Foam Sclerotherapy in the Treatment of Hemangiomas and Venous Malformations.

BACKGROUND: Sclerotherapy has achieved great success in treating most venous malformation (VM) lesions. OBJECTIVE: To compare the effects of foam sclerotherapy on infantile hemangioma and pyogenic granuloma (PG). In addition, we analyzed the data and outcomes of foam sclerotherapy for the VM. MATERIALS AND METHODS: Thirty-nine patients with hemangiomas and 83 patients with VMs were treated, and clinical outcomes, resolution, and complication rates were compared. Sclerotherapy data from the VM group were also analyzed. RESULTS: The average age of the patients and the distribution and tissue involvement of lesions among the 3 groups were significantly different ( p < .001). The average amount of sclerosing foam administered per session in VMs was significantly higher than that in the other 2 groups ( p < .0001) (whereas that in the PG group was lower than that in the infantile hemangioma group [ p < .0001]). However, the overall therapeutic efficacy and side effects in the 3 groups were not significantly different. For VMs, the frequency of ultrasound guided foam sclerotherapy and use of 3% polidocanol increased from superficial to deep lesions, whereas the use of 1% POL decreased ( p < .0001). CONCLUSION: Infantile hemangioma and PG treatments presented good results and minor adverse reactions comparable with those of VMs.

Empagliflozin inhibits neointimal hyperplasia through attenuating endothelial-to-mesenchymal transition via TAK-1/NF-κB pathway.

OBJECTIVE: To investigate whether empagliflozin could prevent injury-induced vascular neointimal hyperplasia and to further explore its mechanism. METHODS: Male C57BL/6J mice were divided into two groups with or without the empagliflozin treatment, and carotid ligation injury was performed to induce neointimal hyperplasia. The injured carotid arteries were collected for Western blotting (WB), histology and immunofluorescence analysis after four weeks. The inflammatory responses were analyzed by qRT-PCR to detect the inflammatory gene mRNA expression. To further explore its mechanism, HUVECs were treated with TGFß-1 to induce EndMT followed by empagliflozin or vehicle treatment in vitro. A23187 (Calcimycin), an agonist of NF-κB signaling was used in the experiment. RESULTS: The wall thickness and the neointima area was significantly reduced in the empagliflozin treatment group on day 28 after artery ligation. The Ki-67 positive cells were 28.33 ± 12.66% and 48.83 ± 10.41% in the empagliflozin-treated group and control group, respectively (P < 0.05). The mRNA expression levels of the inflammatory genes and inflammatory cells were decreased in the empagliflozin treatment group, as well as the MMP2 and MMP9. Meanwhile, empagliflozin can significantly reduce the migratory ability of inflammatory-treated HUVECs. The CD31 was increased in the TGFß1+empagliflozin group, whereas the FSP-1, phosphorylation of TAK-1 (p-TAK-1) and phosphorylation of NF-κB (p- NF-κB) expression level were decreased, compared to the control group without empagliflozin treatment. However, the expression level of FSP-1 and p-NF-κB were reversed after co-treatment with A23187, whereas the p-TAK-1 expression level was without any significant difference. CONCLUSION: Empagliflozin inhibits the inflammation-induced EndMT via the TAK-1/NF-κB signaling pathway.

A nonobstructive condition: Medial arterial calcification. / ä¸å¼•èµ·ç®¡è ”ç‹­çª„çš„è¡€ç®¡ä¸­è†œé’™åŒ–.

Vascular calcification, including intimal and medial calcification, is closely associated with a significant increase in cardiovascular diseases. Although increased understandings were achieved, people still know much more about intimal calcification than medial calcification because the latter doesn't obstruct the arterial lumen, commonly considered as a non-significant finding. We clarified the pathologic characteristic of medial calcification, its difference from intimal calcification, principally focused on its clinical relevance, such as diagnosis, nosogenesis, and hemodynamics. We underline the importance of identifying and distinguishing medial calcification, understanding its effect to local/systematic arterial compliance, and relationship to diabetic neuropathy. Recent studies emphasize do not ignore its predictive role in cardiovascular mortality. It is of great clinical significance to summarize the mechanisms of occurrence, lesion characteristics, diagnostic methods, pathogenic mechanisms, hemodynamic changes, and the distinction as well as association of intimal calcification with intimal calcification.

