in a high rate of compartment syndrome, MNMS, due to ischemia-reperfusion injury. Therefore, appropriate management of these two major complications is an important factor in saving the lives of patients with acute aortic dissection complicated by lower extremity ischemia. Because the possibility of saving a patient's life is improved by prompt diagnosis and treatment, a team approach is required to save lives and save limbs in close collaboration not only with surgeons but also with other departments and multiple professions.

Surgical revision of failed MitraClip procedure for atrial functional mitral regurgitation.

The MitraClip system is used for patients with severe mitral regurgitation (MR) who are at high risk for open surgery. However, some patients need surgical revision for various complications. The acute outcome of MitraClip treatment for atrial functional MR (aFMR) is scarcely reported. Herein, we describe a rare case of an 80-year-old woman treated with a MitraClip for aFMR with mitral annular dilatation and failed leaflet adaptation. The patient suffered from single leaflet device attachment (SLDA) and posterior leaflet injury 3 days posttreatment. The patient successfully underwent mitral valve replacement. The postoperative pulmonary hypertension was markedly improved and the left atrial volume was reduced. A MitraClip should be carefully used for aFMR with mitral annular dilatation and failed leaflet adaptation as it may cause SLDA.

Successful treatment of chronic type B aortic dissection complicated by disseminated intravascular coagulopathy with recombinant human soluble thrombomodulin after thoracic endovascular aortic repair.

OBJECTIVES: We report a case of successful thoracic endovascular aortic repair (TEVAR) of chronic type B aortic dissection complicated by disseminated intravascular coagulopathy. METHODS: The patient suffered from chronic type B aortic dissection coexisting with a large false lumen and an intimal tear. He underwent TEVAR with left common carotid-left subclavian artery bypass. RESULTS: The following day, the patient exhibited a bleeding tendency and marked subcutaneous hemorrhage. He had a low fibrinogen level, a low platelet count, and high levels of fibrin dimer product and D-dimer. We diagnosed the condition as disseminated intravascular coagulopathy and administered recombinant human soluble thrombomodulin (rhTM). The patient recovered successfully from disseminated intravascular coagulopathy and was discharged on postoperative day 6. CONCLUSIONS: We successfully treated a patient with chronic type B aortic dissection with a large intimal tear complicated by postoperative disseminated intravascular coagulopathy using TEVAR followed by rhTM administration. rhTM may be considered in patients with large intimal tear and false lumen.

Extended thoracic endovascular aortic repair for residual aortic dissection after type A aortic dissection repair.

OBJECTIVE: We investigated the outcomes of extended coverage of the descending thoracic aorta by thoracic endovascular aortic repair (TEVAR) for residual chronic type B aortic dissection after type A aortic dissection (TAAD) repair. METHODS: From November 2015 to August 2020, 36 patients underwent extended TEVAR for residual intimal tear after TAAD repair. We specifically investigated the methods and outcomes of this procedure. RESULTS: TEVAR consisted of isolated TEVARs (n = 29), single-vessel debranching TEVAR (6), and two-vessel debranching TEVAR (1). The mean time from TAAD repair to TEVAR was 27 ± 33 months (2-86 months). The TEVAR devices used were Valiant (28 cases), GORETAG (4), Relay plus (2), and TX2 (2). Technical success of TEVAR was 100%. The distal ends of the stent grafts were T 8 (1 case), T 9 (5), T 10 (6), T 11 (9), and T 12 (15), with an average of T 11 ± 1. The average length of hospital stay after TEVAR was 9 ± 3 days (5-17 days). There were no surgical/hospital deaths or complications. The average postoperative follow-up period was 21 ± 15 months without death or reintervention. CONCLUSIONS: The short-term outcomes of extended TEVAR for residual chronic type B aortic dissection after TAAD repair were acceptable without perioperative SCI. Aggressive descending thoracic aorta coverage may prevent aortic events, and extended TEVAR may be a preemptive treatment for the downstream aorta. Mid- to long-term results should be clarified.

Inhibition of VEGF (Vascular Endothelial Growth Factor)-A or its Receptor Activity Suppresses Experimental Aneurysm Progression in the Aortic Elastase Infusion Model.

