Blood Vessels, Thrombosis & Hemostasis最新文献

{"title":"Regional brain volumes and their relationship to neurocognitive outcomes in children with severe hemophilia A","authors":"Silvia Verhofste ,&nbsp;Ahmad Al-Huniti ,&nbsp;Marci Novak ,&nbsp;Amy L. Conrad ,&nbsp;Ellen van der Plas ,&nbsp;Lyndsay Harshman ,&nbsp;Janice M. Staber","doi":"10.1016/j.bvth.2024.100021","DOIUrl":"10.1016/j.bvth.2024.100021","url":null,"abstract":"<div><h3>Abstract</h3><div>The effect of factor VIII (FVIII) deficiency on neurocognitive outcomes in children with hemophilia A (HA) is not well characterized. This study aimed to examine differences in brain volume and neurocognition between children with severe HA and healthy controls.This single-center study included 32 males aged 6 to 16 years, 9 with severe FVIII deficiency and 23 healthy controls. Volumetric data from magnetic resonance imaging and neurocognitive testing were compared using linear models including age to evaluate the association between regional brain volume and function. Cerebellar gray matter volume was significantly smaller in the HA cohort than in healthy controls (estimate, –0.375; 95% confidence interval [CI], –0.732 to –0.019; t₍₂₆₎ = 2.07; <em>P</em> = .049). A reduction in cerebellar gray matter was associated with neurocognitive executive dysfunction as noted by abnormal scores on 2 executive function assessments: the Delis-Kaplan Executive Function System, total switching accuracy (estimate, 0.549; 95% CI, –0.876 to 0.221; t₍₂₅₎ = –3.28; <em>P</em> = .003) and total correct category switching (estimate, 0.538; 95% CI, –0.868 to 0.207; t₍₂₅₎ = –3.19; <em>P</em> = .004), and the Behavior Rating Inventory of Executive Function, behavioral regulation index score (estimate, 0.531; 95% CI, 0.228-0.835; t₍₂₅₎ = 3.44; <em>P</em> = .002). Our study provides key insights into the lower brain volumes found in patients with HA and the corresponding executive dysfunction. Quantitative brain volume assessment in patients with HA may provide an integrated measure and with further research could be a useful clinical tool when assessing risk for neurocognitive dysfunction.</div></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 4","pages":"Article 100021"},"PeriodicalIF":0.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141845275","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":"Vascular biomarkers reveal a unique toxicity profile of posttransplant cyclophosphamide: secondary analysis of BMT CTN 0402 and 1202","authors":"Laura F. Newell ,&nbsp;Najla El Jurdi ,&nbsp;Brian C. Betts ,&nbsp;Corey Cutler ,&nbsp;Joseph H. Antin ,&nbsp;John E. Levine ,&nbsp;Angela Panoskaltsis-Mortari ,&nbsp;Shernan G. Holtan","doi":"10.1016/j.bvth.2024.100020","DOIUrl":"10.1016/j.bvth.2024.100020","url":null,"abstract":"<div><h3>Abstract</h3><p>Posttransplant cyclophosphamide (PTCy)–based graft-versus-host disease (GVHD) prophylaxis regimens are associated with very low rates of severe acute and chronic GVHD after hematopoietic cell transplant (HCT). However, concerns about cardiac and other organ toxicities persist. This study aimed to compare the vascular biomarker profile of PTCy with other GVHD regimens, including tacrolimus/sirolimus (Tac/Sir) and tacrolimus/methotrexate (Tac/MTX), to generate hypotheses for toxicity mitigation strategies. Plasma samples from day +28 after transplant were analyzed against pretransplant baseline measurements in patients receiving PTCy-based GVHD prophylaxis as part of Blood and Marrow Transplant Clinical Trials Network (BMT CTN) 1202 (n = 112) vs Tac/MTX (n = 98) and Tac/Sir (n = 95) regimens from BMT CTN 0402. Compared with Tac/MTX, PTCy was associated with increasing angiopoietin-2 levels and decreasing epidermal growth factor levels at day +28. In contrast, Tac/Sir displayed increasing follistatin and endoglin levels and decreasing vascular endothelial growth factor receptor 2 (VEGFR2) plasma levels after HCT. Across all cohorts, increasing epidermal growth factor was protective from nonrelapse mortality, and decreasing VEGFR2 was associated with subsequent development of extensive chronic GVHD. These distinct biomarker profiles offer insights that could guide strategies to mitigate unique GVHD prophylaxis–associated toxicities.