Purinergic receptor P2X7 contributes to abdominal aortic aneurysm development via modulating macrophage pyroptosis and inflammation.

The purinergic receptor P2X7 has been established as an important mediator of inflammation and participates in a variety of cardiovascular diseases including atherosclerosis, however, its role in abdominal aortic aneurysms (AAA) remains unclear. In this study, we demonstrate that P2X7 plays essential roles in AAA development via modulating macrophage pyroptosis and inflammation. P2X7 is highly expressed in human AAA specimen, as well as in experimental murine AAA lesions (both CaCl2- and Angiotensin II-induced AAA models), and it mainly confines in macrophages. Furthermore, P2X7 deficiency or pharmacological inhibition with its antagonist could significantly attenuate aneurysm formation in experimental murine AAA models, while P2X7 agonist could promote AAA development. The caspase-1 activity, matrix metalloproteinase (MMP) activity, reactive oxygen species (ROS) production and pro-inflammatory gene expression were significantly reduced in experimental AAA lesions in mice with P2X7 deficiency or inhibition. Mechanistically, macrophage P2X7 can mediate the activation of NLRP3 inflammasome and activate its downstream caspase-1 to initiate the pyroptosis pathway. After caspase-1 activation, it further cleaves pro-interleukin (IL)-1ß and gasdermin D (GSDMD). Consequently, the N-terminal fragment of GSDMD forms pores on the cell membrane, leading to macrophage pyroptosis and release of the pro-inflammatory factor IL-1ß. The resulting vascular inflammation further leads to the upregulation of MMP and ROS, thereby promoting AAA development. In summary, these data identify P2X7-mediated macrophage pyroptosis signaling pathway as a novel contributory mechanism of AAA formation.

Treatment strategies for endoleak after endovascular repair of the abdominal aortic aneurysm: A single center retrospective study.

BACKGROUND: Endovascular abdominal aortic aneurysm repair (EVAR) is the most frequently used treatment for aneurysm in abdominal aorta. The endoleak after EVAR causes the aneurysm sac to remain enlarged and risk for rupture. AIMS: The purpose of the study was to assess the efficacy of strategies and techniques for endoleak treatment. METHODS: This study was a single center retrospective study of 30 patients who had kinds of endoleak. The 30 patients were from a cohort of 597 patients who received EVAR from the Secondary Xiangya Hospital, Central South University between Jan 2014 to Dec 2021, what is follow-up well and diagnosed as endoleak. Data included basic clinical information, aspects of the endoleak treatment techniques, and follow-up findings. RESULTS: The 30 patients with endoleak were diagnosed by computed tomography angiography or digital subtraction angiography. Age is 69 ± 7.9 yrs. 26 patients are male with only 4 female patients. Immediate endoleak after EVAR is 46.7%and delayed endoleak is 53.3%. The classification of endoleak is type Ⅰ:76.6%; type Ⅱ 26.7%; type Ⅲ:6.7%; type Ⅳ:6.7%; type Ⅴ:13.3%. Different treatment of endoleak includes: screening, endovascular re-intervention and open surgery. There are 3 patients (10.0%) underwent emergency EVAR due to their rupture condition of aneurysm. All the endoleak patients' CTA image characteristics has been reviewed. The follow-up rate is 93.3%. There are 6 patients (21.4%) died during follow-up. No aneurysm sac rupture death has been recorded. CONCLUSIONS: Endoleak after EVAR is the most frequent complication that directly affects survival and re-intervention rates. Our findings suggested that different treatment strategies based on the individual patient's situation is important for their endoleak treating result.

Long-term outcome of spontaneous isolated superior mesenteric artery dissection in different angiographic types.