OBJECTIVE: We examined the pathogenic significance of VEGF (vascular endothelial growth factor)-A in experimental abdominal aortic aneurysms (AAAs) and the translational value of pharmacological VEGF-A or its receptor inhibition in aneurysm suppression. Approaches and Results: AAAs were created in male C57BL/6J mice via intra-aortic elastase infusion. Soluble VEGFR (VEGF receptor)-2 extracellular ligand-binding domain (delivered in Ad [adenovirus]-VEGFR-2), anti-VEGF-A mAb (monoclonal antibody), and sunitinib were used to sequester VEGF-A, neutralize VEGF-A, and inhibit receptor tyrosine kinase activity, respectively. Influences on AAAs were assessed using ultrasonography and histopathology. In vitro transwell migration and quantitative reverse transcription polymerase chain reaction assays were used to assess myeloid cell chemotaxis and mRNA expression, respectively. Abundant VEGF-A mRNA and VEGF-A-positive cells were present in aneurysmal aortae. Sequestration of VEGF-A by Ad-VEGFR-2 prevented AAA formation, with attenuation of medial elastolysis and smooth muscle depletion, mural angiogenesis and monocyte/macrophage infiltration. Treatment with anti-VEGF-A mAb prevented AAA formation without affecting further progression of established AAAs. Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro. Additionally, sunitinib treatment reduced circulating monocytes in aneurysmal mice. CONCLUSIONS: VEGF-A and its receptors contribute to experimental AAA formation by suppressing mural angiogenesis, MMP and VEGF-A production, myeloid cell chemotaxis, and circulating monocytes. Pharmacological inhibition of receptor tyrosine kinases by sunitinib or related compounds may provide novel opportunities for clinical aneurysm suppression.

The Role of Animal Models in Elucidating the Etiology and Pathology of Abdominal Aortic Aneurysms: Development of a Novel Rupture Mechanism Model.

Existing animal models do not replicate all aspects of abdominal aortic aneurysms (AAAs), including the rupture mechanisms. From histopathological analyses conducted in humans, it has been found that the vasa vasorum of the AAA wall is the starting point of circulatory failure and that bulging and dilatation of the abdominal aorta occurs through inflammation and tissue degeneration. We created a new animal model (the hypoperfusion-induced model) of AAAs. In this study, we describe the current animal models of AAAs and present the utility of our new model of AAAs.

Successful Treatment of Giant Ascending Aortic Aneurysm with Takayasu Arteritis.

A 50-year-old man who suffered from dyspnea on effort with hearing loss was referred to our hospital. Computed tomography angiography revealed a giant 90-mm diameter ascending aortic aneurysm with severe calcification and neck vessel occlusion. Transthoracic echocardiography revealed moderate-to-severe aortic regurgitation. His condition was diagnosed as Takayasu arteritis and he underwent aortic valve reimplantation with total arch replacement. Postoperative computed tomography angiography showed complete aneurysm resection and the patient was discharged without any complications and his hearing loss improved. He is currently being followed up as an outpatient.

Safety and Effectiveness of Tolvaptan Administration after Total Arch Replacement.

BACKGROUND: Postoperative fluid overload in cardiovascular surgery is associated with increased mortality and morbidity. Recently, tolvaptan (TLV), a selective vasopressin V2 antagonist, has been used for perioperative fluid management. This study aimed to validate the safety and effectiveness of TLV administration after total arch replacement (TAR) using selective cerebral perfusion. METHODS: From August 2016 to December 2016, 11 patients who had undergone TAR for thoracic aortic aneurysm were included in this study. In addition to the conventional diuretics furosemide (20 mg) and spironolactone (25 mg), TLV (7.5 mg) was administered orally. RESULTS: TLV increased urine output 1-3 days after administration. Body weight was gradually and steadily reduced until discharge. Neither renal nor liver dysfunction was recognized during the TLV administration. CONCLUSION: The concomitant use of TLV and conventional diuretics is safe and effective for fluid management after TAR using cardiopulmonary bypass, selective cerebral perfusion, and hypothermic circulatory arrest.

Endovascular Aortic Repair for Isolated Infrarenal Aortic Stenosis.

An 87-year-old man with severe intermittent claudication and lower limb pain at rest was referred to our hospital for examination. Computed tomography (CT) angiography imaging showed a severe stenosis in the infrarenal abdominal aorta. The ankle brachial indices (ABIs) were 0.62 (right) and 0.60 (left). Endovascular aortic repair was performed with distal protection. The postoperative course was uneventful, and postoperative CT showed no stenosis or distal embolization. The ABI improved to the normal values of 1.02 (right) and 1.13 (left). The patient was followed up as an outpatient without a cane. Long-term follow-up and randomized controlled trials are necessary to clarify the durability and efficacy of the endovascular approach for this aortic pathology.

Midterm Results of 2-Stage Hybrid Arch Repair for Extensive Aortic Arch Aneurysms.

