JVS-vascular science最新文献

{"title":"Rapid responses of catecholamines, natriuretic peptides and inflammatory markers to acute type B aortic dissection (NeuroendOcrine horMone release in acute type b Aortic Dissection [NOMAD] Study)","authors":"Eric T.A. Lim MB ChB ,&nbsp;David Jardine MD ,&nbsp;Christopher J. Pemberton PhD ,&nbsp;Christopher Frampton PhD ,&nbsp;Richard Troughton PhD ,&nbsp;Adib Khanafer MBBS, FRCS, FRACS","doi":"10.1016/j.jvssci.2026.100422","DOIUrl":"10.1016/j.jvssci.2026.100422","url":null,"abstract":"<div><h3>Background</h3><div>We have recently demonstrated that muscle sympathetic nerve activity and normetanephrine levels are transiently increased for several days immediately after acute type B aortic dissection. We now report other markers of sympathetic activation, natriuresis and inflammation over the same time frame.</div></div><div><h3>Methods</h3><div>In 13 patients with known acute type B aortic dissection (median age, 71 years; 95% confidence interval, 29-89 years), we undertook serial measurements of catecholamine metabolites including normetanephrine, metanephrine, and their second messenger cyclic adenosine monophosphate; renin and aldosterone; N terminal-pro-brain natriuretic peptide (NT-proBNP), and its second messenger cyclic, guanosine monophosphate; C-type natriuretic peptide; the inflammatory growth differentiation factor 15; the stress hormone copeptin; mid-regional-proadrenomedullin; and the marker of cardiac muscle damage Troponin T. Venous sampling times were on admission, then 12 hours, 24 hours, 1 week, and 6 weeks later. Serial measurements were also undertaken in 12 controls (median age, 61 years; 95% confidence interval, 25-86 years) who presented with chest pain.</div></div><div><h3>Results</h3><div>During the first week after dissection, normetanephrine levels were increased: 617 to 792 vs 425 to 489 pmol/L in controls (analysis of variance [ANOVA] <em>P</em> = .01). There was also a simultaneous increase in NT-proBNP levels: 49 to 93 vs 14-21 pmol/L (ANOVA <em>P</em> = .07), and growth differentiation factor 15 levels: 1507 to 2873 vs 1146 to 1448 pg/mL (ANOVA <em>P</em> = .01) over the same period.</div></div><div><h3>Conclusions</h3><div>The increase in normetanephrine levels during the week after type B dissection confirms sympathetic nerve activity as a likely mechanism for hypertension in these patients. This surge of sympathetic activity may be partially antagonized by a simultaneous increase in NT-proBNP, which is possibly triggered by acute inflammation and oxidative stress caused by the dissection.</div></div><div><h3>Clinical Relevance</h3><div>This pilot study focused on assessing the timeline of neuroendocrine hormone release in acute type B aortic dissection. Our results demonstrated an increase in normetanephrine levels suggesting the involvement of the sympathetic nerve activity in driving hypertension in the acute setting of type B aortic dissection. There was also a concurrent increase in N-terminal pro-brain natriuretic peptide and growth differentiation factor 15 levels seen, suggesting an underlying inflammatory process and vascular stress. These can be the focus of future research in the development of pharmaceutical targets or the use of natriuretic drugs and anti-inflammatory agents in the mainstay treatment of type B aortic dissection.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100422"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167359","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":"Histological concordance of medial arterial calcification between tibial and peroneal arteries in advanced peripheral arterial disease","authors":"Snow Adler DO ,&nbsp;Jorge RuizdelRio PhD ,&nbsp;Brian Eliceiri PhD ,&nbsp;Ann C. Gaffey MS, MD","doi":"10.1016/j.jvssci.2026.100426","DOIUrl":"10.1016/j.jvssci.2026.100426","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Medial arterial calcification (MAC) is prevalent in peripheral artery disease (PAD), yet its distribution and clinical significance in infrapopliteal arteries remain poorly defined. Prior histopathological studies of distal tibial segments have not evaluated MAC as a vessel-level lesion. Peroneal arteries (PAs) are frequently regarded as relatively spared revascularization targets based on angiographic assessment alone, despite limited histological validation and emerging evidence that arterial medial remodeling contributes independently to limb ischemia. Accordingly, it remains unclear whether MAC in PAD reflects a diffuse distal arterial phenotype shared across tibial and peroneal segments or a segment-specific process.