OBJECTIVE: This study aimed to compare the follow-up and outcomes of spontaneous isolated superior mesenteric artery dissection (SISMAD) in different angiographic types and to determine the optimal therapeutic options for SISMAD patients. METHODS: This is a retrospective study of 61 SISMAD patients between December 2010 and January 2019 in a single center. Data analysis consisted of demographics, clinical data, radiology review, treatment, follow-up, and outcomes. RESULTS: A total of 61 SISMAD patients were reviewed in this study. Median age was 53 (quartile, 47.5-63.0), 90.2% were males with hypertension (50.8%), dyslipidaemia (54.1%), and smoking history (60.7%). Among all, 43 patients underwent periodic follow-up of computed tomography (CT) angiography for follow-up analysis. 11 (25.6%) patients showed "No Change" during follow-up, including 6 type I patients. 23 patients (53.5%) were "Partially Remodelled" and 18 of them were type II patients. 7 "Completely Remodelled" patients (16.3%) were all in type II group. Two type III patients (4.6%) died after the emergent surgical intervention within 30 days. CONCLUSIONS: Different SISMAD angiographic types present with variant progression. Type I SISMAD may be inclined to remain "unchanged." Type II SISMAD shows a clear trend to remodeling, especially type IIb patients. The progression of type III SISMAD varies in the extent of collateral bypasses.

Empirical Research on the Prediction Effect of Volatility Model Based on the Perspective of Investor Sentiment Health and Market Liquidity.

Healthy investor sentiment has an important impact on stock market volatility. To avoid extreme volatility in the stock market, it becomes crucial to focus on the sentiment health of investors. Therefore, we establish the realized volatility model, the implied volatility model, and the historical volatility model, respectively, introduce investor sentiment and market liquidity into these models, and empirically study the forecast effects of future daily and weekly frequency volatility to play a role in the development of the physical industry and the improvement of organizational performance. The study found that the HAR-RV model has the strongest predictive ability, while the GJR-GARCH model's predictive effect is not ideal; market liquidity and high investor sentiment can improve the predictive effect of most models; compared with long-term (one-week) volatility, the effect of predicting short-term (one-day) volatility is better.

Early Results of a Novel Gutter-Free Chimney Stent-Graft System to Treat Aortic Arch Dissection: Single-Center Data from a Prospective Clinical Trial.

AIMS: Discuss the clinical value, technique characteristics, and early follow-up results of a newly designed gutter-free chimney stent-graft system for aortic arch pathology. METHODS AND RESULTS: About 13 patients with aortic arch dissection were enrolled in a clinical trial testing a novel gutter-free stent-graft between February 2019 and December 2020. All 13 patients were male, age 52.6±10.4 years. The implantation time was 14.0±6.9 minutes; total procedure time was 89.5±19.8 minutes. The volume of contrast was 79.6±7.2 ml. And 15 aortic stent-grafts were implanted, and all 13 patients had chimney branch stent-grafts implanted into the left subclavian artery (LSA). There were 3 (23.1%) cases of immediate type Ιa endoleak after thoracic endovascular aortic repair (TEVAR), and 7.7% type Ιa endoleaks occurred in delayed fashion. Survival at 2 years was 100%, and the 2-year patency of chimney stent-grafts was 100%. CONCLUSIONS: This study reports early success with good freedom from endoleak using a novel stent-graft designed for chimney TEVAR to treat aortic arch dissection. Postoperative survival and patency of the branch stent-grafts were excellent. Additional data from this multicenter clinical trial will be forthcoming.

Endovascular aneurysm repair for aorto-iliac artery pathologies in patients with autosomal dominant polycystic kidney disease.

