Pub Date : 2026-01-01Epub Date: 2025-11-27DOI: 10.1016/j.jvssci.2025.100397
Yasir AlSiraj PhD , Kelly Putnam PhD , Seth I. Brunner BS , Victoria L. English PhD , Charles M. Ensor PhD , Lisa A. Cassis PhD
<div><h3>Objective</h3><div>Adipocytes express renin–angiotensin system (RAS) components, including angiotensinogen (<em>Agt</em>), the precursor to angiotensin II (AngII), and the angiotensin type 1a receptor (<em>AT1aR</em>). The RAS contributes to atherosclerosis, and AngII infusion causes abdominal aortic aneurysm (AAA) formation. We studied effects of adipocyte <em>Agt</em> or <em>AT1aR</em> deficiency on diet-induced atherosclerosis and AngII-induced AAAs in male low-density lipoprotein receptor (<em>Ldlr</em>)-deficient mice.</div></div><div><h3>Methods</h3><div>For atherosclerosis, adipocyte <em>Agt-</em> or <em>AT1aR</em>-deficient <em>Ldlr</em>-deficient mice and littermate controls were fed a Western diet for 3 months. For AAAs, adipocyte <em>Agt-</em> or <em>AT1aR</em>-deficient <em>Ldlr</em><sup><em>−/−</em></sup> mice and littermate controls were fed a Western diet and infused with AngII (1000 ng/kg/min) for 28 days. Atherosclerosis was quantified en face in the aortic arch by the percent of intimal surface area covered by an atherosclerotic lesion. Serum (cholesterol, triglyceride) and plasma renin activity were quantified at study end point. AAAs were quantified in vivo by ultrasound quantification of abdominal aortic lumen diameters in anesthetized mice or at study end point by quantifying maximal external abdominal aortic diameter and AAA incidence (percent). Systolic blood pressure was quantified in AngII-infused mice by tail cuff plethysmography. Adipocyte size was quantified in tissue sections of white adipose tissue. Male <em>Ldlr</em><sup><em>−/−</em></sup> mice were fed a standard diet or a Western diet (1 or 3 months) and <em>Agt</em> or <em>AT1aR</em> messenger RNA (mRNA) abundance quantified in periaortic fat (PAF) by reverse transcriptase polymerase chain reaction.</div></div><div><h3>Results</h3><div>There was no effect of adipocyte <em>Agt</em> deficiency on body weight, serum cholesterol concentrations, or atherosclerotic lesions of Western diet-fed <em>Ldlr</em><sup><em>−/−</em></sup> mice. Adipocyte <em>Agt</em> deficiency had no effect on body weight, serum cholesterol concentrations, abdominal aortic lumen diameter, AAA incidence, or atherosclerosis of AngII-infused <em>Ldlr</em><sup><em>−/−</em></sup> mice. There was no effect of adipocyte AT1aR deficiency on body weight, serum cholesterol concentrations, or atherosclerotic lesions of Western diet-fed <em>Ldlr</em><sup><em>−/−</em></sup> mice. Control, but not adipocyte <em>AT1aR</em>-deficient mice lost weight during AngII infusion. The size of adipocytes in white adipose tissue was increased in adipocyte <em>AT1aR</em>-deficient mice with no significant influences on abdominal aortic lumen diameter, AAA incidence, or atherosclerosis of AngII-infused mice. In mice fed a Western diet for 1 or 3 months, <em>Agt</em> mRNA abundance in abdominal PAF increased over time in both diet groups, with modest diet-induced decreases in thoracic PAF <em>Agt</em> mRNA abunda
{"title":"Role of adipocyte angiotensinogen or angiotensin type 1a receptors in the development of diet-induced atherosclerosis or angiotensin II-induced abdominal aortic aneurysms","authors":"Yasir AlSiraj PhD , Kelly Putnam PhD , Seth I. Brunner BS , Victoria L. English PhD , Charles M. Ensor PhD , Lisa A. Cassis PhD","doi":"10.1016/j.jvssci.2025.100397","DOIUrl":"10.1016/j.jvssci.2025.100397","url":null,"abstract":"<div><h3>Objective</h3><div>Adipocytes express renin–angiotensin system (RAS) components, including angiotensinogen (<em>Agt</em>), the precursor to angiotensin II (AngII), and the angiotensin type 1a receptor (<em>AT1aR</em>). The RAS contributes to atherosclerosis, and AngII infusion causes abdominal aortic aneurysm (AAA) formation. We studied effects of adipocyte <em>Agt</em> or <em>AT1aR</em> deficiency on diet-induced atherosclerosis and AngII-induced AAAs in male low-density lipoprotein receptor (<em>Ldlr</em>)-deficient mice.