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Vascular Loss of Type VIII Collagen Improves Venous Remodeling After Arteriovenous Fistula Creation In Mice
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100220
Xochilt Labissiere, Miguel Gabriel Rojas, Laisel Martinez, Roberto Vazquez-Padron
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引用次数: 0
Patient-specific computational flow simulation reveals significant differences in paravisceral aortic hemodynamics between fenestrated and branched endovascular aneurysm repair 针对患者的计算流模拟揭示了瓣膜和分支血管内动脉瘤修复术在主动脉瓣旁血流动力学方面的显著差异
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2023.100183
Kenneth Tran MD , Celine Deslarzes-Dubuis MD , Sebastien DeGlise MD , Adrien Kaladji MD , Weiguang Yang PhD , Alison L. Marsden PhD , Jason T. Lee MD

Background

Endovascular aneurysm repair with four-vessel fenestrated endovascular aneurysm repair (fEVAR) or branched endovascular aneurysm repair (bEVAR) currently represent the forefront of minimally invasive complex aortic aneurysm repair. This study sought to use patient-specific computational flow simulation (CFS) to assess differences in postoperative hemodynamic effects associated with fEVAR vs bEVAR.

Methods

Patients from two institutions who underwent four-vessel fEVAR with the Cook Zenith Fenestrated platform and bEVAR with the Jotec E-xtra Design platform were retrospectively selected. Patients in both cohorts were treated for paravisceral and extent II, II, and V thoracoabdominal aortic aneurysms. Three-dimensional finite element volume meshes were created from preoperative and postoperative computed tomography scans. Boundary conditions were adjusted for body surface area, heart rate, and blood pressure. Pulsatile flow simulations were performed with equivalent boundary conditions between preoperative and postoperative states. Postoperative changes in hemodynamic parameters were compared between the fEVAR and bEVAR groups.

Results

Patient-specific CFS was performed on 20 patients (10 bEVAR, 10 fEVAR) with a total of 80 target vessels (40 renal, 20 celiac, 20 superior mesenteric artery stents). bEVAR was associated with a decrease in renal artery peak flow rate (−5.2% vs +2.0%; P < .0001) and peak pressure (−3.4 vs +0.1%; P < .0001) compared with fEVAR. Almost all renal arteries treated with bEVAR had a reduction in renal artery perfusion (n = 19 [95%]), compared with 35% (n = 7) treated with fEVAR. There were no significant differences in celiac or superior mesenteric artery perfusion metrics (P = .10-.27) between groups. Time-averaged wall shear stress in the paravisceral aorta and branches also varied significantly depending on endograft configuration, with bEVAR associated with large postoperative increases in renal artery (+47.5 vs +13.5%; P = .002) and aortic time-averaged wall shear stress (+200.1% vs −31.3%; P = .001) compared with fEVAR. Streamline analysis revealed areas of hemodynamic abnormalities associated with branched renal grafts which adopt a U-shaped geometry, which may explain the observed differences in postoperative changes in renal perfusion between bEVAR and fEVAR.

Conclusions

bEVAR may be associated with subtle decreases in renal perfusion and a large increase in aortic wall shear stress compared with fEVAR. CFS is a novel tool for quantifying and visualizing the unique patient-specific hemodynamic effect of different complex EVAR strategies.

Clinical Relevance

This study used patient-specific CFS to compare postoperative hemodynamic effects of four-vessel fenestrated endovascular aneurysm repair (fEVAR) and branched endovascular aneurysm repair