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;This single-center prospective pilot study included 14 patients and 14 limbs (13 patients with PAD and 1 control without PAD) undergoing below-knee amputation. Paired anterior tibial arteries (ATAs) and PAs were harvested, formalin fixed, and paraffin embedded. Hematoxylin and eosin staining was used to assess arterial architecture, intimal plaque, and medial remodeling. MAC was graded 0 to 4 using Alizarin Red staining according to circumferential extent and thickness. Clinical variables included age, sex, ethnicity, diabetes mellitus (DM), hemoglobin A1c, end-stage renal disease stage, smoking status, glucagon-like peptide-1 receptor agonist use, Rutherford category, and limb outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The cohort included 92.3% males with an average age of 69.0 ± 10 years and a high prevalence of DM, consistent with larger PAD series. Moderate to severe (grades 3-4) MAC was common in limbs with PAD. Within-patient concordance of MAC grades between paired ATA and PA was high, with most pairs differing by ≤1 grade, supporting a diffuse rather than a segment-specific distal arterial phenotype. A greater MAC burden was observed in patients with DM, advanced end-stage renal disease, and higher Rutherford categories, but these exploratory associations were not statistically significant. Directional trends were observed between histological MAC burden and adverse limb outcomes, consistent with prior radiographic studies.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;In this pilot human tissue study, MAC appears to represent a shared distal arterial phenotype across ATAs and PAs in PAD rather than a segment-specific lesion. Histology-confirmed MAC burden provides biologic validation of distal calcification patterning and may help to refine our understanding of infrapopliteal disease in advanced PAD. Larger, multicenter studies are warranted to define the prognostic utility of MAC-based indices and to determine how tissue-level calcification patterns relate to clinical imaging and revascularization strategies.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Clinical relevance&lt;/h3&gt;&lt;div&gt;In advanced peripheral artery disease, medial arterial calcification (MAC) appears to be a shared di","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100426"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148230690","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":"Integrative transcriptomics and human tibial artery validation identify ADAM12, PDK4, and RUNX1 as peripheral artery disease-associated genes enriched in calcified tibial arteries","authors":"Snow Adler DO,&nbsp;Jorge RuizdelRio PhD,&nbsp;Brian Eliceiri PhD,&nbsp;Ann C. Gaffey MS, MD","doi":"10.1016/j.jvssci.2026.100434","DOIUrl":"10.1016/j.jvssci.2026.100434","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Medial arterial calcification of tibial vessels is a major obstacle to limb salvage in peripheral artery disease (PAD), yet the molecular drivers remain poorly defined. We used publicly available transcriptomic data to nominate candidate genes relevant to vascular calcification and then tested those candidates in human tibial arteries and in primary PAD-derived vascular cells.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Differential gene expression was analyzed across publicly available PAD/chronic limb-threatening ischemia (CLTI) transcriptomic datasets, comparing PAD/CLTI tissue to non-PAD controls (limma and DESeq&lt;sup&gt;2&lt;/sup&gt; adjusted &lt;em&gt;P&lt;/em&gt; &lt; .05, |log&lt;sub&gt;2&lt;/sub&gt; fold-change| &gt; 1.5). Candidates were prioritized based on predicted roles in calcification processes in endothelial cells and vascular smooth muscle cells. Expression was validated by quantitative polymerase chain reaction in isolated human tibial arteries harvested from patients with PAD/CLTI undergoing below-the-knee amputations and non-PAD control vessels. Following the preparation of primary PAD-derived endothelial cells and vascular smooth muscle cells, the cells were cultured under high-glucose or osmotic control conditions for 7 days to assess the effects of a hyperglycemic challenge.