</div></div><div><h3>Methods</h3><div>For atherosclerosis, adipocyte <em>Agt-</em> or <em>AT1aR</em>-deficient <em>Ldlr</em>-deficient mice and littermate controls were fed a Western diet for 3 months. For AAAs, adipocyte <em>Agt-</em> or <em>AT1aR</em>-deficient <em>Ldlr</em><sup><em>−/−</em></sup> mice and littermate controls were fed a Western diet and infused with AngII (1000 ng/kg/min) for 28 days. Atherosclerosis was quantified en face in the aortic arch by the percent of intimal surface area covered by an atherosclerotic lesion. Serum (cholesterol, triglyceride) and plasma renin activity were quantified at study end point. AAAs were quantified in vivo by ultrasound quantification of abdominal aortic lumen diameters in anesthetized mice or at study end point by quantifying maximal external abdominal aortic diameter and AAA incidence (percent). Systolic blood pressure was quantified in AngII-infused mice by tail cuff plethysmography. Adipocyte size was quantified in tissue sections of white adipose tissue. Male <em>Ldlr</em><sup><em>−/−</em></sup> mice were fed a standard diet or a Western diet (1 or 3 months) and <em>Agt</em> or <em>AT1aR</em> messenger RNA (mRNA) abundance quantified in periaortic fat (PAF) by reverse transcriptase polymerase chain reaction.</div></div><div><h3>Results</h3><div>There was no effect of adipocyte <em>Agt</em> deficiency on body weight, serum cholesterol concentrations, or atherosclerotic lesions of Western diet-fed <em>Ldlr</em><sup><em>−/−</em></sup> mice. Adipocyte <em>Agt</em> deficiency had no effect on body weight, serum cholesterol concentrations, abdominal aortic lumen diameter, AAA incidence, or atherosclerosis of AngII-infused <em>Ldlr</em><sup><em>−/−</em></sup> mice. There was no effect of adipocyte AT1aR deficiency on body weight, serum cholesterol concentrations, or atherosclerotic lesions of Western diet-fed <em>Ldlr</em><sup><em>−/−</em></sup> mice. Control, but not adipocyte <em>AT1aR</em>-deficient mice lost weight during AngII infusion. The size of adipocytes in white adipose tissue was increased in adipocyte <em>AT1aR</em>-deficient mice with no significant influences on abdominal aortic lumen diameter, AAA incidence, or atherosclerosis of AngII-infused mice. In mice fed a Western diet for 1 or 3 months, <em>Agt</em> mRNA abundance in abdominal PAF increased over time in both diet groups, with modest diet-induced decreases in thoracic PAF <em>Agt</em> mRNA abunda","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100397"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145841692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2025-05-23DOI: 10.1016/j.jvssci.2025.100291
Weichen Hong BS , Vijay Tewari BS , Huidan Yu PhD , Jun Chen PhD , Alan P. Sawchuk MD
Compliance mismatch between native arteries and prosthetic grafts contribute to complications such as neointimal hyperplasia and pseudoaneurysms, leading to reduced graft patency. Three-dimensional (3D) printing offers a promising solution by flexibly customizing mechanical properties using elastic polymers. This study investigates whether 3D-printed polymeric grafts can better replicate native arterial compliance compared with commercial prosthetic grafts. We conducted compliance tests on human aortoiliac arteries, polytetrafluoroethylene (PTFE) grafts, Dacron grafts, and 3D-printed arteries with BioMed Elastic Resin within a mock circulation loop. All samples shared controlled geometry and were tested under the same physiological flow conditions. Pressure waveforms and key hemodynamic parameters were recorded and analyzed. The 3D-printed graft demonstrated a compliance of 0.49 cm3/mmHg, more closely matching the human artery than PTFE (0.38 cm3/mmHg) and Dacron (0.45 cm3/mmHg). Its mean arterial pressure (82 ± 0.6 mmHg) and peak pressure (40 ± 0.7 mmHg) in the flow loop also aligned more closely with the native artery compared with conventional grafts. Standard prosthetic graft materials have remained relatively static, whereas there has been immense advancement in new polymer technology. These polymers can match the compliance of native vessels, theoretically reducing complications associated with traditional grafts, and future work should investigate their biocompatibility, durability, and clinical feasibility.