BACKGROUND: This study aims to evaluate the efficacy and safety of endovascular aneurysm repair (EVAR) of abdominal aortic or iliac artery pathologies in patients with autosomal dominant polycystic kidney disease (ADPKD). METHODS: From January 2014 to December 2019, fifteen consecutive patients (13 men, mean age 69.3 years, range 56-82 years) with abdominal aortic or iliac artery pathologies coexisting with ADPKD underwent EVAR in our department. Their general data, perioperative results and follow-up outcomes were retrospectively reviewed and analyzed. RESULTS: Among the fifteen patients, eleven had abdominal aortic aneurysms, one had isolated abdominal aortic dissection and the other three had iliac artery aneurysms. Three patients had thoracic penetrating aortic ulcer and two had intracranial aneurysms as the comorbidities. All patients underwent EVAR with the aorto-iliac pathologies successfully excluded. The average operative time was 171±73 minutes and average contrast volume was 87±12mL. The average follow-up time was 38.4 months (range 6-60). Aorta-bi-iliac stent-grafts were deployed in fourteen patients, while one patient received tubular stent-graft. Two patients underwent simultaneous TEVAR and EVAR, and One underwent EVAR 3 months after TEVAR. One patient was found to have a hematoma at the site of femoral access 3 days after EVAR. One patient was found to have a Type Ib endoleak 5 months after EVAR, and he recovered well with a secondary endovascular intervention. Contrast-induced nephropathy was observed in two patients (13%) post EVAR. Another patient developed renal failure 20 months after EVAR and was treated with regular hemodialysis. All other patients did not have any reported significant deterioration of renal function during follow-up. No other adverse events, such as death, paraplegia, aneurysm rupture, or open surgery conversion occurred during operation and follow-up. CONCLUSIONS: For patients with abdominal aortic or iliac artery diseases coexisting with ADPKD, EVAR had satisfactory mid-term outcomes, without significantly exacerbating the decline of renal function. However, patients with ADPKD might have multiple vascular lesions, especially intracranial aneurysms, which should be paid enough attention in clinical practice.

Application of a Novel Common-Iliac-Artery Skirt Technology (CST) in Treating Challenge Aorto-Iliac or Isolated Iliac Artery Aneurysms.

Purpose: To report a novel common-iliac-artery skirt technology (CST) in treating challenge iliac artery aneurysms. Methods: When required healthy landing zone of common iliac artery (CIA) is not available, CST is a strategy to exclude the internal iliac artery (IIA) and prevent IIA reflux without need of embolization. Patients who received endovascular aneurysm repair (EVAR) in our center from 2014 to 2020 were retrospectively screened, and patients treated with CST or with IIA embolization (IIAE) were enrolled. Results: After retrospective screen of 524 EVAR patients, 39 CST patients, 26 IIAE patients, and 7 CST + IIAE patients were enrolled in this study. CST group suggested to have more aged, hyperlipemia, and smoking patients than IIAE group. Two groups had comparable maximal diameter of abdominal aorta (AA), CIA, EIA, but larger diameter of IIA (CST 19.82 ± 2.281 vs. IIAE 27.82 ± 3.401, p = 0.048), and CIA bifurcation (CST 25.01 ± 1.316 vs. IIAE 29.76 ± 2.775, p = 0.087) was found in IIAE group. Anatomy of 79.5% of CST patients and 92.3% of IIAE patients (p = 0.293) was not suitable for potential use of iliac branch device. CST group had significant shorter surgery time (CST 97.42 ± 3.891 vs. IIAE 141.0 ± 8.010, p < 0.001), shorter hospital stay (CST 15.35 ± 0.873 vs. IIAE 19.32 ± 1.067, p = 0.009), lower in-hospital [CST 0% (0/39) vs. IIAE 11.5% (3/26), p = 0.059] and 1-year follow-up stent related MAEs [CST 6.7% (2/30) vs. IIAE 28.6% (6/21), p = 0.052], but comparable mortality and stent related MAEs for all-cohort follow-up analysis comparing to IIAE group. In our study, a lower in-hospital buttock claudication (BC) rate for CST (CST 20.5% vs. IIAE 46.2%, p = 0.053) and a comparable erectile dysfunction (ED) rate (CST 10.3% vs. IIAE 23.1%, p = 0.352) were found between CST and IIAE groups. After 1 year, both groups had about one third relief of BC symptoms [CST 33.3% (4/12) vs. IIAE 30.7% (4/13), p = 1.000]. Subgroup analysis of 14 patents concomitant with IIA aneurysm in CST group and the 7 CST + IIAE patients were carried out, and no difference was found in mortality, stent MAEs, sac dilation, or reintervention rate. Last, illustration of seven typical CST cases was presented. Conclusion: In selected cases, the CST is a safe, feasible-and-effective choose in treating challenge iliac artery aneurysms and preventing IIA endoleak.

Midterm Results of Retrograde In Situ Needle Fenestration During Thoracic Endovascular Aortic Repair of Aortic Arch Pathologies.