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100020"},"PeriodicalIF":0.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000202/pdfft?md5=01eb3abe1f0fcdbe3c0117bbf8ef11b8&pid=1-s2.0-S2950327224000202-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141850752","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":"Genetic variants contribute to modulation of renal function in patients with immune thrombotic thrombocytopenic purpura","authors":"Wenjing Cao ,&nbsp;Malay K. Basu ,&nbsp;Elizabeth Staley ,&nbsp;X. Long Zheng","doi":"10.1016/j.bvth.2024.100019","DOIUrl":"10.1016/j.bvth.2024.100019","url":null,"abstract":"<div><h3>Abstract</h3><div>Immune thrombotic thrombocytopenic purpura (iTTP) is a potentially fatal blood disorder, resulting from autoantibodies against ADAMTS13. However, the contribution of genetic variations that may modulate its clinical presentations remains unknown. This study aimed to determine the potential contribution of variants in the genes associated with coagulation, complement activation or regulation, and platelet activation to pathophysiology of iTTP. Multicenter case series, whole-exome sequencing, and bioinformatic approaches were used. We focused on analysis of 20 genes that are involved in regulation of coagulation (eg, <em>ADAMTS13</em>, <em>THBD</em>, <em>MMACHC</em>, <em>INF2</em>, and <em>PLG</em>), complement activation (eg, <em>C3</em>, <em>C3AR1</em>, <em>C5</em>, <em>CFB</em>, <em>CFH</em>, <em>CFI</em>, <em>C4BPA</em>, <em>CD46</em> [<em>MCP</em>], <em>CD59</em>, and <em>CFHR1</em>-<em>CFHR5</em>), and platelet activation (eg, <em>DGKE</em>) from 40 adult patients with iTTP. Multiple genetic variations were identified in 12 of 20 genes of interest. More than 80% of patients harbored genetic variants in <em>CFI</em>, <em>CFH</em>, <em>C5</em>, and <em>ADAMTS13</em>; 15% to 55% of patients had variants in <em>C3</em>, <em>INF2</em>, <em>CFHR5</em>, and <em>PLG</em>; and &lt;10% of patients had variants in <em>CD46</em>, <em>C3AR1</em>, <em>DGKE</em>, and <em>THBD</em>. Of these, the variants in <em>C5</em> are associated with a more favorable renal function, whereas the variants in <em>DGKE</em> are associated with more persistently elevated creatinine levels. These results demonstrate that variants in the genes involved in coagulation, complement, and platelet activation are common in patients with iTTP, which may contribute to phenotypical modulations of or predispose to iTTP resulting from severe ADAMTS13 deficiency.</div></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 4","pages":"Article 100019"},"PeriodicalIF":0.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141709314","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":"Structural basis of MPL activation by thrombopoietin","authors":"Amirhossein Mafi ∗ ,&nbsp;Matthew Bratkowski ∗ ,&nbsp;Jiefei Geng ,&nbsp;Alyssa A. Brito ,&nbsp;Janani Sridar ,&nbsp;Dongjian Hu ,&nbsp;Anhdao T. Darcy ,&nbsp;Dhaval Nanavati ,&nbsp;Nathan J. Brown ,&nbsp;Manoj K. Rathinaswamy ,&nbsp;Yuliya Kutskova ,&nbsp;Dan Eaton ,&nbsp;Qi Hao † ,&nbsp;Marcia Paddock †","doi":"10.1016/j.bvth.2024.100018","DOIUrl":"10.1016/j.bvth.2024.100018","url":null,"abstract":"<div><h3>Abstract</h3><p>Myeloproliferative leukemia protein (MPL), also known as thrombopoietin (TPO) receptor, is a class I cytokine receptor that is expressed on hematopoietic progenitors, promoting growth and differentiation toward the megakaryocyte lineage and is critical for normal platelet production. Mutations in MPL, TPO, or Janus kinase 2 (JAK2) have been implicated in multiple diseases from congenital thrombocytopenias to myeloproliferative neoplasms. The ligand for MPL, TPO, stimulates platelet production by inducing MPL dimerization and results in an active conformation that allows downstream JAK2/STAT5 signaling. Despite the biological importance of this pathway, the molecular signaling mechanism remained unclear. Here, we present a 3.39-Å cryo-electron microscopy structure of the ectodomain of mouse MPL bound to TPO. The structure revealed both low and high affinity sites between MPL and TPO that contain