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Analysis of 14 datasets identified 89 differentially expressed genes enriched in inflammatory, osteogenic, and metabolic pathways. Fourteen candidates were selected for validation. Among them, &lt;em&gt;ADAM12&lt;/em&gt;, &lt;em&gt;PDK4&lt;/em&gt;, and &lt;em&gt;RUNX1&lt;/em&gt; were confirmed in PAD tibial arteries as the most relevant candidates from the prespecified panel, consistent with their prioritization from the transcriptomic and literature-guided candidate-selection strategy.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;A candidate-first translational strategy integrating public transcriptomic prioritization with validation in human tibial arteries confirmed &lt;em&gt;PDK4&lt;/em&gt; and &lt;em&gt;RUNX1&lt;/em&gt; as significantly upregulated medial arterial calcification-associated genes in PAD tibial arteries, and identified &lt;em&gt;ADAM12&lt;/em&gt; as a biologically prioritized candidate showing a concordant but statistically nonsignificant trend in the same direction. Their expression in diseased tissue, together with the absence of acute glucose responsiveness in primary PAD-derived vascular cells, supports a model in which these genes are linked to chronic vascular remodeling rather than transient hyperglycemic signaling. These findings refine the molecular landscape of PAD-associated calcification and establish a focused framework for potential mechanistic studies.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Clinical relevance&lt;/h3&gt;&lt;div&gt;Tibial medial arterial calcification is a major barrier to limb salvage in patients with peripheral artery disease (PAD)/chronic limb-threatening ischemia because it makes revascularization more difficult and less durable. By validating candidate genes in human tibial arter","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100434"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148958294","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":"Undiseased and diseased abdominal aortas contain environmentally relevant micronanoplastics","authors":"Pierce L. Massie MD,&nbsp;Marcus A. Garcia PharmD,&nbsp;Daniel F. Gallego MD,&nbsp;Christopher Schlosser PA,&nbsp;Sakshi Patil PhD,&nbsp;Eliane El Hayek PhD,&nbsp;Aerlin Decker BSPS,&nbsp;Rui Liu PhD,&nbsp;Milad MazloumiBakhshayesh MPharm,&nbsp;Erin Risotto-Urbanowicz MD,&nbsp;Matthew P. Justus MS,&nbsp;Carolyn Pace BS,&nbsp;Rowza T. Rumma MD,&nbsp;Matthew J. Campen PhD,&nbsp;Ross M. Clark MD, MBA, FACS, FSVS","doi":"10.1016/j.jvssci.2026.100449","DOIUrl":"10.1016/j.jvssci.2026.100449","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Plastics production has accelerated, with most products ultimately residing in the environment. Plastics degrade into micro- (&lt;5 mm) and nano- (&lt;1000 nm) plastic particles (MNPs) that can be ingested or inhaled by humans. In the literature, MNPs have been found in higher concentrations in diseased arteries, but the mechanisms remain unclear. Studies have found MNPs in tissue from ascending aortic dissections, but data on infrarenal aortic aneurysms, occlusive plaques, and cadaveric aortas have not been reported.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;MNPs from aortic aneurysmal walls, aortic occlusive plaques, and fresh cadaveric aortas were measured using pyrolysis-gas chromatography/mass spectroscopy; the MNPs assessed included polyethylene (PE), polypropylene (PP), polystyrene, acrylonitrile butadiene styrene, styrene-butadiene (SBR), poly(methyl methacrylate), polycarbonate, polyvinylchloride (PVC), polyurethane, polyethylene terephthalate, nylon 6, and nylon 66. Scanning electron microscopy/energy dispersive X ray spectroscopy was used to visualize MNPs and characterize the milieu of a single aortic plaque for hypothesis generation.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Nine aneurysms (n = 9 male; mean age, 71 years), six occlusive plaques (n = 4 male; mean age, 67 years), and twelve cadaveric aortas (n = 4 male; mean age, 35 years) were collected. In non-atherosclerotic, cadaveric aortas, the most prevalent polymers were PE (33.7 μg/g tissue), PVC (33.5 μg/g), and PP (21.3 μg/g). In atherosclerotic cadaveric aortas, the most prevalent polymers were PE (99.5 μg/g), PP (66.7 μg/g), and PVC (58 μg/g). In aneurysms, the most prevalent polymers were PE (115.8 μg/g), SBR (114.7 μg/g), and PVC (67.3 μg/g). In plaques, the most prevalent polymers were PE (745.5 μg/g), PVC (47.5 μg/g), and SBR (40.3 μg/g). Numerous within-group differences between polymers were noted, often following a common theme of which was the most prevalent. Single plaque scanning electron microscopy/energy dispersive X ray spectroscopy revealed shard-like MNPs surrounded by calcium/phosphorus, suggesting that MNPs accumulate within plaque calcifications in occlusive disease.