PURPOSE: To evaluate the safety and feasibility of the in situ needle fenestration (ISNF) technique for reconstruction of the left subclavian artery (LSA) during thoracic endovascular aortic repair (TEVAR) of complicated aortic arch pathologies. MATERIALS AND METHODS: A retrospective review was conducted from January 2014 to December 2019 of 50 patients (mean age 60.2±11.1; 45 men) who underwent ISNF to revascularize the LSA during TEVAR. Twenty-one of the patients also required revascularization of the left common carotid artery (LCCA; n=19) and innominate artery (IA; n=2) using physician-modified in vitro fenestration. Overall, 73 supra-aortic branches were targeted for revascularization. RESULTS: ISNF was successful in 48 patients (96%); one LSA could not be stented and a tortuous LSA prevented the needle from fenestrating the graft. No perioperative major adverse event occurred. There were no type I and 4 type III endoleaks (8%), 3 of which occurred among the first 20 cases. Types II and IV endoleaks were found in 3 (6%) and 6 (12%) cases, respectively; all disappeared during a median follow-up of 15 months (range 3-66). One death (2%) occurred within 12 months due to cerebral hemorrhage. Two patients (4%) required open reinterventions at 6 and 62 months. CONCLUSION: ISNF for revascularization of the LSA during TEVAR seems to be feasible with acceptable midterm outcomes. The learning curve and evolving patient selection criteria affected technical success, complications, and the need for reinterventions. Long-term durability requires further evaluation.

EphB4 signaling maintains the contractile phenotype of adult venous smooth muscle cells.

BACKGROUND: Autologous vein grafting remains the gold standard for surgical bypass grafts. However, vein bypasses still have significant incidence of failure. Ephrin type-B receptor 4 (EphB4), the embryonic venous determinant, may modulate vein graft adaptation. Although EphB4 is expressed in venous endothelial and smooth muscle cells (SMCs), it is not known whether EphB4 is functional in human SMCs. MATERIALS AND METHODS: Human adult venous SMCs were obtained from the inferior vena cava of an adult human liver donor. Primary SMCs were stimulated with EphrinB2/Fc or transfected with an EphB4-expression vector (GV219-EphB4). Expression of SMC phenotype markers, migration, and proliferation were evaluated. RESULTS: Activation of EphB4 with EphrinB2/Fc increased the mRNA and protein expression of the venous SMC contractile markers alpha actin, calponin-1, SM22, and MYH11, while decreasing the expression of the synthetic marker osteopontin. EphrinB2/Fc treatment inhibited SMC migration, but not proliferation. In addition, overexpression of EphB4 increased mRNA expression of SMC contractile markers, while decreasing expression of the apoptosis marker caspase-9. CONCLUSIONS: EphB4 was present and functional in adult human venous SMCs. Stimulation of EphB4 increased expression of contractile SMC phenotypic markers and decreased SMC migration in vitro, functioning to retain the contractile phenotype of SMCs. EphB4 activation, therefore, recapitulates changes observed during vein graft adaptation to the arterial environment in vivo. EphB4 represents a new strategy to inhibit neointimal hyperplasia during vein graft adaption.

SUMO1 modification of methyltransferase-like 3 promotes tumor progression via regulating Snail mRNA homeostasis in hepatocellular carcinoma.

Rationale: Hepatocellular carcinoma (HCC) is one of the leading causes of mortality worldwide. Methyltransferase-like 3 (Mettl3), an RNA N6-methyladenosine (m6A) methyltransferase, has been shown to act as an oncogene in several human cancers. However, the regulatory role of posttranslational modifications of Mettl3 in liver cancer remains elusive. Methods: SUMOylation was analyzed using immunoprecipitation and western blot assays. In vitro and in vivo biological functions were examined using MTS, colony formation, wound healing, transwell, apoptosis, and viability assays and the BALB/c nude mouse model, respectively. Immunohistochemistry was conducted to evaluate the prognostic value of Mettl3 expression in HCC. The regulatory mechanism of Mettl3 in HCC was investigated by m6A dot blot, immunofluorescence, dual luciferase reporter, protein stability, and RNA stability assays. Results: Mettl3 was found to be SUMOylated by a small ubiquitin-like modifier SUMO1. Further, SUMOylation of Mettl3 was increased upon mitogen stimulation, which correlated with UBC9 upregulation, and was positively correlated with high metastatic potential of liver cancer. Finally, SUMOylation of Mettl3 was found to regulate HCC progression via controlling Snail mRNA homeostasis in an m6A methyltransferase activity-dependent manner. Conclusions: This study revealed a novel mechanism of SUMOylated Mettl3-mediated Snail mRNA homeostasis, identifying the UBC9/SUMOylated Mettl3/Snail axis as a novel mediator of the SUMO pathway involved in HCC progression.