背景四血管腔内动脉瘤修补术(fEVAR)或分支血管腔内动脉瘤修补术(bEVAR)目前代表了微创复杂主动脉瘤修补术的前沿。本研究试图使用患者特异性计算流模拟(CFS)来评估 fEVAR 与 bEVAR 术后血流动力学效应的差异。方法回顾性地选择了两家机构的患者,他们分别接受了使用 Cook Zenith Fenestrated 平台的四血管 fEVAR 术和使用 Jotec E-xtra Design 平台的 bEVAR 术。两组患者均接受了内脏旁和 II、II 和 V 度胸腹主动脉瘤的治疗。根据术前和术后的计算机断层扫描创建了三维有限元体积网格。根据体表面积、心率和血压调整了边界条件。在术前和术后状态相同的边界条件下进行了搏动流模拟。结果对 20 位患者(10 位 bEVAR,10 位 fEVAR)共 80 根目标血管(40 根肾动脉、20 根腹腔动脉、20 根肠系膜上动脉支架)进行了患者特异性 CFS 分析。与 fEVAR 相比,bEVAR 可降低肾动脉峰值流速(-5.2% vs +2.0%;P < .0001)和峰值压力(-3.4 vs +0.1%;P < .0001)。几乎所有接受 bEVAR 治疗的肾动脉灌注都减少了(19 例 [95%]),而接受 fEVAR 治疗的比例为 35% (7 例)。各组间腹腔动脉或肠系膜上动脉灌注指标无明显差异(P = .10-.27)。内植物配置不同,腹主动脉旁和分支的时间平均壁剪应力也有显著差异,与fEVAR相比,bEVAR术后肾动脉(+47.5 vs +13.5%;P = .002)和主动脉时间平均壁剪应力(+200.1% vs -31.3%;P = .001)大幅增加。流线分析显示了与采用 U 型几何形状的分支肾移植物相关的血流动力学异常区域,这可能解释了所观察到的 bEVAR 和 fEVAR 术后肾脏灌注变化的差异。本研究使用患者特异性 CFS 比较了复杂主动脉瘤患者术后四血管腔内动脉瘤修补术(fEVAR)和分支血管腔内动脉瘤修补术(bEVAR)对血流动力学的影响。研究结果表明,与 fEVAR 相比,bEVAR 可能会导致肾动脉灌注的细微减少和主动脉壁剪应力的显著增加。这些差异与临床相关,为临床医生选择这些方法提供了启示。了解 CFS 揭示的复杂 EVAR 策略对患者特异性血流动力学的影响有助于未来的个性化治疗决策,并有可能减少主动脉瘤修复术后并发症。
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引用次数: 0
Serum detection of blood brain barrier injury in subjects with a history of stroke and transient ischemic attack 在有中风和短暂性脑缺血发作病史的受试者血清中检测血脑屏障损伤
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100206
Scott French , Juan Arias MD , Ikeoluwapo Bolakale-Rufai MD , Summan Zahra MD , Kaneez Zahra Rubab Khakwani MD , Edward J. Bedrick PhD , Geidy E. Serrano PhD , Thomas G. Beach MD, PhD , Eric Reiman MD , Craig Weinkauf MD, PhD

Objective

Stroke and transient ischemic attack may have long-term negative effects on the blood-brain barrier (BBB) and promote endothelial inflammation, both of which could increase neurodegeneration and dementia risk beyond the cell death associated with the index event.

Methods

Serum from 88 postmortem subjects in the Arizona Study of Aging and Neurodegenerative Disorders were analyzed by sandwich ELISA for specific biomarkers to investigate the effects of cerebrovascular accidents (CVAs) on BBB integrity and endothelial activation. Statistical analyses were performed using the Mann-Whitney U Test, Spearman rank correlation, and linear/logistic regressions adjusted for potential confounders; a P-value < .05 was considered significant for all analyses.

Results

Serum PDGFRẞ, a putative biomarker of BBB injury, was significantly increased in subjects with vs without a history of CVA who had similar cardiovascular risk factors (P < .01). This difference was stable after adjusting for age, hypertension, and other potential confounders in regression analysis (odds ratio, 27.02; 95% confidence interval, 2.61-411.7; P < .01). In addition, PDGFRẞ was positively associated with VCAM-1, a biomarker of endothelial inflammation (ρ = 0.42; P < .01).

Conclusions

Our data suggest that patients with stroke or transient ischemic attack have lasting changes in the BBB. Still more, this demonstrates the utility of PDGFRẞ as a serum-based biomarker of BBB physiology, a potentially powerful tool in studying the role of the BBB in various neurodegenerative diseases and COVID infection sequelae.

Clinical Relevance

Our data demonstrate the utility of serum PDGFRẞ, a putative biomarker of BBB integrity in the setting of stroke and TIA (CVA). A serum biomarker of BBB integrity could be a useful tool to detect early BBB damage and allow prospective work to study how such damage affects long-term neurodegenerative risk. Since BBB disruption occurs early in ADRD development, it could be monitored to help better understand disease progression and involvement of vascular pathways in ADRD.