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Detectable levels of MNPs were found in aortic atherosclerotic occlusive plaques, aortic aneurysms, and both normal and diseased cadaveric aortas. Nanoplastics were visualized within plaque calcifications in occlusive disease. Further study is needed to elucidate the mechanisms through which MNPs play a role in atherosclerotic and degenerative vascular disease development.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Clinical relevance&lt;/h3&gt;&lt;div&gt;This work examines the levels of micronanoplastics in human aortic aneurysms and aortoiliac atherosclerotic plaques and reports the levels in healthy and diseased cadaveric aortic tissues. No clear associations between age and micronanoplastic levels were demonstrated among patients. Of the polymers measured, polyethe","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100449"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149211069","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":"Changes in local hemodynamic forces associated with arch branched endografts","authors":"William J. Yoon MD, PhD ,&nbsp;Andres Schanzer MD ,&nbsp;Kevin Mani MD, PhD ,&nbsp;Anders Wanhainen MD, PhD","doi":"10.1016/j.jvssci.2026.100413","DOIUrl":"10.1016/j.jvssci.2026.100413","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;Different zone 0 endograft designs have been introduced. This study sought to assess postimplantation hemodynamic changes induced by zone 0 endografts, with varied configuration of side branches, using computational models.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Twenty-nine patients who underwent zone 0 endovascular repair with single-, double-, or triple-branched endografts (n = 7, n = 11, n = 11, respectively), using different configurations of antegrade (A) and retrograde (R) branches, were included. Computational simulations were used to assess postimplantation changes in peak flow rate, systolic blood pressure (SBP) and time-averaged wall shear stress (TAWSS) at the innominate artery (IA), right subclavian artery, right common carotid artery (CCA), left CCA (LCCA), left subclavian artery (LSA), and distal aortic arch, as well as the total displacement force (DF) of the endograft.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Regardless of orientation, IA side branch implantation increased the IA peak flow rate across all endograft designs, an effect significant only in single-branched devices (+70%, &lt;em&gt;P&lt;/em&gt; = .02). This increase was accompanied by a significant decrease in peak flow in the LCCA and LSA for single- (&lt;em&gt;P&lt;/em&gt; = .02 and &lt;em&gt;P&lt;/em&gt; = .02, respectively) and double-branched devices (&lt;em&gt;P&lt;/em&gt; = .01 and &lt;em&gt;P&lt;/em&gt; &lt; .001, respectively), whereas no such effect was observed with triple-branched devices. Notably, the two antegrade branches supplying the IA and LCCA and one retrograde branch to the LSA- and three retrograde branches (3R)-triple-branched designs had the opposite effect on LCCA blood flow (+8.3% vs −6.7% [&lt;em&gt;P&lt;/em&gt; = .02], respectively), although their impact on LSA flow did not differ significantly (−7.5% vs −8.1% [&lt;em&gt;P&lt;/em&gt; = .92], respectively). This resulted in disparate effects on distal arch flow (−0.3% vs +6.3% [&lt;em&gt;P&lt;/em&gt; = .02], respectively). Postimplantation alteration in distal arch flow was progressively attenuated with more branches. The preimplantation to postimplantation SBP differences in the IA, LCCA, and LSA mirrored the corresponding changes in peak flow. Elevated peak flow in the IAs led to a significant postimplantation increase in the TAWSS across all device designs. In contrast, the LSA side branches with retrograde orientation in the two antegrade branches supplying the IA and LCCA and one retrograde branch to the LSA-triple-branched and 3R-triple-branched endografts demonstrated marked increases in TAWSS (36.1% vs 50.2%, respectively), despite there being no significant change in the mean flow rate. Although maximum DF varied between devices (single-branched, 32.8 N; double-branched, 23.9 N; 2A+1-triple-branched, 22.9 N; 3R-triple-branched, 28.9 N), a post hoc analysis showed that branch configuration did not significantly influence DF.