Endovascular treatment for aortic arch pathologies: chimney, on-the-table fenestration, and in-situ fenestration techniques.

BACKGROUND: Revascularization of the supra-aortic major branches in thoracic endovascular aortic repair (TEVAR) is challenging owing to the complex anatomic configuration of aortic arch pathologies. This study aims to evaluate the feasibility, effectiveness, and safety of three major techniques-chimney, fenestrated, and in-situ fenestration-for patients with aortic arch pathologies. METHODS: A retrospective analysis was performed involving 234 patients with aortic arch lesions, who underwent TEVAR with adaptations in technique (chimney, fenestrated, or in-situ fenestration) between January 2016 and December 2017. RESULTS: One hundred and twenty-six patients underwent the chimney technique (98 single chimneys, 24 double chimneys, and four triple chimneys); one hundred and two patients (102/234) were treated with on-the-table fenestration technique (92 single fenestrations, nine double fenestrations, and one double fenestration plus innominate artery chimney); and the remaining six patients underwent in-situ needle fenestration technique. Overall, indications included aortic dissections (99/234), aortic arch aneurysms (60/234), penetrating aortic ulcers (72/234), and re-interventions (3/234). The technical success rates were 99.6%. There were five cases of early all-cause mortality. The patency rates of overall branches were 99.6%. There were 15 cases with type Ia endoleak-14 in the chimney group (11.1%) and one in the on-the-table fenestration group (1%). Five patients underwent re-interventions. The median follow-up time for all patients was 28 (range, 16-41) months. CONCLUSIONS: Our experience suggests that chimney, on-the-table fenestration, and in-situ needle fenestration techniques are feasible, effective, and safe treatment options for aortic arch pathologies with encouraging mid-term results. Long-term durability concerns require further evaluation.

Early experience and technical aspects of physician-modified fenestration in thoracic endovascular aortic repair for aortic arch pathologies.

OBJECTIVE: This study was performed to describe the treatment of aortic arch pathologies with a physician-modified fenestration (PMF) technique in thoracic endovascular aortic repair (TEVAR). METHODS: From August 2015 to August 2017, 32 patients with aortic arch pathologies underwent TEVAR with the PMF technique. All patients' clinical data were analyzed with GraphPad Prism 7.0. RESULTS: Thirty-four aortic stent-grafts were implanted in 32 patients. The mean proximal diameter of the stent-graft was 32.4 ± 3.4 cm, and the mean length was 170.0 ± 25.2 cm. Twenty-nine PMF procedures were performed to preserve the left subclavian artery (LSA) and three to preserve both the LSA and left common carotid artery. The mean distance between the pathology and LSA was 8.4 ± 4.0 mm. The mean procedure time (from first to last digital subtraction angiography) was 22.8 ± 20.8 min. The mean follow-up time was 8.3 ± 5.3 months. During follow-up, the all-cause survival rate was 83.3% and the patency rate of the branch artery after PMF was 96.0%. CONCLUSION: The PMF technique is a relatively safe, feasible, and time-saving method to preserve the branch artery in TEVAR for aortic arch pathologies. The short- to middle-term result of this technique is satisfactory.

Thoracic Endovascular Aortic Repair With Single/Double Chimney Technique for Aortic Arch Pathologies.