{"title":"Evaluating compliance in three-dimensional-printed polymeric vascular grafts compared to human arteries and commercial grafts in a mock circulation loop compliance in three-dimensional-printed polymeric vascular grafts","authors":"Weichen Hong BS , Vijay Tewari BS , Huidan Yu PhD , Jun Chen PhD , Alan P. Sawchuk MD","doi":"10.1016/j.jvssci.2025.100291","DOIUrl":"10.1016/j.jvssci.2025.100291","url":null,"abstract":"<div><div>Compliance mismatch between native arteries and prosthetic grafts contribute to complications such as neointimal hyperplasia and pseudoaneurysms, leading to reduced graft patency. Three-dimensional (3D) printing offers a promising solution by flexibly customizing mechanical properties using elastic polymers. This study investigates whether 3D-printed polymeric grafts can better replicate native arterial compliance compared with commercial prosthetic grafts. We conducted compliance tests on human aortoiliac arteries, polytetrafluoroethylene (PTFE) grafts, Dacron grafts, and 3D-printed arteries with BioMed Elastic Resin within a mock circulation loop. All samples shared controlled geometry and were tested under the same physiological flow conditions. Pressure waveforms and key hemodynamic parameters were recorded and analyzed. The 3D-printed graft demonstrated a compliance of 0.49 cm<sup>3</sup>/mmHg, more closely matching the human artery than PTFE (0.38 cm<sup>3</sup>/mmHg) and Dacron (0.45 cm<sup>3</sup>/mmHg). Its mean arterial pressure (82 ± 0.6 mmHg) and peak pressure (40 ± 0.7 mmHg) in the flow loop also aligned more closely with the native artery compared with conventional grafts. Standard prosthetic graft materials have remained relatively static, whereas there has been immense advancement in new polymer technology. These polymers can match the compliance of native vessels, theoretically reducing complications associated with traditional grafts, and future work should investigate their biocompatibility, durability, and clinical feasibility.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100291"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2025-04-29DOI: 10.1016/j.jvssci.2025.100289
Drew J. Braet MD , Moritz Lindquist Liljeqvist MD, PhD
{"title":"Toward the “slope of enlightenment”: The role of adiposity in abdominal aortic aneurysms","authors":"Drew J. Braet MD , Moritz Lindquist Liljeqvist MD, PhD","doi":"10.1016/j.jvssci.2025.100289","DOIUrl":"10.1016/j.jvssci.2025.100289","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100289"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2025-04-15DOI: 10.1016/j.jvssci.2025.100288
Kota Mitsui RT, BSc , Yunosuke Nishihara MD, PhD , Norisato Tsuda RT, MSc , Manabu Sato MD, PhD
Objective
This study aimed to: (1) investigate the hemodynamic characteristics of type II endoleaks using mathematical simulations based on pharmacokinetic analysis; and (2) validate the simulation results using clinical data from four-dimensional computed tomography (4D-CT) to assess the relationship between time-enhanced curves (TECs) and aneurysm enlargement.