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The hemodynamic stability within the aortic arch improves with a greater number of endograft","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100413"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538356","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":"Thoracic duct outflow obstruction increases thoracic duct pressure above central venous pressure supporting thoracic duct decompression","authors":"Takuji Maruyama MD,&nbsp;Shuji Kariya MD, PhD,&nbsp;Miyuki Nakatani MD, PhD,&nbsp;Yutaka Ueno MD,&nbsp;Yasuyuki Ono MD,&nbsp;Yuki Tanaka MD,&nbsp;Kanji Sugiura MD,&nbsp;Noboru Tanigawa MD, PhD","doi":"10.1016/j.jvssci.2026.100425","DOIUrl":"10.1016/j.jvssci.2026.100425","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;Thoracic duct outflow obstruction is a recognized cause of refractory lymphatic leakage; however, the physiological consequences of such obstruction on thoracic duct pressure and its relationship to central venous pressure have not been fully characterized in vivo. This study aimed to evaluate changes in thoracic duct pressure and the pressure gradient between the thoracic duct and the central venous system in an experimental model of thoracic duct outflow obstruction.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;In a swine model, thoracic duct pressure and central venous pressure were directly measured using intravascular catheters positioned at matched vertebral levels. Thoracic duct embolization was performed at the upper thoracic level using coils and cyanoacrylate and was used as an experimental model of thoracic duct outflow obstruction. Pressure measurements were obtained before embolization and after confirmation of complete thoracic duct occlusion. Changes in thoracic duct pressure, central venous pressure, and the pressure relationship between the two systems were analyzed using paired statistical comparisons.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Thoracic duct outflow obstruction resulted in a significant increase in upstream thoracic duct pressure, with a median increase of approximately 6 to 8 mmHg compared with preobstruction values. Following obstruction, thoracic duct pressure consistently exceeded central venous pressure, creating a pressure gradient indicative of lymphatic hypertension. In contrast, central venous pressure did not change significantly after thoracic duct obstruction. No consistent cranio-caudal longitudinal pressure gradient along the thoracic duct was identified.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Thoracic duct outflow obstruction induces lymphatic hypertension, as demonstrated by an increase in thoracic duct pressure relative to central venous pressure. This experimentally demonstrated pressure gradient provides physiological support for decompressive interventions by demonstrating a pressure gradient favorable for lymphatic drainage into the venous system. By directly quantifying intralymphatic and venous pressures in vivo, this study offers mechanistic insight into the pathophysiology of lymphatic leakage associated with thoracic duct obstruction and may help inform treatment selection between occlusive and decompressive strategies in lymphatic interventions.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Clinical Relevance&lt;/h3&gt;&lt;div&gt;Thoracic duct outflow obstruction is a cause of lymphatic leakage, yet the consequences of obstruction on thoracic duct pressure and its relationship to central venous pressure have remained unclear. In this experimental study, in vivo measurements demonstrated that thoracic duct outflow obstruction results in an increase in thoracic duct pressure, creating a pressure gradient relative to central venous pressure. This pressure relationship reflects lymphatic hypertension caused by ","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100425"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167501","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":"A narrative review of recent literature of circulating biomarkers of abdominal aortic aneurysm","authors":"Yae Hyun Rhee MD ,&nbsp;Joshua M. Spin MD, PhD ,&nbsp;Philip S. Tsao PhD","doi":"10.1016/j.jvssci.2025.100399","DOIUrl":"10.1016/j.jvssci.2025.100399","url":null,"abstract":"<div><h3>Objective</h3><div>Abdominal aortic aneurysms (AAAs) arise through complex pathogenesis, and good methods of risk stratification have proved elusive. Further, the lack of medical options short of surgery for treatment, and the requirement for dedicated imaging for identification, result in delayed diagnosis and hamper patient outcomes. Application of circulating biomarkers to effectively assess disease presence and predict progression would improve clinical management and support patient well-being. Exploration for suitable circulating biomarkers of AAAs is still very much in process; however, no disease-specific biomarker has yet been established for effective diagnosis and prognosis. This review aims to contribute enhanced tools for utilizing biomarkers for risk stratification and management of AAA disease.