BACKGROUND: This report evaluated the perioperative and midterm results of the 2-stage hybrid arch procedure. This procedure involves total arch replacement with an elephant trunk as the first stage and thoracic endovascular aortic repair as the second stage for patients with extended aortic arch pathology. METHODS: Between April 2010 and April 2017, 55 consecutive patients (age, 74.2 ± 6.4 years) with extended aortic arch atherosclerotic pathology involving the aortic arch and descending aorta underwent first-stage total arch replacement with the elephant trunk procedure. The second stage was completed for 53 (96.4%) of the 55 patients. The mean duration between the 2 procedures was 2.4 ± 2.2 months. Postoperative follow-up was completed after a mean of 36.6 ± 24.9 months. RESULTS: The in-hospital mortality rate for the first stage was 0%. Two patients died during the interval between surgeries. The in-hospital mortality rate for the second stage was 0%. Two (3.6%) of the 55 first-stage patients and none of the 53 second-stage patients experienced a postoperative stroke. No spinal cord dysfunction occurred during the first-stage and second-stage procedures. The 3- and 5-year survival rates were 88.2% and 67.0%, respectively. The 5-year thoracic aortic intervention-free rate was 95.5%. CONCLUSIONS: Extended aortic arch aneurysms were repaired using a 2-stage hybrid arch repair. Perioperative mortality and midterm results were acceptable. Use of an elephant trunk provided a secure landing zone for thoracic endovascular aneurysm repair. This 2-stage hybrid procedure is an alternative approach to extended aortic arch pathology.

Successful Thoracic Endovascular Aortic Repair using 2- and 3-Dimensional Fusion Imaging without Further Contrast Enhancement.

We report a case of successful thoracic endovascular aortic repair using a 3-dimensional computed tomography (3D CT) roadmap for a patient with severe contrast media allergy. As 3D CT image data were previously obtained, we integrated the data with the fluoroscopic image three dimensionally and constructed a 3D CT roadmap. This method is anticipated to be effective in patients who require less contrast enhancement or radiological dose by examining the appropriate imaging protocol for the kinds, shapes, and positions of the benchmarks for fusion.

Ectopic Expression of PCSK9 by Smooth Muscle Cells Contributes to Aortic Dissection.

BACKGROUND: Acute aortic dissection (AAD) is a common disease among the elderly. Although several risk factors of AAD have been reported, the molecular mechanism underlying AAD development remains to be elucidated. Proprotein convertase subtilisin/kexin type 9 (PCSK9) increases low-density lipoprotein cholesterol levels in blood by preventing its clearance. Therefore, PCSK9 inhibition is a promising therapeutic approach to treat cardiovascular diseases (CVDs). The objective of this study was to elucidate the role of PCSK9 in the pathogenesis of AAD. METHODS: We used fluorescence immunohistochemistry to assess PCSK9 expression in aortic tissues resected from 10 AAD patients and in the normal aorta from 5 autopsy samples as well as in spontaneously hyperlipidemic apolipoprotein E-deficient mice used as an experimental AD model. RESULTS: We revealed a characteristic distribution pattern of PCSK9 in atherosclerotic plaques and the degenerated tunica media in AAD tissues, which was rarely observed in normal aortic tissues. Furthermore, PCSK9 was notably expressed around calcification areas formed by vascular smooth muscle cells, especially those of the synthetic phenotype. The results obtained in the animal model were consistent with PCSK9 expression in AAD tissues. CONCLUSIONS: Our findings suggest that PCSK9 overexpression in the aorta may promote AAD. This study adds to the growing body of evidence supporting the use of PCSK9 inhibitors for the management of CVDs.

Elevated Plasma Levels of LDL Cholesterol Promote Dissecting Thoracic Aortic Aneurysms in Angiotensin II-Induced Mice.

BACKGROUND: Plasma low-density lipoprotein (LDL) cholesterol is implicated in abdominal aorta (AA) and aortic dissection (AD); however, its role in the pathogenesis of AA and AD, a disease with a high mortality rate, is unknown. The existing animal models such as apolipoprotein E-deficient (Apoe-/-) mice cannot reproduce all the conditions of AA/AD, including elevated LDL-cholesterol levels and spontaneous atheroma formation; therefore, a more reliable in vivo model is required. Here, we analyzed angiotensin II (Ang II)-induced mice with combined deficiency of the LDL receptor and the catalytic component of the apolipoprotein B-edisome complex (Ldlr-/-/Apobec1-/- [WKO]) to understand AA formation and AD occurrence in relation to plasma lipid composition. METHODS: AAs and ADs were created in 18- to 22- week-old male Apoe-/- and Ldlr-/-/Apobec1-/- mice by Ang II infusion. Immunostaining allowed assessment of smooth muscle cells and mural monocytes/macrophages. RESULTS: Ldlr-/-/Apobec1-/- mice had elevated LDL-cholesterol levels characteristic for human type IIa hyperlipidemia, resulting in atherogenesis, which promoted mortality, AA formation, and AD development. Interestingly, variations in the distribution of atheromas and inflammatory sites between Apoe-/- and Ldlr-/-/Apobec1-/- mice depending on lipid profiles resulted in differences in AA formation and AD occurrence in the thoracic aorta. CONCLUSIONS: Our results indicate the presence of a pathogenic pathway involving serum lipid composition that plays a key role in AA formation and AD occurrence in Ang II-induced mice.

