JVS-vascular science最新文献

{"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 ,&nbsp;Vijay Tewari BS ,&nbsp;Huidan Yu PhD ,&nbsp;Jun Chen PhD ,&nbsp;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 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.</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}

{"title":"Glucose transporter 1 in vascular smooth muscle cells is dispensable for abdominal aortic aneurysm induced by angiotensin II","authors":"Keiichi Torimoto MD, PhD ,&nbsp;Hymavathi Reddy Vari PhD ,&nbsp;Yuki Nakayama MD, PhD ,&nbsp;Hirotoshi Utsunomiya PhD ,&nbsp;Masatoshi Takeda MD, PhD ,&nbsp;Tomoki Hashimoto MD, PhD ,&nbsp;Victor Rizzo PhD ,&nbsp;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}

{"title":"Hemodynamic subtype classification of type II endoleaks using time-enhanced curves and its association with aneurysmal enlargement","authors":"Kota Mitsui RT, BSc ,&nbsp;Yunosuke Nishihara MD, PhD ,&nbsp;Norisato Tsuda RT, MSc ,&nbsp;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_feeder (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}

{"title":"Toward the “slope of enlightenment”: The role of adiposity in abdominal aortic aneurysms","authors":"Drew J. Braet MD ,&nbsp;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}

{"title":"Analysis of the relationship between central adiposity and biomechanical, histological, and immunohistochemical properties of the anterior wall of abdominal aortic aneurysms","authors":"Alexandre Malta Brandão MD, PhD ,&nbsp;Marcos Vinícius Melo de Oliveira MD, PhD ,&nbsp;Gina Camillo Rocha Silvestre BS ,&nbsp;Alexandre Queiroz Silva BS ,&nbsp;Michele Alberto Marques BS ,&nbsp;Suely Aparecida Pinheiro Palomino MSc ,&nbsp;Maria de Lourdes Higuchi MD, PhD ,&nbsp;Erasmo Simão da Silva MD, PhD","doi":"10.1016/j.jvssci.2025.100283","DOIUrl":"10.1016/j.jvssci.2025.100283","url":null,"abstract":"<div><h3>Objective</h3><div>Adipose tissue plays a role in atherogenesis and degeneration of the vascular wall. However, the relationship between aortic abdominal aneurysm (AAA) and adipose tissue is controversial. This study aimed to correlate the biomechanical properties (elasticity and resistance), histology and immunohistochemistry findings of aortic tissue fragments from abdominal aortic aneurysms (AAAs) with the abdominal fat distribution determined by computed tomography scans.</div></div><div><h3>Methods</h3><div>This retrospective study analyzed data from biomechanical tests performed on fragments of the anterior wall of AAA obtained during open surgical repair. A uniaxial test was used to determine the tissue's failure tensile strength, tension, stress, and elasticity (strain). Preoperative computed tomography scans were used to quantify abdominal circumference at the L3-L4 and umbilical levels. Visceral and subcutaneous fat areas were quantified at these levels using tissue radiodensity. Univariate analysis and multiple regression models were used to correlate adiposity measures with biomechanical variables, considering factors such as hypertension, diabetes, and smoking status. Histological analysis (hematoxylin and eosin staining) was performed on twenty-five specimens, and immunohistochemical analysis (CD20, CD68, CD45, peroxisome proliferator activated receptor-γ [PPAR-γ], KLF5, and tumor necrosis factor-α) was performed on 13 specimens.</div></div><div><h3>Results</h3><div>The most common risk factors were hypertension (82%) and smoking (85%). Diabetes mellitus was present in 21.8%. No correlation was found between visceral fat area and biomechanical parameters or maximum AAA diameter. Predominance of visceral adipose tissue at L3-L4 and the umbilical level was associated with lower fibrosis in all layers of the abdominal wall (subcutaneous, 61% vs visceral, 41%), higher PPAR-γ expression in the tunica media (subcutaneous, 170.5-199.0 positive cells/mm² vs visceral, 957.88-1038.50 positive cells/mm²; <em>P</em> = .033), and lower elastic fiber concentration in the tunica media. (subcutaneous, 40.5% vs visceral, 31.5%).</div></div><div><h3>Conclusions</h3><div>No relationship was found between the biomechanical parameters of the AAA wall and visceral or subcutaneous fat areas. The predominance of visceral fat was associated with increased adipocyte cellularity and decreased elastic fiber concentration in the tunica media of the anterior AAA wall.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100283"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697011","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}

{"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 ,&nbsp;Camilo Polania-Sandoval MD ,&nbsp;Ganesh P. Pujari MD ,&nbsp;Kiran K. Mangalaparthi PhD ,&nbsp;M. Cristine Charlesworth PhD, MS ,&nbsp;Mercedes Prudencio PhD ,&nbsp;Tania Gendron PhD ,&nbsp;Sukhwinder J.S. Sandhu MD ,&nbsp;Aziza Nassar MD, MPH ,&nbsp;Leonard Petrucelli PhD ,&nbsp;James F. Meschia MD ,&nbsp;Akhilesh Pandey MD, PhD ,&nbsp;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> &lt; .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> &lt; .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}