</div></div><div><h3>Methods</h3><div>Utilizing MEDLINE/PubMed, we summarize 44 recent publications covering circulating AAA biomarkers. The biomarkers were categorized and tiered into six subgroups by study design, with prospective studies tiered higher than retrospective observational studies. The classification system separately describes a list of post-interventional monitoring biomarkers. Part of the review also deals with recent approaches to identifying potential AAA biomarkers by genetic inference.</div></div><div><h3>Results</h3><div>Forty individual circulating biomarkers, two plasma protein panels (consisting of 9 or 7 proteins), one plasma-multiomic study, and two micro-RNA (miR) panels revealed correlations to AAA disease risk. Among those, many have already been established as biomarkers for other cardiovascular diseases, meaning feasibility has been proven but disease specificity is lacking.</div></div><div><h3>Conclusions</h3><div>Multiple circulating proteins and miRs have been investigated for their utility as AAA-specific diagnostic or prognostic biomarkers. This work may ultimately identify not only novel AAA biomarkers that are specific for cell type, proteins, metabolites, genetic polymorphisms, and miRNA, but permit framing of comprehensive networks of disease-participating molecules. More robust data with higher disease sensitivity and specificity are needed, along with more multi-centered longitudinal clinical studies with large sample sizes.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100399"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146023639","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":"Proteomic signatures of carotid plaque vulnerability: Proteolysis, inflammation, metabolic reprogramming, and lipid dysregulation","authors":"Camilo Polania Sandoval MD ,&nbsp;James F. Meschia MD ,&nbsp;Mercedes Prudencio PhD ,&nbsp;Tania Gendron PhD ,&nbsp;Christopher Jacobs MD ,&nbsp;Richard D. Beegle MD ,&nbsp;Sukhwinder J.S. Sandhu MD ,&nbsp;Kiran K. Mangalaparthi PhD ,&nbsp;Jaeyun Sung PhD ,&nbsp;Xiaowei Zhao PhD ,&nbsp;Aziza Nassar MD, MPH, MBA ,&nbsp;Houssam Farres MD ,&nbsp;Leonard Petrucelli PhD ,&nbsp;Akhilesh Pandey MD, PhD ,&nbsp;Young Erben MD","doi":"10.1016/j.jvssci.2025.100404","DOIUrl":"10.1016/j.jvssci.2025.100404","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Carotid plaque vulnerability is a current feature that aids in the decision-making for ischemic stroke risk. Proteomic analysis of plaque tissue can reveal molecular indicators of instability that complement imaging findings. We sought to identify a proteomic signature distinguishing vulnerable from stable carotid plaques in patients undergoing endarterectomy, with the aim of uncovering candidate biomarkers for potential diagnostic and therapeutic targets.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Twenty-eight carotid plaque specimens were collected from 27 patients (including 1 patient with bilateral endarterectomy). Samples were classified as vulnerable (n = 14) or nonvulnerable (n = 14) based on preoperative magnetic resonance angiography with vessel wall imaging. A tandem mass tag-based multiplexing strategy followed by mass spectrometric analysis was used to profile the proteomes of all samples. Normalized and log&lt;sub&gt;2&lt;/sub&gt;-transformed protein intensities were compared using two-sample &lt;em&gt;t&lt;/em&gt; tests with unequal variances, and &lt;em&gt;P&lt;/em&gt; values were adjusted for multiple testing with the Benjamini-Hochberg method to obtain false discovery rate &lt;em&gt;q&lt;/em&gt; values. Proteins with a &lt;em&gt;q&lt;/em&gt; value of ≤0.25 were designated high-confidence candidates, and those with a &lt;em&gt;P&lt;/em&gt; value of &lt;.05 but a &lt;em&gt;q&lt;/em&gt; value of &gt;0.25 were considered exploratory.