Methods
A mathematical model was created to simulate the hemodynamics of type II endoleaks, incorporating nine compartments representing various cardiovascular components. Simulations were performed under different conditions, leading to the classification of endoleaks into four hemodynamic types. Clinical data were collected from 45 patients who underwent 4D-CT scans at a single center between April 2017 and April 2022. The study cohort included two groups: 20 patients with type II endoleaks identified within 1 week after endovascular aortic repair and 25 patients with persistent type II endoleaks diagnosed during follow-up imaging ranging from 6 months to 9 years post endovascular aortic repair. To evaluate aneurysm volume changes, follow-up CT scans were conducted 6 months or 1 year after the 4D-CT. The primary outcome was evaluating the consistency between simulation results and clinical TEC data obtained from 4D-CT. The secondary outcomes assessed the relationship between individual TEC parameters derived from clinical TEC data and aneurysm enlargement.
Results
The mathematical simulations successfully classified type II endoleaks into four hemodynamic types. Clinical validation showed a high concordance between simulation and clinical TEC shapes. A significant difference was observed in various TEC parameters between the stable and enlarged groups. The simulation-based analysis revealed a strong association between aneurysm enlargement and the most informative parameters, including 80% enhancement duration (area under the curve [AUC], 0.88; sensitivity, 0.87; specificity, 0.80; 95% confidence interval [CI], 0.779-0.990; cutoff, 16.9), peak-to-peak timefeeder (AUC, 0.78; sensitivity, 0.93; specificity, 0.60; 95% CI, 0.621-0.937; cutoff, 13.0), and upslope (AUC, 0.86; sensitivity, 0.73; specificity, 0.93; 95% CI, 0.740-0.972; cutoff, 11.7).
Conclusions
This study utilized mathematical simulations and clinical validation to characterize the hemodynamics of type II endoleaks. The results demonstrate the strong association of TEC parameters, derived from 4D-CT, with aneurysm enlargement, highlighting their potential for guiding timely intervention in clinical practice.
{"title":"Hemodynamic subtype classification of type II endoleaks using time-enhanced curves and its association with aneurysmal enlargement","authors":"Kota Mitsui RT, BSc , Yunosuke Nishihara MD, PhD , Norisato Tsuda RT, MSc , Manabu Sato MD, PhD","doi":"10.1016/j.jvssci.2025.100288","DOIUrl":"10.1016/j.jvssci.2025.100288","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to: (1) investigate the hemodynamic characteristics of type II endoleaks using mathematical simulations based on pharmacokinetic analysis; and (2) validate the simulation results using clinical data from four-dimensional computed tomography (4D-CT) to assess the relationship between time-enhanced curves (TECs) and aneurysm enlargement.</div></div><div><h3>Methods</h3><div>A mathematical model was created to simulate the hemodynamics of type II endoleaks, incorporating nine compartments representing various cardiovascular components. Simulations were performed under different conditions, leading to the classification of endoleaks into four hemodynamic types. Clinical data were collected from 45 patients who underwent 4D-CT scans at a single center between April 2017 and April 2022. The study cohort included two groups: 20 patients with type II endoleaks identified within 1 week after endovascular aortic repair and 25 patients with persistent type II endoleaks diagnosed during follow-up imaging ranging from 6 months to 9 years post endovascular aortic repair. To evaluate aneurysm volume changes, follow-up CT scans were conducted 6 months or 1 year after the 4D-CT. The primary outcome was evaluating the consistency between simulation results and clinical TEC data obtained from 4D-CT. The secondary outcomes assessed the relationship between individual TEC parameters derived from clinical TEC data and aneurysm enlargement.