Progress in best medical treatment have made identification of best candidates for carotid surgery more difficult. New diagnostic modalities could be helpful in this perspective. Microwaves (MWs) can quantify dielectric properties (complex relative permittivity) of biological tissues and MW technology has emerged as a promising field of research for distinguishing abnormal tissues from healthy ones. We here evaluated the ability of a dedicated MW sensor developed in our laboratory to identify vulnerable carotid lesions.
Methods
We included 50 carotid lesions in this study. The plaques were analyzed and classified preoperatively by ultrasound (US) examination, computed tomography angiography and tested postoperatively using a MW sensor. Histopathological analysis was used as a gold standard to separate vulnerable plaques (VPs) from nonvulnerable plaques (NVPs).
Results
VPs were more frequently types 2 or 3 plaques (on US examination), had a greater proportion of low (<60 Hounsfield unit) and moderate (60-130 Hounsfield unit) attenuation components (computed tomography angiography) and displayed higher dielectric constant values (MW) than NVPs, which had an opposite profile. NVPs were more frequently asymptomatic plaques compared with VPs (P = .035). Multivariate analysis showed that US examination and MW identified VPs with a sensitivity of 77% and a specificity of 76% (cutoff value, –0.045; area under the curve, 0.848; P < .0001).
Conclusions
We found that the presence of types 2 to 3 (on US examination) and high dielectric constant plaques in vitro was highly indicative of a VP based on histological analysis. Further studies are needed to determine the potential of MW to identify the most dangerous asymptomatic carotid lesions.
{"title":"In vitro analysis of carotid lesions using a preliminary microwave sensor to detect vulnerable plaques: Correlation with histology, Duplex ultrasound examination, and computed tomography scanner: The Imaging and Microwave Phenotyping Assessment of Carotid stenosis Threat (IMPACT) study","authors":"Rania Shahbaz PhD , Etienne Charpentier MD , Maharajah Ponnaiah PhD , Frédérique Deshours PhD , Hamid Kokabi PhD , Isabelle Brochériou MD, PhD , Gilles Le Naour PhD , Alban Redheuil MD, PhD , Fabien Koskas MD, PhD , Jean-Michel Davaine MD, PhD","doi":"10.1016/j.jvssci.2023.100182","DOIUrl":"10.1016/j.jvssci.2023.100182","url":null,"abstract":"<div><h3>Objective</h3><p>Progress in best medical treatment have made identification of best candidates for carotid surgery more difficult. New diagnostic modalities could be helpful in this perspective. Microwaves (MWs) can quantify dielectric properties (complex relative permittivity) of biological tissues and MW technology has emerged as a promising field of research for distinguishing abnormal tissues from healthy ones. We here evaluated the ability of a dedicated MW sensor developed in our laboratory to identify vulnerable carotid lesions.</p></div><div><h3>Methods</h3><p>We included 50 carotid lesions in this study. The plaques were analyzed and classified preoperatively by ultrasound (US) examination, computed tomography angiography and tested postoperatively using a MW sensor. Histopathological analysis was used as a gold standard to separate vulnerable plaques (VPs) from nonvulnerable plaques (NVPs).</p></div><div><h3>Results</h3><p>VPs were more frequently types 2 or 3 plaques (on US examination), had a greater proportion of low (<60 Hounsfield unit) and moderate (60-130 Hounsfield unit) attenuation components (computed tomography angiography) and displayed higher dielectric constant values (MW) than NVPs, which had an opposite profile. NVPs were more frequently asymptomatic plaques compared with VPs (<em>P</em> = .035). Multivariate analysis showed that US examination and MW identified VPs with a sensitivity of 77% and a specificity of 76% (cutoff value, –0.045; area under the curve, 0.848; <em>P</em> < .0001).</p></div><div><h3>Conclusions</h3><p>We found that the presence of types 2 to 3 (on US examination) and high dielectric constant plaques in vitro was highly indicative of a VP based on histological analysis. Further studies are needed to determine the potential of MW to identify the most dangerous asymptomatic carotid lesions.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266635032300086X/pdfft?md5=afffd8fbb14ab1c4a89531bcf8ce250b&pid=1-s2.0-S266635032300086X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138992631","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}
Pub Date : 2024-01-01DOI: 10.1016/j.jvssci.2024.100197
Sharon C. Kiang MD, FACS
{"title":"Artificial intelligence: The magic 8 ball for vascular surgery","authors":"Sharon C. Kiang MD, FACS","doi":"10.1016/j.jvssci.2024.100197","DOIUrl":"https://doi.org/10.1016/j.jvssci.2024.100197","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000087/pdfft?md5=506c99565c872936917c1c97d9bd2319&pid=1-s2.0-S2666350324000087-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140344813","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}
Pub Date : 2024-01-01DOI: 10.1016/j.jvssci.2024.100213
Objective
Implantation of an endovascular device disrupts the homeostatic CD31:CD31 interactions among quiescent endothelial cells (ECs), platelets, and circulating leukocytes. The aim of this study was to design an endothelial-mimetic coating of nitinol and cobalt-chromium (CoCr) surfaces and stents using synthetic CD31 peptides, to promote device endothelialization and pacific integration within the arterial wall.