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;From 3267 proteins identified, 398 reached nominal significance (&lt;em&gt;P&lt;/em&gt; &lt; .05). From those, 29 reached at least log&lt;sub&gt;2&lt;/sub&gt;(fold-change) of +1, whereas 3 of −1 log&lt;sub&gt;2&lt;/sub&gt;(fold change), yielding a total of 32 proteins. Fifteen were significant for a &lt;em&gt;q&lt;/em&gt; value ≤0.25. All were upregulated in vulnerable lesions and these included: matrix-degrading enzymes (matrix metalloproteinase [MMP]7, MMP9, MMP1, and ADAM-like decysin-1), neutrophil-derived effectors (azurocidin, cathelicidin antimicrobial peptide, lactotransferrin, and myeloperoxidase), inflammatory regulators (interleukin-1 receptor antagonist and interleukin-4-induced protein), glycolytic enzymes (hexokinase-3 and hexokinase-2), and lipid-handling proteins (lipoprotein-associated phospholipase A&lt;sub&gt;2&lt;/sub&gt;, apolipoprotein B, and paraoxonase-1). An additional 17 exploratory proteins showed nominal significance (&lt;em&gt;P&lt;/em&gt; &lt; .05, &lt;em&gt;q&lt;/em&gt; &gt; 0.25) with at least log&lt;sub&gt;2&lt;/sub&gt;(fold-change) of 1, and 366 proteins with nominal significance but with a log&lt;sub&gt;2&lt;/sub&gt;(fold-change) of &lt;1.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Our proteomic profiling delineates a robust vulnerability signature marked by enhanced proteolysis, neutrophil activation, inflammatory signaling, metabolic reprogramming, and lipid dysregulation. High-confidence proteins emerged as tissue biomarkers of plaque instability. Validating their association with future cerebrovascular events is the next step toward clinically actionable stroke prediction. Exploratory candidates w","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100404"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078304","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":"Endovascular dual internal-external iliac balloon occlusion creates a reproducible porcine survival model of unilateral acute hindlimb ischemia","authors":"Ariyan Tabesh MD,&nbsp;Sahil Patel MD,&nbsp;Tripti Mathur MBBS,&nbsp;Priya Dhawan MD,&nbsp;Zosia Zawacki VMD, DACLAM,&nbsp;Diana Bauer VMD,&nbsp;Pedro Ruivo VMD,&nbsp;Rachel M. Russo MD,&nbsp;Shahram Aarabi MD, MPH","doi":"10.1016/j.jvssci.2026.100432","DOIUrl":"10.1016/j.jvssci.2026.100432","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;Large-animal models are essential for studying acute limb ischemia (ALI), yet most existing porcine ALI models are nonsurvival designs intended for short-term physiologic or metabolic investigation. In contrast, current survival models predominantly replicate chronic limb ischemia by surgically ligating the external iliac artery (EIA) or common femoral artery (CFA), an approach that does not generate a complete acute ischemic insult. In our previous studies, single-segment occlusion of the external iliac artery or CFA failed to produce profound unilateral ischemia because of robust collateral reconstitution through the internal iliac system and pelvic vasculature. To address this limitation, we developed a reproducible, minimally invasive survival model of unilateral hindlimb ALI using simultaneous balloon occlusion of the ipsilateral internal artery and EIA (ie, “dual internal-external iliac balloon occlusion”), enabling reliable 7-day survival and longitudinal assessment of functional, electrophysiologic, and histologic outcomes of ALI.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Female Yorkshire pigs (50-55 kg) underwent general anesthesia, surgical exposure and vascular access of the common carotid artery, and percutaneous vascular access of the CFA using the Seldinger technique. Angiography confirmed the characteristic porcine anatomy, demonstrating an aortic trifurcation with right and left EIAs and a single internal iliac trunk providing extensive collateral flow. Iterative testing compared tourniquet application, distal aortic balloon occlusion, selective external iliac balloon occlusion, and simultaneous EIA and internal iliac artery balloon occlusion. Sustained 6-hour unilateral hindlimb ischemia was ultimately achieved with balloon occlusion of both the external and internal iliac arteries and validated by angiography, Doppler ultrasound study, and pulse oximetry. Primary outcomes included Tarlov gait score, electrophysiologic testing, and blinded terminal histologic analysis of peroneus tertius muscle and tibial nerve at 7 days postoperatively.