PURPOSE: To summarize a single-center experience using the single/double chimney technique in association with thoracic endovascular aortic repairs (TEVAR) for aortic arch pathologies. METHODS: From November 2007 to March 2016, 122 patients (mean age 50.4±12.7 years, range 29-80; 92 men) with aortic arch pathologies underwent TEVAR combined with single (n=101) or double (n=21) chimney grafts to reconstruct the supra-aortic branches: 21 innominate arteries, 114 left common carotid arteries, and 8 left subclavian arteries (LSA). Pathologies included type B aortic dissection (n=47), aortic arch dissection (n=49), retrograde type A aortic dissection (n=8), thoracic aortic aneurysm (n=7), penetrating aortic arch ulcer (n=9), and post-TEVAR type I endoleak (n=2). Follow-up examinations included computed tomography at 0.5, 3, 6, and 12 months and yearly thereafter. RESULTS: The aortic stent-grafts were deployed in zone 0 (n=21), zone 1 (n=93), and zone 2 (n=8). One (0.8%) of the 122 patients died at 4 days due to a perforated peptic ulcer. Type Ia endoleaks were found intraoperatively in 13 (10.7%) patients, including 3 with the double chimney technique. Type II endoleaks occurred in 6 (4.9%) patients; 3 were treated with duct occluders in the LSA. Postoperative chimney graft migration occurred in 1 (0.8%) patient with double chimneys; additional stent-grafts were deployed in both chimneys. Median follow-up was 32.3 months, during which 1 (0.8%) patient died after a stroke at 3 months. Chimney stent-graft patency was observed in the remaining 120 patients. Two (1.7%) secondary TEVARs were performed for distal aortic dissection. Nine asymptomatic type Ia endoleaks and 1 type II endoleak persisted in follow-up; a type II endoleak in 1 patient with Marfan syndrome sealed in 52 months. CONCLUSION: TEVAR with the chimney technique provides a safe, minimally invasive alternative with good chimney graft patency and low postoperative mortality during midterm follow-up. The double chimney technique should be used judiciously owing to its potential complications.

Epigallocatechin-3-gallate is a potent phytochemical inhibitor of intimal hyperplasia in the wire-injured carotid artery.

OBJECTIVE: Epigallocatechin-3-gallate (EGCG), a catechin gallate ester, is the major component of green tea and has been demonstrated to inhibit tumor growth as well as inhibit smooth muscle cell migration. We evaluated the effect of the phytochemicals resveratrol, allicin, sulforaphane (SFN), and EGCG on intimal hyperplasia in the carotid artery injury model. METHODS: Intimal hyperplasia was induced in carotid arteries of adult Sprague-Dawley rats with a wire injury. Experimental animals received intraperitoneal injections of one of the four phytochemicals daily beginning 1 day prior to surgery and continued for up to 4 weeks. Control animals were administered saline. Carotid specimens were harvested at 2 weeks and subjected to quantitative image analysis. In addition, EGCG specimens were analyzed for cell proliferation, immunohistochemistry, and Western blot analysis. RESULTS: Quantitative image analysis showed significant phytochemical suppression of intimal hyperplasia at 2 and 4 weeks postoperatively with EGCG (62% decrease in intimal area). Significant decreases were also noted at 2 weeks for SFN (56%) and resveratrol (44%), whereas the decrease with allicin (24%) was not significant. Quantification of intimal hyperplasia by intima:media ratio showed similar results. Cell proliferation assay of specimens demonstrated suppression by EGCG. Immunohistochemical staining of EGCG-treated specimens showed extracellular signal-regulated kinase (ERK) suppression but not of the c-jun N-terminal kinase or p38 pathways. Western blot analysis confirmed reduced ERK activation in arteries treated with EGCG. CONCLUSIONS: Intraperitoneal injection of the phytochemicals EGCG, SFN, resveratrol, and allicin have suppressive effects on the development of intimal hyperplasia in the carotid artery injury model, with maximal effect due to EGCG. The mechanism of EGCG action may be due to inhibition of ERK activation. EGCG may affect a common pathway underlying either neoplastic cellular growth or vascular smooth muscle cellular proliferation.

Vascular endothelial growth factor-A inhibits EphB4 and stimulates delta-like ligand 4 expression in adult endothelial cells.