several pathologic mutations. To better understand TPO-driven MPL signaling, we expanded upon this structure by molecular dynamic (MD) simulations to model the full-length human MPL/TPO complex, and showed that MPL D4-D4 domain interactions are functionally relevant in activity assays. To build on our understanding of downstream activation, we added JAK2 to the MPL/TPO complex by MD simulations. This ternary complex illustrates JAK2 dimerization through the pseudokinase domain, illustrates residues important for MPL interactions, and reveals the constitutive activation mechanism of patient mutant V617F. The model also suggests the mechanism of JAK2 tyrosine kinase domain transphosphorylation. Overall, our studies illuminate TPO/MPL/JAK2 signaling mechanisms and provide additional insight into the nature of receptor signaling, which will further benefit human health.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100018"},"PeriodicalIF":0.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000184/pdfft?md5=a1683a278ce551192c96b84e0e3238ed&pid=1-s2.0-S2950327224000184-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141706607","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":"Characterizing the association between complement-mediated TMA and cognitive dysfunction using MRI and neurocognitive assessment","authors":"Pauline K. Kosalka ,&nbsp;Fahad Hannan ,&nbsp;Jeff Hamilton ,&nbsp;Christopher J. Patriquin ,&nbsp;Katerina Pavenski ,&nbsp;Michael T. Jurkiewicz ,&nbsp;Leandro Tristao ,&nbsp;Adrian M. Owen ,&nbsp;Sean C. L. Deoni ,&nbsp;Jean Théberge ,&nbsp;Jennifer Mandzia ,&nbsp;Jonathan D. Thiessen ,&nbsp;Jocelyn S. Garland ,&nbsp;Susan B. McGrath ,&nbsp;Shih-Han Susan Huang","doi":"10.1016/j.bvth.2024.100016","DOIUrl":"10.1016/j.bvth.2024.100016","url":null,"abstract":"<div><h3>Abstract</h3><p>Complement-mediated thrombotic microangiopathy (CM-TMA) is a rare, life-threatening thrombotic microangiopathy caused by a defect in the alternative complement pathway. It is associated with renal failure and acute encephalopathy, but long-term neurocognitive effects are uncertain. Using magnetic resonance imaging (MRI) and neurocognitive tests, we can further evaluate the long-term neurocognitive complications in CM-TMA and compare them with controls. In this study, we analyzed microstructural changes in the cerebral white matter and neurocognitive testing results of patients with CM-TMA. Seven adult patients with CM-TMA in remission and 6 healthy controls were included. All patients were treated with C5 complement blockade. They were followed-up for 12 months after study entry. All patients had consecutive MRI scans (standard-of-care and quantitative sequences) to assess for white matter changes and concurrent neurocognitive testing. Patients with CM-TMA had increased white matter signal intensity in most regions of the brain compared with controls. This was accompanied by increased depression and neurocognitive dysfunction (impaired concentration, short-term memory, and verbal memory). These findings were also present up to 12 months after the initial study visit. In summary, patients with previous CM-TMA were found to have significant, albeit nonspecific, cerebral white matter abnormalities, with impaired memory and concentration. Larger studies with longitudinal follow-up to assess neurocognitive complications in CM-TMA are required. This trial was registered at Clinical Trials Ontario (ctontario.ca; project ID: 1318).</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100016"},"PeriodicalIF":0.0,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000160/pdfft?md5=3b1b128f43da6772edde9663874a5a96&pid=1-s2.0-S2950327224000160-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142020948","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":"Targeting the P-selectin/PSGL-1 pathway: discovery of disease-modifying therapeutics for disorders of thromboinflammation","authors":"Samira Escopy ,&nbsp;Elliot L. Chaikof","doi":"10.1016/j.bvth.2024.100015","DOIUrl":"10.1016/j.bvth.2024.100015","url":null,"abstract":"<div><h3>Abstract</h3><p>P-selectin is a membrane glycoprotein and a member of the selectin family of cell adhesion