Seminars in thrombosis and hemostasis最新文献_第5页

The History of Rare Bleeding Disorders. 罕见出血性疾病的历史。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-11-04 DOI: 10.1055/s-0044-1792032

Akbar Dorgalaleh, Behnaz Tavasoli, Saeed Hassani, Narjes Ramezanzadeh, Kimia Fathalizade, Farzaneh Hashemi, Zahra Feily, Melika Khademi, Zhino Kohzadi, Roghayeh Gholizadeh Doran Mahalleh, Mohammad S Torkamandi, Mahya S Yassini

{"title":"The History of Rare Bleeding Disorders.","authors":"Akbar Dorgalaleh, Behnaz Tavasoli, Saeed Hassani, Narjes Ramezanzadeh, Kimia Fathalizade, Farzaneh Hashemi, Zahra Feily, Melika Khademi, Zhino Kohzadi, Roghayeh Gholizadeh Doran Mahalleh, Mohammad S Torkamandi, Mahya S Yassini","doi":"10.1055/s-0044-1792032","DOIUrl":"10.1055/s-0044-1792032","url":null,"abstract":"Deficiencies in coagulation factors I (FI), FII, FV, combined FV and FVIII (CF5F8) and vitamin K-dependent coagulation factors FVII, FX, FXI, and FXIII have been referred to as rare bleeding disorders (RBDs), rare coagulation factor deficiencies (RCFDs), or recessively inherited coagulation disorders. Fibrinogen was most likely the first member of this group to be identified, with reports of its discovery spanning from 1859 to 1966. If not, then the first coagulation factor to be identified was prothrombin in 1894, and the last coagulation factor to be found was FX in 1956, about 60 years later. The first patient to be diagnosed with an RBD was a 9-year-old boy with afibrinogenemia in 1920 and the vitamin K-dependent coagulation factors deficiency was the most recent RBD in this group to be identified in a 3-month-old child in 1966. The initial therapeutic option for nearly all patients with RBDs was whole blood transfusion; this was replaced in 1941 by fresh frozen plasma (FFP), and then in later years by cryoprecipitate and coagulation factor concentrates. Fibrinogen concentrate was the first coagulation factor concentrate produced in 1956. Coagulation factor concentrate is now available for FI, FVII, FX, FXI, and FXIII; however, FFP and/or platelet transfusion are the only treatments available for FV deficiency. The only recombinant concentrates available for RBDs are for FVII and FXIII, which date from 1988 and the 2000s, respectively. Even though the clinical presentations, diagnosis, and management of lesser-known bleeding disorders have improved significantly in recent decades, more studies are needed to reveal the hidden aspects of these disorders in order to overcome diagnostic and therapeutic challenges and ultimately improve the quality of life for those who are affected.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"236-252"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Platelet-Type von Willebrand Disease: Complex Pathophysiology and Insights on Novel Therapeutic and Diagnostic Strategies. 血小板型 von Willebrand 病：复杂的病理生理学以及对新型治疗和诊断策略的见解。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-08-27 DOI: 10.1055/s-0044-1789183

Anne Fu, Thomas D D Kazmirchuk, Calvin Bradbury-Jost, Ashkan Golshani, Maha Othman

{"title":"Platelet-Type von Willebrand Disease: Complex Pathophysiology and Insights on Novel Therapeutic and Diagnostic Strategies.","authors":"Anne Fu, Thomas D D Kazmirchuk, Calvin Bradbury-Jost, Ashkan Golshani, Maha Othman","doi":"10.1055/s-0044-1789183","DOIUrl":"10.1055/s-0044-1789183","url":null,"abstract":"von Willebrand disease (VWD) is the most common well-studied genetic bleeding disorder worldwide. Much less is known about platelet-type VWD (PT-VWD), a rare platelet function defect, and a \"nonidentical\" twin bleeding phenotype to type 2B VWD (2B-VWD). Rather than a defect in the von Willebrand factor (VWF) gene, PT-VWD is caused by a platelet GP1BA mutation leading to a hyperaffinity of the glycoprotein Ibα (GPIbα) platelet surface receptor for VWF, and thus increased platelet clearing and high-molecular-weight VWF multimer elimination. Nine GP1BA gene mutations are known. It is historically believed that this enhanced binding was enabled by the β-switch region of GPIbα adopting an extended β-hairpin form. Recent evidence suggests the pathological conformation that destabilizes the compact triangular form of the R-loop-the GPIbα protein's region for VWF binding. PT-VWD is often misdiagnosed as 2B-VWD, even the though distinction between the two is crucial for proper treatment, as the former requires platelet transfusions, while the latter requires VWF/FVIII concentrate administration. Nevertheless, these PT-VWD treatments remain unsatisfactory, owing to their high cost, low availability, risk of alloimmunity, and the need to carefully balance platelet administration. Antibodies such as 6B4 remain undependable as an alternative therapy due to their questionable efficacy and high costs for this purpose. On the other hand, synthetic peptide therapeutics developed with In-Silico Protein Synthesizer to disrupt the association between GPIbα and VWF show preliminary promise as a therapy based on in vitro experiments. Such peptides could serve as an effective diagnostic technology for discriminating between 2B-VWD and PT-VWD, or potentially all forms of VWD, based on their high specificity. This field is rapidly growing and the current review sheds light on the complex pathology and some novel potential therapeutic and diagnostic strategies.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"219-226"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142081457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Precision Medicine in Rare Bleeding Disorders. 罕见出血性疾病的精准医学。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-12-05 DOI: 10.1055/s-0044-1800833