</div></div><div><h3>Results</h3><div>The mathematical simulations successfully classified type II endoleaks into four hemodynamic types. Clinical validation showed a high concordance between simulation and clinical TEC shapes. A significant difference was observed in various TEC parameters between the stable and enlarged groups. The simulation-based analysis revealed a strong association between aneurysm enlargement and the most informative parameters, including 80% enhancement duration (area under the curve [AUC], 0.88; sensitivity, 0.87; specificity, 0.80; 95% confidence interval [CI], 0.779-0.990; cutoff, 16.9), peak-to-peak time<sub>feeder</sub> (AUC, 0.78; sensitivity, 0.93; specificity, 0.60; 95% CI, 0.621-0.937; cutoff, 13.0), and upslope (AUC, 0.86; sensitivity, 0.73; specificity, 0.93; 95% CI, 0.740-0.972; cutoff, 11.7).</div></div><div><h3>Conclusions</h3><div>This study utilized mathematical simulations and clinical validation to characterize the hemodynamics of type II endoleaks. The results demonstrate the strong association of TEC parameters, derived from 4D-CT, with aneurysm enlargement, highlighting their potential for guiding timely intervention in clinical practice.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100288"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile. A mouse model of inducible VSMC GLUT1 deletion was created and aortic GLUT1 silencing was confirmed. Without Ang II plus β-aminopropionitrile treatment, no difference was observed regarding the external aortic diameter (control 1.06 ± 0.18 mm vs deletion 0.97 ± 0.26 mm) or systolic blood pressure (control 102 ± 9 mm Hg vs deletion 107 ± 11 mm Hg) between control or GLUT1-silenced mice. With treatment, control mice as well as VSMC GLUT1-silenced mice equally developed AAA (control 2.37 ± 0.75 mm vs deletion 2.41 ± 0.93 mm), whereas a tendency toward lower blood pressure was observed in GLUT1 silenced mice (control 150 ± 9 mm Hg vs deletion 135 ± 22 mm Hg). No significant difference was observed regarding the rate of rupture-dependent mortality. We concluded that VSMC GLUT1 is dispensable for AAA development induced by Ang II in mice.
研究表明，使用葡萄糖转运体（GLUT）葡萄糖利用抑制剂可减轻小鼠实验性腹主动脉瘤（AAA）的发生。血管平滑肌细胞（VSMC）信号传导似乎对血管紧张素 II（Ang II）诱导的小鼠 AAA 至关重要。因此，我们测试了一个假设，即血管平滑肌细胞（VSMC）沉默主要的 GLUT（GLUT1）可防止血管紧张素 II 加 β-氨基丙腈治疗小鼠 AAA 的发生和破裂。建立了诱导性血管内皮细胞 GLUT1 缺失的小鼠模型，并证实了主动脉 GLUT1 沉默。在未接受 Ang II 和 β-氨基丙腈治疗的情况下，对照组和 GLUT1 沉默小鼠的主动脉外径（对照组为 1.06 ± 0.18 mm，缺失组为 0.97 ± 0.26 mm）或收缩压（对照组为 102 ± 9 mm Hg，缺失组为 107 ± 11 mm Hg）均无差异。经过治疗后，对照组小鼠和 VSMC GLUT1 沉默小鼠同样发展为 AAA（对照组 2.37 ± 0.75 mm vs 基因缺失组 2.41 ± 0.93 mm），而 GLUT1 沉默小鼠的血压趋于降低（对照组 150 ± 9 mm Hg vs 基因缺失组 135 ± 22 mm Hg）。在破裂依赖性死亡率方面没有观察到明显差异。我们的结论是，血管内皮细胞 GLUT1 对于 Ang II 诱导的小鼠 AAA 的发展是不可或缺的。
{"title":"Glucose transporter 1 in vascular smooth muscle cells is dispensable for abdominal aortic aneurysm induced by angiotensin II","authors":"Keiichi Torimoto MD, PhD , Hymavathi Reddy Vari PhD , Yuki Nakayama MD, PhD , Hirotoshi Utsunomiya PhD , Masatoshi Takeda MD, PhD , Tomoki Hashimoto MD, PhD , Victor Rizzo PhD , Satoru Eguchi MD, PhD","doi":"10.1016/j.jvssci.2024.100270","DOIUrl":"10.1016/j.jvssci.2024.100270","url":null,"abstract":"<div><div>Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile. A mouse model of inducible VSMC GLUT1 deletion