亚利桑那州衰老与神经退行性疾病研究(Arizona Study of Aging and Neurodegenerative Disorders)用夹心酶联免疫吸附分析法(Sandwich ELISA)分析了88例受试者死后血清中的特定生物标记物,以研究脑血管意外(CVA)对血脑屏障(BBB)完整性和内皮活化的影响。结果血清PDGFRẞ是BBB损伤的一种假定生物标志物,在具有类似心血管风险因素的有CVA病史和无CVA病史的受试者中显著增加(P< .01)。在回归分析中对年龄、高血压和其他潜在混杂因素进行调整后,这一差异保持稳定(几率比,27.02;95% 置信区间,2.61-411.7;P < .01)。此外,PDGFRẞ 与血管内皮炎症的生物标志物 VCAM-1 呈正相关(ρ = 0.42;P <;.01)。临床相关性我们的数据证明了血清 PDGFRẞ 的实用性,它是中风和短暂性脑缺血发作(CVA)时 BBB 完整性的潜在生物标志物。BBB 完整性的血清生物标志物可作为检测早期 BBB 损伤的有用工具,并可用于研究此类损伤如何影响长期神经退行性风险的前瞻性工作。由于 BBB 破坏发生在 ADRD 发病的早期,因此对其进行监测有助于更好地了解 ADRD 的疾病进展和血管通路的参与情况。
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引用次数: 0
Inhibition of Endothelial Cell-Mediated Efferocytosis Promotes Abdominal Aortic Aneurysm Formation
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100244
Jeff Arni C. Valisno, Gang Su, Paolo Bellotti, Jonathan Krebs, Guoshuai Cai, Guanyi Lu, Ashish K. Sharma, Gilbert R. Upchurch Jr.
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引用次数: 0
Modeling Varicose Vein Using Induced Pluripotent Stem Cells
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100265
Chikage Noishiki, Shaunak S. Adkar, David Wu, Lu Liu, Naima C. Turbes, Dipti Tripathi, Amit Manhas, Dilip Thomas, Karim Sallam, Jason T. Lee, Nick J. Leeper, Derek Klarin, Eri Fukaya, Nazish Sayed
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引用次数: 0
Pathological PERK/ATF4 Activation in Vascular Smooth Muscle Cells Drives Abdominal Aortic Aneurysm Development
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100249
Brennan Callow, Kevin Dale Mangum, Tyler Bauer, Xianying Xing, Mary O'Riordan, Johann Gudjonsson, Andrea T. Obi, Katherine A. Gallagher, Frank M. Davis
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引用次数: 0
Three-Dimensional Characterization of Sex Differences in Abdominal Aortic Aneurysm Progression Via Vascular Deformation Mapping
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100251
Drew Braet, Luciano Delbono, Greg Spahlinger, Nathan Graham, Akul Arora, C. Alberto Figueroa, Jonathan Eliason, Nicholas S. Burris
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引用次数: 0
The role of 6-phosphogluconate dehydrogenase in vascular smooth muscle cell phenotypic switching and angioplasty-induced intimal hyperplasia 6- 磷酸葡萄糖酸脱氢酶在血管平滑肌细胞表型转换和血管成形术诱导的内膜增生中的作用
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100214
Amy L. Lu , Li Yin PhD , Yitao Huang BS , Zain Husain Islam , Rohan Kanchetty , Campbell Johnston , Kaijie Zhang MD , Xiujie Xie PhD , Ki Ho Park PhD , Charles E. Chalfant PhD , Bowen Wang PhD

Background

Restenosis poses a significant challenge for individuals afflicted with peripheral artery diseases, often leading to considerable morbidity and necessitating repeated interventions. The primary culprit behind the pathogenesis of restenosis is intimal hyperplasia (IH), in which the hyperproliferative and migratory vascular smooth muscle cell (VSMC) accumulate excessively in the tunica intima. 6-Phosphogluconate dehydrogenase (6PGD), sometimes referred to as PGD, is one of the critical enzymes in pentose phosphate pathway (PPP). In this study, we sought to probe whether 6PGD is aberrantly regulated in IH and contributes to VSMC phenotypic switching.

Methods

We used clinical specimens of diseased human coronary arteries with IH lesions and observed robust upregulation of 6PGD at protein level in both the medial and intimal layers in comparison with healthy arterial segments.

Results

6PGD activity and protein expression were profoundly stimulated upon platelet-derived growth factor-induced VSMC phenotypic switching. Using gain-of-function (dCas9-mediated transcriptional activation) and loss-of-function (small interfering RNA-mediated) silencing, we were able to demonstrate the pathogenic role of 6PGD in driving VSMC hyperproliferation, migration, dedifferentiation, and inflammation. Finally, we conducted a rat model of balloon angioplasty in the common carotid artery, with Pluronic hydrogel-assisted perivascular delivery of Physcion, a selective 6PGD inhibitor with poor systemic bioavailability, and observed effective mitigation of IH.

Conclusions

We contend that aberrant 6PGD expression and activity—indicative of a metabolic shift toward pentose phosphate pathway—could serve as a new disease-driving mechanism and, hence, an actionable target for the development of effective new therapies for IH and restenosis after endovascular interventions.