Methods
Peptides mimicking the domains 1 (D1) and 2 (D2) of CD31 were synthetized and immobilized onto experimental nitinol and CoCr surfaces using a three-step, dip-coating, mussel-inspired protocol using copper-free click chemistry. Human aortic EC phenotype and endothelialization assessment using parallel scratch tests were carried out using five synthetic CD31 peptides coated on 4.8-mm nitinol and CoCr flat disks and were compared with control disks. The CD31 peptide exhibiting the best results in vitro was then immobilized on clinical-grade 3 × 40-mm self-expanding nitinol and 2.5 × 20.0-mm balloon-expandable CoCr stents. Such devices were implanted in native arteries of White New Zealand rabbits, and compared with control uncoated bare metal stents (BMS) and drug-eluting stents 7 and 30 days after implantation using resin cross-sections and scanning electron microscopy (n = 2-3 per group at each time point).
Results
Membrane-distal CD31 D1 and D2 peptides exhibited a distinct capability to foster a healthy endothelial phenotype and to promote endothelialization in vitro. By day 7 after implantation, CD31 nitinol and CoCr stents were evenly covered by wholesome ECs, devoid of thromboinflammatory signs, in contrast with both BMS and drug-eluting stents. Such results were consistent until day 30.
Conclusions
Membrane-distal CD31 biomimetic peptides seem to camouflage the device surface effectively, preventing local reactions and promoting rapid and seamless endovascular integration.
{"title":"Camouflaging endovascular stents with an endothelial coat using CD31 domain 1 and 2 mimetic peptides","authors":"","doi":"10.1016/j.jvssci.2024.100213","DOIUrl":"10.1016/j.jvssci.2024.100213","url":null,"abstract":"<div><h3>Objective</h3><p>Implantation of an endovascular device disrupts the homeostatic CD31:CD31 interactions among quiescent endothelial cells (ECs), platelets, and circulating leukocytes. The aim of this study was to design an endothelial-mimetic coating of nitinol and cobalt-chromium (CoCr) surfaces and stents using synthetic CD31 peptides, to promote device endothelialization and pacific integration within the arterial wall.</p></div><div><h3>Methods</h3><p>Peptides mimicking the domains 1 (D1) and 2 (D2) of CD31 were synthetized and immobilized onto experimental nitinol and CoCr surfaces using a three-step, dip-coating, mussel-inspired protocol using copper-free click chemistry. Human aortic EC phenotype and endothelialization assessment using parallel scratch tests were carried out using five synthetic CD31 peptides coated on 4.8-mm nitinol and CoCr flat disks and were compared with control disks. The CD31 peptide exhibiting the best results in vitro was then immobilized on clinical-grade 3 × 40-mm self-expanding nitinol and 2.5 × 20.0-mm balloon-expandable CoCr stents. Such devices were implanted in native arteries of White New Zealand rabbits, and compared with control uncoated bare metal stents (BMS) and drug-eluting stents 7 and 30 days after implantation using resin cross-sections and scanning electron microscopy (n = 2-3 per group at each time point).</p></div><div><h3>Results</h3><p>Membrane-distal CD31 D1 and D2 peptides exhibited a distinct capability to foster a healthy endothelial phenotype and to promote endothelialization in vitro. By day 7 after implantation, CD31 nitinol and CoCr stents were evenly covered by wholesome ECs, devoid of thromboinflammatory signs, in contrast with both BMS and drug-eluting stents. Such results were consistent until day 30.</p></div><div><h3>Conclusions</h3><p>Membrane-distal CD31 biomimetic peptides seem to camouflage the device surface effectively, preventing local reactions and promoting rapid and seamless endovascular integration.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000245/pdfft?md5=586568decde158b644a6988f3b5e2f40&pid=1-s2.0-S2666350324000245-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141851075","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}
Pub Date : 2024-01-01DOI: 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
{"title":"Patient-specific computational flow simulation reveals significant differences in paravisceral aortic hemodynamics between fenestrated and branched endovascular aneurysm repair","authors":"Kenneth Tran MD , Celine Deslarzes-Dubuis MD , Sebastien DeGlise MD , Adrien Kaladji MD , Weiguang Yang PhD , Alison L. Marsden PhD , Jason T. Lee MD","doi":"10.1016/j.jvssci.2023.100183","DOIUrl":"10.1016/j.jvssci.2023.100183","url":null,"abstract":"<div><h3>Background</h3><p>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.</p></div><div><h3>Methods</h3><p>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.</p></div><div><h3>Results</h3><p>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%; <em>P</em> < .0001) and peak pressure (−3.4 vs +0.1%; <em>P</em> < .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 (<em>P</em> = .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%; <em>P</em> = .002) and aortic time-averaged wall shear stress (+200.1% vs −31.3%; <em>P</em> = .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.</p></div><div><h3>Conclusions</h3><p>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.</p></div><div><h3>Clinical Relevance</h3><p>This study used patient-specific CFS to compare postoperative hemodynamic effects of four-vessel fenestrated endovascular aneurysm repair (fEVAR) and branched endovascular aneurysm repair ","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350323000871/pdfft?md5=a80815d2199cb6cf5b972868ccdb2934&pid=1-s2.0-S2666350323000871-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139298688","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}
Pub Date : 2024-01-01DOI: 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.