molecules. It is prestored in α-granules of platelets and Weibel-Palade bodies of endothelial cells and is rapidly expressed on their surfaces upon activation during the course of an inflammatory response. Although a critical component of the innate immune system, the interaction of P-selectin with its cognate ligand, P-selectin glycoprotein ligand 1 (PSGL-1) may mediate maladaptive events central to the pathophysiology of venous thromboembolism, cardiovascular disease, stroke, metabolic syndrome, and sickle cell disease, among other disorders. As a consequence, a growing understanding of the significance of P-selectin and PSGL-1 in human disease has motivated the design of inhibitors that target the P-selectin/PSGL-1 pathway. Herein, we review the development and evaluation of both biologic and small-molecule inhibitors, including preclinical studies and clinical trials that have evaluated therapeutic potential of these agents for a variety of diseases linked to dysregulated inflammatory and thrombotic responses.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100015"},"PeriodicalIF":0.0,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000159/pdfft?md5=62bf22670a3a660320054f729ff7f483&pid=1-s2.0-S2950327224000159-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141637597","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":"Association of IVCF use with mortality and intracranial hemorrhage in patients with selected cancers and brain metastasis","authors":"Renata Abrahão ,&nbsp;Ann Brunson ,&nbsp;Vaibhav Kumar ,&nbsp;Anjlee Mahajan ,&nbsp;Nigel S. Key ,&nbsp;Theresa Keegan ,&nbsp;Ted Wun","doi":"10.1016/j.bvth.2024.100011","DOIUrl":"10.1016/j.bvth.2024.100011","url":null,"abstract":"<div><h3>Abstract</h3><p>We investigated the association of inferior vena cava filter (IVCF) usage with early mortality and intracranial hemorrhage (ICH) in patients with cancer and venous thromboembolism (VTE) with and without brain metastasis. We used the California Cancer Registry data linked to hospitalization and emergency department databases to identify patients (all ages) with melanoma, kidney, breast, or lung cancers who had acute VTE between 2005 and 2017 at hospital admission. The primary outcomes were 30-day mortality and 180-day ICH post-index VTE hospitalization. Of the 16 847 patients with cancer and VTE, 19.1% had brain metastasis. Patients with brain metastasis were more likely to receive an IVCF (odds ratio, 2.24; 95% confidence interval [CI], 2.01-2.50). Among patients with active bleeding, IVCF placement was associated with ∼50% reduction in 30-day mortality (hazard ratio [HR], 0.53; 95% CI, 0.42-0.68), regardless of the presence or absence of brain metastasis. In patients without active bleeding, 30-day mortality decreased by nearly 30% among those with brain metastasis who received IVCF (HR, 0.72; 95% CI, 0.60-0.85), with no difference among those without brain metastasis who had an IVCF inserted. Patients with brain metastasis had an elevated hazard of 180-day mortality (HR, 5.14; 95% CI, 2.99-8.83), but no association was found between IVCF insertion and 180-day ICH. Our study suggests a potential mortality benefit of IVCF use among patients with selected cancers and VTE, particularly among patients with active bleeding and those with brain metastasis with no bleeding. IVCF use was not associated with 180-day ICH. Randomized clinical trials are warranted to confirm our results.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100011"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000111/pdfft?md5=559af1b9e3cabfa47b8ac390a94d6f5b&pid=1-s2.0-S2950327224000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141134550","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":"Incorporating point-of-care technologies to assess treatment response in sickle cell disease","authors":"Bindu Parachalil Gopalan ∗ ,&nbsp;Timothy Quang ∗ ,&nbsp;Maria A. Lizarralde-Iragorri ,&nbsp;Dianna Lovins ,&nbsp;Ann Cullinane ,&nbsp;Alina Dulau-Florea ,&nbsp;Bruce Tromberg ,&nbsp;Arun