{"title":"Three-dimensional characterization of ascending aortic strain, motion and growth in patients undergoing thoracic endovascular aortic repair","authors":"Nicasius Tjahjadi MD ,&nbsp;Carlos Campello Jorge MD ,&nbsp;Prabhvir S. Marway MD ,&nbsp;Taeouk Kim MSc ,&nbsp;Timothy Baker PhD ,&nbsp;Constantijn Hazenberg MD, PhD ,&nbsp;Joost A. van Herwaarden MD, PhD ,&nbsp;C. Alberto Figueroa PhD ,&nbsp;Himanshu J. Patel MD ,&nbsp;Nicholas S. Burris MD","doi":"10.1016/j.jvssci.2025.100293","DOIUrl":"10.1016/j.jvssci.2025.100293","url":null,"abstract":"<div><h3>Objective</h3><div>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.</div></div><div><h3>Methods</h3><div>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 (&gt;4.0 cm) and a non-dilated control group.</div></div><div><h3>Results</h3><div>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; <em>P</em> = .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 <em>P</em> &lt; .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%; <em>P</em> &lt; .001) and PA (pre-TEVAR, 6.3% ± 3.0%; post-TEVAR, 9.0% ± 4.6%; <em>P</em> &lt; .001). A moderate, negative correlation (R = −0.57; <em>P</em> = .007) between MA aortic growth rate and aortic strain was observed post-TEVAR.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100293"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144571870","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}

{"title":"Using computational modeling and four-dimensional computed tomography to predict type II endoleaks","authors":"Leah M. Gober MD ,&nbsp;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}

{"title":"Changes in vascular identity during vascular remodeling","authors":"Yukihiko Aoyagi MD ,&nbsp;Andrew W. Schwartz BS ,&nbsp;Zhuo Li MD, PhD ,&nbsp;Hualong Bai MD, PhD ,&nbsp;Luis Gonzalez PhD ,&nbsp;Cayetana Lazcano Etchebarne BS ,&nbsp;Yuichi Ohashi MD ,&nbsp;Masaki Kano MD ,&nbsp;Bryan Ho MD ,&nbsp;Kathleen Martin PhD ,&nbsp;Alan Dardik MD, PhD","doi":"10.1016/j.jvssci.2025.100282","DOIUrl":"10.1016/j.jvssci.2025.100282","url":null,"abstract":"<div><h3>Background</h3><div>Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity.</div></div><div><h3>Methods</h3><div>This is a review of experimental literature.</div></div><div><h3>Results</h3><div>These proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype.</div></div><div><h3>Conclusions</h3><div>Changes in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases.</div></div><div><h3>Clinical Relevance</h3><div>Vascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100282"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143685844","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}

{"title":"Evaluation of sex-based differences in below-the-knee plaque histology in patients who underwent amputation for chronic limb-threatening ischemia","authors":"Fouzul Kansul ,&nbsp;Deborah Vela MD ,&nbsp;Judit Csore MD ,&nbsp;Bright Benfor MD ,&nbsp;Sasha Suarez MD ,&nbsp;Anahita Dua MD, MBA, MSC ,&nbsp;Trisha L. Roy MD, PhD","doi":"10.1016/j.jvssci.2024.100269","DOIUrl":"10.1016/j.jvssci.2024.100269","url":null,"abstract":"<div><h3>Objective</h3><div>With the growing incidence of peripheral arterial disease (PAD) and the historic under-representation of female patients in cardiovascular trials, a comprehensive evaluation of sex-based variances in PAD presentation and treatment outcomes is needed. This study aims to evaluate sex-based differences in the vessel wall characteristics of patients who underwent amputation owing to critical limb-threatening ischemia to optimize personalized treatment planning and aid in the selection of endovascular devices for PAD patients.</div></div><div><h3>Methods</h3><div>A total of 35 lower limbs were collected from 34 patients with end-stage PAD undergoing major amputation. We selected, harvested, and cross-sectioned at 3- to 4-mm intervals 163 diseased below-the-knee arterial segments resulting in 1260 arterial rings. Histological analyses were conducted on each individual ring and later summarized by arterial segment.</div></div><div><h3>Results</h3><div>Male and female patients were remarkably similar across multiple plaque characteristics, including degree of stenosis, calcification severity and localization, and atherosclerotic patterns. A significant sex-based difference was noted in the presence of luminal thrombus, which was more prevalent in females (38.7% vs 25.0%; <em>P</em> = .016). Histopathological differences were noted between popliteal and tibial lesions, with popliteal segments demonstrating increased chronic total occlusion presence and atherosclerosis, whereas severe calcification occurred more often in tibial segments. A sex-based evaluation of the popliteal segments showed increased calcification (60.71% vs 28.0%; <em>P</em> = .003) and atherosclerosis (96.4% vs 73.0%; <em>P</em> = .028) in males compared with females.</div></div><div><h3>Conclusions</h3><div>Differences in the degree of calcification, incidence of atherosclerosis, and presence of luminal thrombus may pose important clinical implications for antiplatelet and anticoagulation regimen choice and guide treatment options. Further studies are warranted to evaluate the impact of these differences on outcomes of endovascular procedures.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"6 ","pages":"Article 100269"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143082227","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}