{"title":"Serum detection of blood brain barrier injury in subjects with a history of stroke and transient ischemic attack","authors":"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","doi":"10.1016/j.jvssci.2024.100206","DOIUrl":"https://doi.org/10.1016/j.jvssci.2024.100206","url":null,"abstract":"<div><h3>Objective</h3><p>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.</p></div><div><h3>Methods</h3><p>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 <em>U</em> Test, Spearman rank correlation, and linear/logistic regressions adjusted for potential confounders; a <em>P</em>-value < .05 was considered significant for all analyses.</p></div><div><h3>Results</h3><p>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 (<em>P</em> < .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; <em>P</em> < .01). In addition, PDGFRẞ was positively associated with VCAM-1, a biomarker of endothelial inflammation (ρ = 0.42; <em>P</em> < .01).</p></div><div><h3>Conclusions</h3><p>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.</p></div><div><h3>Clinical Relevance</h3><p>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.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000178/pdfft?md5=2882cf384347395014f8173be3bf2f3e&pid=1-s2.0-S2666350324000178-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141240412","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}
Arterial stiffening is associated with adverse cardiovascular patient outcomes; stiffness may also be associated with postsurgical events and has been suggested to be a fundamental mechanism in the pathogenesis of aortic aneurysms. Although open repair of aneurysms decreases aortic stiffness, implantation of a rigid endograft is associated with increased aortic stiffness after endovascular aneurysm repair (EVAR). This review provides an overview of aortic wall physiology and the contemporary understanding of aortic stiffness and its implications for patients undergoing abdominal aortic aneurysm repair. Recent data suggests that increased central arterial stiffness, estimated preoperatively using the pulse wave velocity (PWV), may predict aneurysm sac behavior after EVAR, with elevated preoperative PWV associated with less sac shrinkage, and even sac enlargement, after EVAR. With the development of several simple noninvasive methods to measure PWV, such as brachial-ankle PWV and single cuff brachial oscillometry, there may be a role for monitoring ambulatory PWV to predict outcomes after EVAR. Additionally, because aortic stiffness is associated with adverse cardiovascular outcomes, and EVAR increases aortic stiffness, assessment of aortic stiffness before aortic interventions may help to guide therapeutic decisions as well as surveillance protocols, leading to optimized patient outcomes.