背景再狭窄是外周动脉疾病患者面临的一个重大挑战,通常会导致相当高的发病率,并需要反复进行干预。再狭窄发病机制的罪魁祸首是内膜增生(IH),在这种情况下,过度增殖和移行的血管平滑肌细胞(VSMC)在内膜中过度聚集。6-磷酸葡萄糖酸脱氢酶(6PGD),有时也称为 PGD,是磷酸戊糖途径(PPP)的关键酶之一。本研究试图探究 6PGD 是否在 IH 中受到异常调控并导致 VSMC 表型转换。结果 6PGD 的活性和蛋白表达在血小板衍生生长因子诱导的 VSMC 表型转换时受到显著刺激。利用功能获得(dCas9 介导的转录激活)和功能丧失(小干扰 RNA 介导的)沉默,我们能够证明 6PGD 在驱动 VSMC 过度增殖、迁移、去分化和炎症中的致病作用。最后,我们在大鼠颈总动脉中进行了球囊血管成形术模型,并在 Pluronic 水凝胶辅助下在血管周围输送 Physcion(一种全身生物利用度较低的选择性 6PGD 抑制剂),观察到 IH 得到了有效缓解。结论我们认为,6PGD 的异常表达和活性--表明新陈代谢转向磷酸戊糖途径--可作为一种新的疾病驱动机制,从而成为开发治疗 IH 和血管内介入术后再狭窄的有效新疗法的可行靶点。
{"title":"The role of 6-phosphogluconate dehydrogenase in vascular smooth muscle cell phenotypic switching and angioplasty-induced intimal hyperplasia","authors":"Amy L. Lu ,&nbsp;Li Yin PhD ,&nbsp;Yitao Huang BS ,&nbsp;Zain Husain Islam ,&nbsp;Rohan Kanchetty ,&nbsp;Campbell Johnston ,&nbsp;Kaijie Zhang MD ,&nbsp;Xiujie Xie PhD ,&nbsp;Ki Ho Park PhD ,&nbsp;Charles E. Chalfant PhD ,&nbsp;Bowen Wang PhD","doi":"10.1016/j.jvssci.2024.100214","DOIUrl":"10.1016/j.jvssci.2024.100214","url":null,"abstract":"<div><h3>Background</h3><p>Restenosis poses a significant challenge for individuals afflicted with peripheral artery diseases, often leading to considerable morbidity and necessitating repeated interventions. The primary culprit behind the pathogenesis of restenosis is intimal hyperplasia (IH), in which the hyperproliferative and migratory vascular smooth muscle cell (VSMC) accumulate excessively in the tunica intima. 6-Phosphogluconate dehydrogenase (6PGD), sometimes referred to as PGD, is one of the critical enzymes in pentose phosphate pathway (PPP). In this study, we sought to probe whether 6PGD is aberrantly regulated in IH and contributes to VSMC phenotypic switching.</p></div><div><h3>Methods</h3><p>We used clinical specimens of diseased human coronary arteries with IH lesions and observed robust upregulation of 6PGD at protein level in both the medial and intimal layers in comparison with healthy arterial segments.</p></div><div><h3>Results</h3><p>6PGD activity and protein expression were profoundly stimulated upon platelet-derived growth factor-induced VSMC phenotypic switching. Using gain-of-function (dCas9-mediated transcriptional activation) and loss-of-function (small interfering RNA-mediated) silencing, we were able to demonstrate the pathogenic role of 6PGD in driving VSMC hyperproliferation, migration, dedifferentiation, and inflammation. Finally, we conducted a rat model of balloon angioplasty in the common carotid artery, with Pluronic hydrogel-assisted perivascular delivery of <em>Physcion</em>, a selective 6PGD inhibitor with poor systemic bioavailability, and observed effective mitigation of IH.</p></div><div><h3>Conclusions</h3><p>We contend that aberrant 6PGD expression and activity—indicative of a metabolic shift toward pentose phosphate pathway—could serve as a new disease-driving mechanism and, hence, an actionable target for the development of effective new therapies for IH and restenosis after endovascular interventions.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100214"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000257/pdfft?md5=015a2d171ee9d906e05a42573e145c34&pid=1-s2.0-S2666350324000257-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction notice to “Neointimal hyperplasia after carotid transection and anastomosis surgery is associated with degradation of decorin and platelet-derived growth factor signaling” [JVS–Vascular Science 2 (2021) 2 - 12] 颈动脉横断和吻合手术后的新内膜增生与去甲斑素降解和血小板衍生生长因子信号传导有关》的撤稿通知 [JVS-Vascular Science 2 (2021) 2 - 12]
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100216
Roshan J. D'Cruz MD , Valerie B. Sampson PhD , Carly A. Askinas MD , Rebecca A. Scott PhD , Karyn G. Robinson MS , Claude A. Beaty MD , Anne M. Hesek AS , Robert E. Akins PhD, FAHA
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引用次数: 0
A surgeon-scientist's approach to improving arteriovenous fistula patency 外科医生-科学家改善动静脉瘘通畅的方法
Q3 Medicine Pub Date : 2024-01-01 DOI: 10.1016/j.jvssci.2024.100207
Alan Dardik MD, PhD
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引用次数: 0
期刊
JVS-vascular science
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