was created and aortic GLUT1 silencing was confirmed. Without Ang II plus β-aminopropionitrile treatment, no difference was observed regarding the external aortic diameter (control 1.06 ± 0.18 mm vs deletion 0.97 ± 0.26 mm) or systolic blood pressure (control 102 ± 9 mm Hg vs deletion 107 ± 11 mm Hg) between control or GLUT1-silenced mice. With treatment, control mice as well as VSMC GLUT1-silenced mice equally developed AAA (control 2.37 ± 0.75 mm vs deletion 2.41 ± 0.93 mm), whereas a tendency toward lower blood pressure was observed in GLUT1 silenced mice (control 150 ± 9 mm Hg vs deletion 135 ± 22 mm Hg). No significant difference was observed regarding the rate of rupture-dependent mortality. We concluded that VSMC GLUT1 is dispensable for AAA development induced by Ang II in mice.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100270"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11728061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985642","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 : 2025-01-01Epub Date: 2025-05-24DOI: 10.1016/j.jvssci.2025.100292
Leah M. Gober MD , Alan Dardik MD PhD
{"title":"Using computational modeling and four-dimensional computed tomography to predict type II endoleaks","authors":"Leah M. Gober MD , Alan Dardik MD PhD","doi":"10.1016/j.jvssci.2025.100292","DOIUrl":"10.1016/j.jvssci.2025.100292","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100292"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2025-01-21DOI: 10.1016/j.jvssci.2025.100281
Benjamin J. Madden BSc , Camilo Polania-Sandoval MD , Ganesh P. Pujari MD , Kiran K. Mangalaparthi PhD , M. Cristine Charlesworth PhD, MS , Mercedes Prudencio PhD , Tania Gendron PhD , Sukhwinder J.S. Sandhu MD , Aziza Nassar MD, MPH , Leonard Petrucelli PhD , James F. Meschia MD , Akhilesh Pandey MD, PhD , Young Erben MD
Objective
Extracranial carotid artery pathology accounts for 15% to 20% of ischemic strokes. Advancements in magnetic resonance angiography (MRA) with vessel wall imaging (VWI) have enabled the identification of vulnerable plaques, aiding in risk stratification for neurovascular events. This pilot study aimed to identify proteins in plaques with and without vulnerable features on MRA with VWI.
Methods
Consecutive patients undergoing carotid endarterectomy were included in the study cohort with preoperative MRA with VWI. A retrospective chart review was conducted to extract pertinent clinical data including cardiovascular risk factors and medications. Proteomic analysis involved Tandem Mass Tag (TMTpro) labeling of peptides, basic pH high-performance liquid chromatography fractionation, and NanoLC-tandem mass spectrometry.
Results
Proteomic analysis revealed 23 proteins significantly elevated in vulnerable plaques, including Proteinase 3 (PRTN3), Phospholipid Transfer Protein (PLTP), and S100 Calcium-Binding Protein A12 (S100A12), with increased abundance exceeding two-fold changes or above (P < .001). Conversely, three proteins exhibited reduced abundance in vulnerable plaques including Dynamin-3 (DNM3), Transmembrane Protein 181 (TMEM181), and Adducin-3 (ADD3) (P < .05).
Conclusions
This study contributes to the understanding of protein biomarkers associated with carotid plaque vulnerability, offering insights into disease progression and stroke prevention. Proteins secreted by vulnerable plaques may offer not only the potential for early disease recognition; but can also become a target for future pharmacologic therapy prior to a devastating neurologic event. Further validation studies and multi-center trials will be needed to confirm the value of these potential biomarkers.