{"title":"Implications of preoperative arterial stiffness for patients treated with endovascular repair of abdominal aortic aneurysms","authors":"Carly Thaxton MD , Masaki Kano MD, PhD , Daniel Mendes-Pinto MD, PhD , Túlio Pinho Navarro MD, PhD , Toshiya Nishibe MD, PhD , Alan Dardik MD, PhD","doi":"10.1016/j.jvssci.2024.100209","DOIUrl":"10.1016/j.jvssci.2024.100209","url":null,"abstract":"<div><p>Arterial stiffening is associated with adverse cardiovascular patient outcomes; stiffness may also be associated with postsurgical events and has been suggested to be a fundamental mechanism in the pathogenesis of aortic aneurysms. Although open repair of aneurysms decreases aortic stiffness, implantation of a rigid endograft is associated with increased aortic stiffness after endovascular aneurysm repair (EVAR). This review provides an overview of aortic wall physiology and the contemporary understanding of aortic stiffness and its implications for patients undergoing abdominal aortic aneurysm repair. Recent data suggests that increased central arterial stiffness, estimated preoperatively using the pulse wave velocity (PWV), may predict aneurysm sac behavior after EVAR, with elevated preoperative PWV associated with less sac shrinkage, and even sac enlargement, after EVAR. With the development of several simple noninvasive methods to measure PWV, such as brachial-ankle PWV and single cuff brachial oscillometry, there may be a role for monitoring ambulatory PWV to predict outcomes after EVAR. Additionally, because aortic stiffness is associated with adverse cardiovascular outcomes, and EVAR increases aortic stiffness, assessment of aortic stiffness before aortic interventions may help to guide therapeutic decisions as well as surveillance protocols, leading to optimized patient outcomes.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000208/pdfft?md5=1cd6d8eee65627db4bd2b983b5be5f8c&pid=1-s2.0-S2666350324000208-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141134147","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}
Pub Date : 2024-01-01DOI: 10.1016/j.jvssci.2024.100214
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":"","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":null,"pages":null},"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}
Pub Date : 2024-01-01DOI: 10.1016/j.jvssci.2024.100191
Anand Brahmandam MD , Rafael Alves BM , Hao Liu (刘灏) MD , Luis Gonzalez PhD , Yukihiko Aoyagi (青栁 幸彦) MD , Yuichi Ohashi (大橋 雄一) MD , John T. Langford MD , Carly Thaxton MD , Ryosuke Taniguchi (谷口 良輔) MD, PhD , Weichang Zhang (张惟常) MD, PhD , Hualong Bai (白华龙) MD, PhD , Bogdan Yatsula PhD , Alan Dardik MD, PhD
Objective
A central arteriovenous fistula (AVF) has been proposed as a potential novel solution to treat patients with refractory hypertension. We hypothesized that venous remodeling after AVF creation in the hypertensive environment reduces systemic blood pressure but results in increased AVF wall thickness compared with remodeling in the normotensive environment.
Methods
A central AVF was performed in C57BL6/J mice previously made hypertensive with angiotensin II (Ang II); mice were sacrificed on postoperative day 7 or 21.
Results
In mice treated with Ang II alone, the mean systolic blood pressure increased from 90 ± 5 mmHg to 160 ± 5 mmHg at day 21; however, in mice treated with both Ang II and an AVF, the blood pressure decreased with creation of an AVF. There were significantly more PCNA-positive cells, SM22α/PCNA-positive cells, collagen I deposition, and increased Krüppel-like Factor 2 immunoreactivity in hypertensive mice with an AVF compared with normotensive mice with an AVF.
Conclusions
These data show that a central AVF decreases systemic hypertension as well as induces local alterations in venous remodeling.
{"title":"A central arteriovenous fistula reduces systemic hypertension in a mouse model","authors":"Anand Brahmandam MD , Rafael Alves BM , Hao Liu (刘灏) MD , Luis Gonzalez PhD , Yukihiko Aoyagi (青栁 幸彦) MD , Yuichi Ohashi (大橋 雄一) MD , John T. Langford MD , Carly Thaxton MD , Ryosuke Taniguchi (谷口 良輔) MD, PhD , Weichang Zhang (张惟常) MD, PhD , Hualong Bai (白华龙) MD, PhD , Bogdan Yatsula PhD , Alan Dardik MD, PhD","doi":"10.1016/j.jvssci.2024.100191","DOIUrl":"10.1016/j.jvssci.2024.100191","url":null,"abstract":"<div><h3>Objective</h3><p>A central arteriovenous fistula (AVF) has been proposed as a potential novel solution to treat patients with refractory hypertension. We hypothesized that venous remodeling after AVF creation in the hypertensive environment reduces systemic blood pressure but results in increased AVF wall thickness compared with remodeling in the normotensive environment.</p></div><div><h3>Methods</h3><p>A central AVF was performed in C57BL6/J mice previously made hypertensive with angiotensin II (Ang II); mice were sacrificed on postoperative day 7 or 21.</p></div><div><h3>Results</h3><p>In mice treated with Ang II alone, the mean systolic blood pressure increased from 90 ± 5 mmHg to 160 ± 5 mmHg at day 21; however, in mice treated with both Ang II and an AVF, the blood pressure decreased with creation of an AVF. There were significantly more PCNA-positive cells, SM22α/PCNA-positive cells, collagen I deposition, and increased Krüppel-like Factor 2 immunoreactivity in hypertensive mice with an AVF compared with normotensive mice with an AVF.</p></div><div><h3>Conclusions</h3><p>These data show that a central AVF decreases systemic hypertension as well as induces local alterations in venous remodeling.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000026/pdfft?md5=60786e70b011585e96e3a0ee22d68666&pid=1-s2.0-S2666350324000026-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139832835","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}
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