RGD targeting of human ferritin iron oxide nanoparticles enhances in vivo MRI of vascular inflammation and angiogenesis in experimental carotid disease and abdominal aortic aneurysm.

PURPOSE: To evaluate Arg-Gly-Asp (RGD)-conjugated human ferritin (HFn) iron oxide nanoparticles for in vivo magnetic resonance imaging (MRI) of vascular inflammation and angiogenesis in experimental carotid disease and abdominal aortic aneurysm (AAA). MATERIALS AND METHODS: HFn was genetically engineered to express the RGD peptide and Fe3 O4 nanoparticles were chemically synthesized inside the engineered HFn (RGD-HFn). Macrophage-rich left carotid lesions were induced by ligation in FVB mice made hyperlipidemic and diabetic (n = 14), with the contralateral right carotid serving as control. Murine AAAs were created by continuous angiotensin II infusion in ApoE-deficient mice (n = 12), while control mice underwent saline infusion (n = 8). All mice were imaged before and after intravenous injection with either RGD-HFn-Fe3 O4 or HFn-Fe3 O4 using a gradient-echo sequence on a whole-body 3T clinical scanner, followed by histological analysis. The nanoparticle accumulation was assessed by the extent of T2*-induced carotid lumen reduction (% lumen loss) or aortic T2*-weighted signal intensity reduction (% SI [signal intensity] loss). RESULTS: RGD-HFn-Fe3 O4 was taken up more than HFn-Fe3 O4 in both the ligated left carotid arteries (% lumen loss; 69 ± 9% vs. 36 ± 7%, P = 0.01) and AAAs (% SI loss; 47 ± 6% vs. 20 ± 5%, P = 0.01). The AAA % SI loss correlated positively with AAA size (r = 0.89, P < 0.001). Histology confirmed the greater accumulation and colocalization of RGD-HFn-Fe3 O4 to both vascular macrophages and endothelial cells. CONCLUSION: RGD-HFn-Fe3 O4 enhances in vivo MRI by targeting both vascular inflammation and angiogenesis, and provides a promising translatable MRI approach to detect high-risk atherosclerotic and aneurysmal vascular diseases. LEVEL OF EVIDENCE: 1 J. Magn. Reson. Imaging 2017;45:1144-1153.

Peptide inhibitor of CXCL4-CCL5 heterodimer formation, MKEY, inhibits experimental aortic aneurysm initiation and progression.

OBJECTIVE: Macrophages are critical contributors to abdominal aortic aneurysm (AAA) disease. We examined the ability of MKEY, a peptide inhibitor of CXCL4-CCL5 interaction, to influence AAA progression in murine models. APPROACH AND RESULTS: AAAs were created in 10-week-old male C57BL/6J mice by transient infrarenal aortic porcine pancreatic elastase infusion. Mice were treated with MKEY via intravenous injection either (1) before porcine pancreatic elastase infusion or (2) after aneurysm initiation. Immunostaining demonstrated CCL5 and CCR5 expression on aneurysmal aortae and mural monocytes/macrophages, respectively. MKEY treatment partially inhibited migration of adaptively transferred leukocytes into aneurysmal aortae in recipient mice. Although all vehicle-pretreated mice developed AAAs, aneurysms formed in only 60% (3/5) and 14% (1/7) of mice pretreated with MKEY at 10 and 20 mg/kg, respectively. MKEY pretreatment reduced aortic diameter enlargement, preserved medial elastin fibers and smooth muscle cells, and attenuated mural macrophage infiltration, angiogenesis, and aortic metalloproteinase 2 and 9 expression after porcine pancreatic elastase infusion. MKEY initiated after porcine pancreatic elastase infusion also stabilized or reduced enlargement of existing AAAs. Finally, MKEY treatment was effective in limiting AAA formation after angiotensin II infusion in apolipoprotein E-deficient mice. CONCLUSIONS: MKEY suppresses AAA formation and progression in 2 complementary experimental models. Peptide inhibition of CXCL4-CCL5 interactions may represent a viable translational strategy to limit progression of human AAA disease.