S. Shet","doi":"10.1016/j.bvth.2024.100009","DOIUrl":"10.1016/j.bvth.2024.100009","url":null,"abstract":"","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100009"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000093/pdfft?md5=2720a428b76bb505612843d72b3e3c38&pid=1-s2.0-S2950327224000093-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141138195","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":"HMGA2 promotes platelet-neutrophil complex formation and pulmonary tissue damage in myelodysplastic syndromes","authors":"Natsumi Matsunuma ,&nbsp;Yoshihiro Hayashi ,&nbsp;Marina Fukuda ,&nbsp;Kanako Yuki ,&nbsp;Yasushige Kamimura-Aoyagi ,&nbsp;Hiroki Kobayashi ,&nbsp;Naoki Shingai ,&nbsp;Yuka Harada ,&nbsp;Hironori Harada","doi":"10.1016/j.bvth.2024.100014","DOIUrl":"10.1016/j.bvth.2024.100014","url":null,"abstract":"<div><h3>Abstract</h3><p>High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that functions as an oncogene in various cancers. Although overexpression of HMGA2 has been reported in several myeloid malignancies, its role varies considerably in different disease contexts. Here, we identified a distinct role of HMGA2 as a mediator of noninfectious pneumonia in myelodysplastic syndrome (MDS). The expression level of <em>HMGA2</em> in CD34⁺ hematopoietic stem cells and progenitors (HSC/Ps) was significantly associated with the incidence of noninfectious pneumonia, a common systemic complication in patients with MDS. Consistent with this clinical investigation, HMGA2 overexpression in a mouse model of an MDS-associated mutation led to the development of lethal noninfectious pneumonia. Mechanistically, HMGA2 overexpression conferred a megakaryocytic lineage bias to HSC/Ps and contributed to platelet activation in MDS mice. P-selectin–positive activated platelets interacted with MDS clone–derived neutrophils that exhibit increased susceptibility to cell death and formed platelet-neutrophil complexes (PNCs). Both the frequency of PNCs and neutrophil cell death within the lung microenvironment increased in MDS mice overexpressing HMGA2. Genetic inhibition of P-selectin attenuated pulmonary tissue damage in MDS mice. These findings indicate that PNCs could be a new therapeutic target for noninfectious pneumonia in patients with MDS and provide new insights into the mechanistic basis of the systemic complications of MDS.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100014"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000147/pdfft?md5=bb4a2c0bb20376bb8b90b0688c5371f3&pid=1-s2.0-S2950327224000147-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141144779","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":"Venous anomalies: an underrecognized but important cause of venous thromboembolism","authors":"Joanne So ,&nbsp;Caroline Dix ,&nbsp;Warren Clements ,&nbsp;Harry Gibbs ,&nbsp;Huyen Tran ,&nbsp;James D. McFadyen","doi":"10.1016/j.bvth.2024.100013","DOIUrl":"10.1016/j.bvth.2024.100013","url":null,"abstract":"<div><h3>Abstract</h3><p>Anatomical variants, such as May-Thurner syndrome (MTS) and inferior vena cava (IVC) variants, are underrecognized causes of deep venous thrombosis (DVT), despite affecting management. We aimed to identify the proportion of anatomical variants in proximal lower limb DVT. A retrospective cohort study was performed with cases of acute proximal DVT from 2014 to 2021 identified from ICD-10 codes. We identified 4731 DVTs and included 1268 proximal DVTs. Thirty-six (2.84%) had an anatomical variant (25 MTS and 11 IVC variants), with a rate of 14.39% in females &lt;50 years old. Compared with nonvariant DVTs, they were more likely to be unprovoked (81% vs 23%), younger (median age, 37 vs 63 years), female (67% vs 37%), and have postthrombotic syndrome (22% vs 9%). Variants frequently received thrombolysis (58% vs 1%) or angioplasty (47% vs 0%) and indefinite anticoagulation (83% vs 40%). Further investigation for variants should be considered for high-risk patients, as variants affect management.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100013"},"PeriodicalIF":0.0,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000135/pdfft?md5=101383f35f94ec4ed05c4461416ff731&pid=1-s2.0-S2950327224000135-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141133282","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}