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Dual internal-external iliac balloon occlusion consistently produced complete hindlimb ischemia for 6 hours without mortality or systemic morbidity. Pulse oximetry and Doppler ultrasound study confirmed absent distal flow during occlusion, with angiographic validation of no reconstitution. Pigs survived to day 7, exhibiting immediate postoperative functional impairment. Histology showed acute ischemic injury with myofiber necrosis, inflammatory infiltration, coagulative necrosis, mineralization and architectural disruption. Nerve conduction studies demonstrated complete loss of compound muscle action potentials in most specimens.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;In our porcine survival model, a minimally invasive dual internal-external iliac balloon occlusion technique consistently induced profound hindlimb ischemia consistent wi","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100432"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769995","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":"Poor glycemic control is independently associated with fibrinolysis shutdown in patients with peripheral artery disease","authors":"Swechha Bhatt MBBS,&nbsp;Aseman Bagheri Sheshdeh BS,&nbsp;Shezan Fouzdar MBBS,&nbsp;Radha Bansal MBBS,&nbsp;Prajakta Lokhande MBBS,&nbsp;Shanaya Vimadalal BA,&nbsp;Shiv Patel BA,&nbsp;Anahita Dua MD, MBA, FACS","doi":"10.1016/j.jvssci.2026.100441","DOIUrl":"10.1016/j.jvssci.2026.100441","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;Fibrinolysis plays a critical role in regulating thrombotic potential by facilitating the breakdown of fibrin-rich thrombi after clot formation. Impaired fibrinolysis, often referred to as hypofibrinolysis or fibrinolytic shutdown, results in reduced clot degradation and promotes thrombus persistence, propagation, and recurrent vascular occlusion. Consequently, impaired fibrinolysis is increasingly recognized as an important contributor to thrombotic risk in patients with peripheral artery disease (PAD). Poor glycemic control has been associated with a prothrombotic milieu through mechanisms including enhanced platelet activation, increased fibrin clot density, and reduced fibrinolytic capacity; however, its relationship with fibrinolytic shutdown in PAD remains poorly defined. Therefore, we aimed to evaluate the association between glycemic control and fibrinolytic shutdown using viscoelastic testing.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We performed a retrospective cohort study of 192 patients with PAD who underwent revascularization. Patients were stratified by glycated hemoglobin (HbA1c) &lt; 7% and ≥7%. Viscoelastic testing was performed using thromboelastography. Fibrinolysis was assessed using lysis at 30 minutes, and phenotypes were defined as severe shutdown (≤0.3%), partial shutdown (0.3%-0.8%), physiologic (0.8%-3.0%), and hyperfibrinolysis (&gt;3.0%). Multivariable logistic regression evaluated the association between HbA1c and severe fibrinolysis shutdown, adjusting for demographic, clinical, and treatment variables.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Patients with HbA1c ≥ 7% demonstrated lower lysis at 30 minutes values compared with those with HbA1c &lt; 7% (median, 0.00 [interquartile range, 0.00-0.35] vs median, 0.30 [interquartile range, 0.00-0.90]; &lt;em&gt;P&lt;/em&gt; = .015) and a higher prevalence of severe fibrinolysis shutdown (74.7% vs 51.3%; &lt;em&gt;P&lt;/em&gt; = .009). After adjustment, patients with HbA1c ≥ 7% had a higher predicted probability of severe shutdown (68.8% [95% CI, 51.4-82.2] vs 41.0% [CI, 26.3-57.4]; &lt;em&gt;P&lt;/em&gt; &lt; .001). In continuous analysis, each 1% increase in HbA1c was associated with increased odds of severe shutdown (adjusted odds ratio, 1.50; 95% CI, 1.19-1.93; &lt;em&gt;P&lt;/em&gt; = .001). Severe shutdown was additionally associated with thrombosis-driven reintervention (22.2% vs 8.0%; adjusted odds ratio, 3.60; 95% CI, 1.42-10.54; &lt;em&gt;P&lt;/em&gt; = .011).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Poor glycemic control was independently associated with severe fibrinolysis shutdown in patients with PAD, and severe shutdown was associated with increased thrombosis-driven reintervention. A dose-dependent relationship between HbA1c and impaired fibrinolysis suggests a mechanistic link between hyperglycemia and prothrombotic risk. Hence, patients with higher glucose levels may need increased thromboprophylaxis strategies to mitigate thrombotic risk. These findings may have implications for risk stratifi","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100441"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149051131","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}