{"title":"Proteomic analysis of carotid artery plaques with and without vulnerable features on magnetic resonance angiography with vessel wall imaging: a pilot study","authors":"Benjamin J. Madden BSc , Camilo Polania-Sandoval MD , Ganesh P. Pujari MD , Kiran K. Mangalaparthi PhD , M. Cristine Charlesworth PhD, MS , Mercedes Prudencio PhD , Tania Gendron PhD , Sukhwinder J.S. Sandhu MD , Aziza Nassar MD, MPH , Leonard Petrucelli PhD , James F. Meschia MD , Akhilesh Pandey MD, PhD , Young Erben MD","doi":"10.1016/j.jvssci.2025.100281","DOIUrl":"10.1016/j.jvssci.2025.100281","url":null,"abstract":"<div><h3>Objective</h3><div>Extracranial carotid artery pathology accounts for 15% to 20% of ischemic strokes. Advancements in magnetic resonance angiography (MRA) with vessel wall imaging (VWI) have enabled the identification of vulnerable plaques, aiding in risk stratification for neurovascular events. This pilot study aimed to identify proteins in plaques with and without vulnerable features on MRA with VWI.</div></div><div><h3>Methods</h3><div>Consecutive patients undergoing carotid endarterectomy were included in the study cohort with preoperative MRA with VWI. A retrospective chart review was conducted to extract pertinent clinical data including cardiovascular risk factors and medications. Proteomic analysis involved Tandem Mass Tag (TMTpro) labeling of peptides, basic pH high-performance liquid chromatography fractionation, and NanoLC-tandem mass spectrometry.</div></div><div><h3>Results</h3><div>Proteomic analysis revealed 23 proteins significantly elevated in vulnerable plaques, including Proteinase 3 (PRTN3), Phospholipid Transfer Protein (PLTP), and S100 Calcium-Binding Protein A12 (S100A12), with increased abundance exceeding two-fold changes or above (<em>P</em> < .001). Conversely, three proteins exhibited reduced abundance in vulnerable plaques including Dynamin-3 (DNM3), Transmembrane Protein 181 (TMEM181), and Adducin-3 (ADD3) (<em>P</em> < .05).</div></div><div><h3>Conclusions</h3><div>This study contributes to the understanding of protein biomarkers associated with carotid plaque vulnerability, offering insights into disease progression and stroke prevention. Proteins secreted by vulnerable plaques may offer not only the potential for early disease recognition; but can also become a target for future pharmacologic therapy prior to a devastating neurologic event. Further validation studies and multi-center trials will be needed to confirm the value of these potential biomarkers.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100281"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143403651","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 : 2025-01-01Epub Date: 2025-06-10DOI: 10.1016/j.jvssci.2025.100293
Nicasius Tjahjadi MD , Carlos Campello Jorge MD , Prabhvir S. Marway MD , Taeouk Kim MSc , Timothy Baker PhD , Constantijn Hazenberg MD, PhD , Joost A. van Herwaarden MD, PhD , C. Alberto Figueroa PhD , Himanshu J. Patel MD , Nicholas S. Burris MD
Objective
We utilized vascular deformation mapping (VDM) to assess ascending aortic motion, regional stiffness and growth in patients who underwent zone 2/3 thoracic endovascular aortic repair (TEVAR) to quantify changes in ascending aorta biomechanics after endograft implantation.
Methods
Multi-planar, multi-directional aortic motion, aortic strain, and three-dimensional aortic growth was extracted by VDM from electrocardiography-gated computed tomography angiograms. Aortic displacement and strain were compared between patients who underwent TEVAR (both pre- and post-procedure) and in patients with dilated ascending aorta (>4.0 cm) and a non-dilated control group.
Results
One hundred twenty subjects were included for analysis. Between pre-TEVAR and post-TEVAR, total displacement decreased (4.87 ± 1.52 mm vs 4.13 ± 1.43 mm; P = .03). Ascending aortic cross-sectional area strain at the sinuses (SVS), mid-ascending (MA), and proximal arch (PA) were lower in the pre-TEVAR group (SVS, 8.3% ± 4.7%; MA, 6.2% ± 3.2%; PA, 6.3% ± 3.0%; all P < .001) compared with non-dilated controls (SVS, 14.0% ± 6.6%; MA, 14.9% ± 6.6%; PA, 14.9% ± 6.9%). TEVAR increased aortic strain at the MA (pre-TEVAR, 6.2% ± 3.2%; post-TEVAR, 8.5% ± 4.6%; P < .001) and PA (pre-TEVAR, 6.3% ± 3.0%; post-TEVAR, 9.0% ± 4.6%; P < .001). A moderate, negative correlation (R = −0.57; P = .007) between MA aortic growth rate and aortic strain was observed post-TEVAR.
Conclusions
Zone 2/3 TEVAR introduces changes in ascending aortic biomechanics. Patients with lower post-TEVAR strain, suggesting higher aortic stiffness, may be at highest risk of progressive growth. Imaging-based assessment of aortic biomechanics may help improve risk stratification for long-term outcomes post-TEVAR.
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