BACKGROUND: During vein graft adaptation to the arterial circulation, vascular endothelial growth factor (VEGF) A expression transiently increases before becoming downregulated; however, the role of VEGF-A in venous remodeling is not clear. In addition, although VEGF-A stimulates angiogenesis and determines arterial identity in nascent arterial endothelial cells (EC), the role of VEGF-A in regulating identity in adult venous EC is also not clear. MATERIALS AND METHODS: EC, wild type (EphB4+/+) or heterozygous knockout (EphB4+/-), were stimulated with VEGF-A (0-100 ng/mL) and examined with quantitative polymerase chain reaction and western blotting. RESULTS: VEGF-A (100 ng/mL) inhibited expression of EphB4 and stimulated expression of delta-like ligand 4 (dll4) but did not stimulate either notch or EphrinB2 expression in adult venous EC. Pretreatment with VEGF receptor 2-neutralizing antibody abolished VEGF-stimulated downregulation of EphB4 but not the upregulation of dll4. Pretreatment with PD98059 or wortmannin showed that VEGF-A downregulation of EphB4 and upregulation of dll4 are mitogen-activated protein kinase kinase and extracellular signal-regulated kinase dependent but phosphatidylinositol 3 kinase-Akt independent. Compared with VEGF-induced EphB4 downregulation and dll4 upregulation in control EC, reduced EphB4 signaling in EphB4+/- EC showed even further downregulation of EphB4 and upregulation of dll4. CONCLUSIONS: Despite the genetic programming of arterial and venous EC fate, VEGF-A can repress venous identity in adult venous EC without induction of arterial identity. These changes in adult EC in vitro recapitulate the changes in identity described during vein graft adaptation to the arterial environment in vivo.

Reduced adult endothelial cell EphB4 function promotes venous remodeling.

Reduced EphB4 expression is observed during vein graft adaptation and is associated with increased venous wall thickening. These findings suggest that EphB4 may mediate normal adult venous endothelial cell (EC) function and vein graft adaptation. We therefore tested the functional significance of EphB4 using EC with genetically reduced EphB4 signaling. EC were isolated from EphB4(+/+) and EphB4(+/-) mice. In vitro function was assessed through EC proliferation, migration, nitric oxide (NO) synthesis, and chemokine production. A mouse vein graft model was used to correlate in vitro findings with in vivo vein grafts. Smooth muscle cells (SMC) were subjected to proliferation and migration assays using EphB4(+/+) and EphB4(+/-) EC-conditioned medium. EphB4(+/-) EC exhibited diminished proliferation (P < 0.0001, n = 6), migration (P < 0.0001, n = 3), and NO production (P = 0.0012, n = 3). EphB4(+/-) EC had increased VEGF-A mRNA (P = 0.0006, n = 6) and protein (P = 0.0106, n = 3) as well as increased secretion of VEGF-A (P = 0.0010, n = 5), PDGF-BB (P < 0.0001, n = 6), and TGF-ß1 (P < 0.0001, n = 6). EphB4(+/-)-conditioned medium promoted SMC proliferation (P < 0.0001, n = 7) and migration (P = 0.0358, n = 3). Vein grafts and EphB4(+/-) EC showed similarity with regard to VEGF-A and eNOS mRNA and protein expression. In conclusion, reduced venous EC EphB4 function is associated with a proangiogenic and mitogenic phenotype. EphB4(+/-) EC have increased secretion of SMC mitogens and reduced NO production that correlate with the thickened neointima formed during vein graft adaptation. These findings suggest that EphB4 remains active in adult venous EC and that loss of EphB4 plays a role in vein graft adaptation.

Aberrant subclavian artery pathologies and Kommerell's diverticulum: a review and analysis of published endovascular/hybrid treatment options.

Aberrant subclavian artery (ASA) is one of the most common congenital vascular anomalies of the aortic arch. The incidences of aberrant right subclavian artery (ARSA) and aberrant left subclavian artery (ALSA) are 0.4% to 2.3% and 0.05%, respectively. Approximately 60% of ARSA patients will have a Kommerell's diverticulum at the origin of the ASA. Symptomatic or aneurysmal ASAs need to be treated. Historically, open operation was the favored method to reconstruct ASA anatomy; however, novel endovascular techniques are now available. Following a brief discussion of embryonic development, symptoms, and treatment history of the ASA and Kommerell's diverticulum, the results of a literature review to collect the worldwide experience of endovascular/hybrid treatment of ASA is presented.