Clinical Characteristics of Cryopyrin-Associated Periodic Syndrome and Long-Term Real-World Efficacy and Tolerability of Canakinumab in Japan: Results of a Nationwide Survey.

OBJECTIVE: We assess the clinical characteristics of patients with cryopyrin-associated periodic syndrome (CAPS) in Japan and evaluate the real-world efficacy and safety of interleukin-1 (IL-1) inhibitors, primarily canakinumab. METHODS: Clinical information was collected retrospectively, and serum concentrations of canakinumab and cytokines were analyzed. RESULTS: A total of 101 patients were included, with 86 and 15 carrying heterozygous germline and somatic mosaic mutations, respectively. We identified 39 mutation types, and the common CAPS-associated symptoms corresponded with those in previous reports. Six patients (5.9% of all patients) died, with four of the deaths caused by CAPS-associated symptoms. Notably, 73.7% of patients (100%, 79.6%, and 44.4% of familial cold autoinflammatory syndrome, Muckle-Wells syndrome, and chronic infantile neurological cutaneous articular syndrome/neonatal onset multisystem inflammatory disease, respectively) achieved complete remission with canakinumab, and early therapeutic intervention was associated with better auditory outcomes. In some patients, canakinumab treatment stabilized the progression of epiphysial overgrowth and improved height gain, visual acuity, and renal function. However, 23.7% of patients did not achieve inflammatory remission with crucial deterioration of organ damage, with two dying while receiving high-dose canakinumab treatment. Serological analysis of canakinumab and cytokine concentrations revealed that the poor response was not related to canakinumab shortage. Four inflammatory nonremitters developed inflammatory bowel disease (IBD)-unclassified during canakinumab treatment. Dual biologic therapy with canakinumab and anti-tumor necrosis factor-α agents was effective for IBD- and CAPS-associated symptoms not resolved by canakinumab monotherapy. CONCLUSION: This study provides one of the largest epidemiologic data sets for CAPS. Although early initiation of anti-IL-1 treatment with canakinumab is beneficial for improving disease prognosis, some patients do not achieve remission despite a high serum concentration of canakinumab. Moreover, IBD may develop in CAPS after canakinumab treatment.

Flanged elephant trunk technique at distal anastomosis for total arch replacement with multibranched arch graft.

Bleeding from the distal anastomosis suture line in total arch replacement is a serious and major concern for surgeons. We present a simple, flanged elephant trunk technique to reduce or eliminate bleeding from the distal anastomosis suture line in total arch replacement using a multibranched arch graft. This method allows not only a secure and reinforced distal anastomosis, but also simultaneous elephant trunk insertion.

Clinical outcomes of Najuta thoracic stent graft system for arch aneurysms.

Objectives: We aimed to elucidate the perioperative and short-term clinical outcomes of the Najuta thoracic stent graft system with fenestrations for supra-aortic vessels. Methods: We retrospectively investigated the perioperative and short-term clinical outcomes of 20 patients treated for arch or distal arch aneurysms using the Najuta thoracic stent graft system during the period from May 2019 to February 2023. Results: The technical success rate of the Najuta thoracic stent graft system was 95%. Of the 20 patients, 17 patients (85.0%) underwent concomitant extra-anatomical supra-aortic bypass. Postoperative CT revealed type Ia (n = 2) and type II (n = 3) endoleaks which disappeared on follow-up. The postoperative complications were stroke (n = 2, 10.0%), paraplegia (n = 1, 5.0%), and paraparesis (n = 1, 5.0%). In a very old patient, a blood transfusion was performed from the common iliac artery using the retroperitoneal approach. There were no aorta-related complications such as retrograde type A dissection or distal stent graft-induced new entry. Conclusions: We treated arch or distal arch thoracic aneurysms by inserting a tube-type stent graft as a scaffold on the peripheral site and placing the Najuta thoracic stent graft on the proximal site. By extending the landing zone to Zone 0 and using a low radial force, which is a feature of the Najuta thoracic stent graft system, postoperative bird-beak and aorta-related complications were avoided. The treatment of arch and distal arch aortic aneurysms using the Najuta thoracic stent graft system showed acceptable perioperative and short-term clinical outcomes. Thoracic endovascular aortic repair using the Najuta thoracic stent graft system may be a potential treatment option for arch and distal arch aortic aneurysms, warranting further studies.