Akbar Dorgalaleh, Maha Othman

引用次数: 0

Clinical, Laboratory, and Molecular Aspects of Congenital Fibrinogen Disorders. 先天性纤维蛋白原紊乱的临床、实验室和分子方面。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-08-16 DOI: 10.1055/s-0044-1788898

Alessandro Casini, Philippe de Moerloose, Marguerite Neerman-Arbez

{"title":"Clinical, Laboratory, and Molecular Aspects of Congenital Fibrinogen Disorders.","authors":"Alessandro Casini, Philippe de Moerloose, Marguerite Neerman-Arbez","doi":"10.1055/s-0044-1788898","DOIUrl":"10.1055/s-0044-1788898","url":null,"abstract":"Congenital fibrinogen disorders (CFDs) include afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, and hypodysfibrinogenemia. The fibrinogen levels, the clinical features, and the genotype define several sub-types, each with specific biological and clinical issues. The diagnosis of CFDs is based on the measurement of activity and antigen fibrinogen levels as well as on the genotype. While relatively easy in quantitative fibrinogen disorders, the diagnosis can be more challenging in qualitative fibrinogen disorders depending on the reagents and methods used, and the underlying fibrinogen variants. Overall, quantitative and qualitative fibrinogen defects lead to a decrease in clottability, and usually in a bleeding tendency. The severity of the bleeding phenotype is moreover related to the concentration of fibrinogen. Paradoxically, patients with CFDs are also at risk of thrombotic events. The impact of the causative mutation on the structure and the fibrinogen level is one of the determinants of the thrombotic profile. Given the major role of fibrinogen in pregnancy, women with CFDs are particularly at risk of obstetrical adverse outcomes. The study of the fibrin clot properties can help to define the impact of fibrinogen disorders on the fibrin network. The development of next generation sequencing now allows the identification of genetic modifiers able to influence the global hemostasis balance in CFDs. Their integration in the assessment of the patient risk on an individual scale is an important step toward precision medicine in patients with such a heterogeneous clinical course.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"103-110"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141996398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inherited Disorders of the Fibrinolytic Pathway: Pathogenic Phenotypes and Diagnostic Considerations of Extremely Rare Disorders. 纤维蛋白溶解途径的遗传性疾病：极罕见疾病的致病表型和诊断注意事项》（Pathogenic Phenotypes and Diagnostic Considerations of Extremely Rare Disorders）。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-09-19 DOI: 10.1055/s-0044-1789596

Maha Al-Ghafry, Mouhamed Yazan Abou-Ismail, Suchitra S Acharya

{"title":"Inherited Disorders of the Fibrinolytic Pathway: Pathogenic Phenotypes and Diagnostic Considerations of Extremely Rare Disorders.","authors":"Maha Al-Ghafry, Mouhamed Yazan Abou-Ismail, Suchitra S Acharya","doi":"10.1055/s-0044-1789596","DOIUrl":"10.1055/s-0044-1789596","url":null,"abstract":"Fibrinolysis is initiated by the activation of plasminogen to plasmin via tissue-plasminogen activator (tPA) and urokinase-plasminogen activator (uPA); plasmin then converts fibrin to fibrin degradation products (FDPs). The antifibrinolytics counterbalancing this system include plasminogen activator inhibitor-1 (PAI-1), which inhibits tPA and uPA, α-2 antiplasmin (α2AP), which inhibits plasmin, and thrombin activatable fibrinolysis inhibitor, which inhibits the conversion of fibrin to FDP. Inherited disorders of the fibrinolytic pathway are rare and primarily have hemorrhagic phenotypes in humans: PAI-1 deficiency, α2AP deficiency, and Quebec platelet disorder. Patients with these disorders are usually treated for bleeds or receive prophylaxis to prevent bleeds in the surgical setting, with pharmacological antifibrinolytics such as aminocaproic acid and tranexamic acid. Disorders of the fibrinolytic pathway with fibrin deposition are extremely rare, mostly noted in patients with plasminogen deficiency, who have more recently benefited from advances in human plasma-derived plasminogen concentrates administered intravenously or locally. These disorders can be very difficult to diagnose using conventional or even specialized coagulation testing, as testing can be nonspecific or have low sensitivity. Testing of the corresponding protein's activity and antigen (where applicable) can be obtained in specialized centres, and routine laboratory measures are not diagnostic. Genetic testing of the pathogenic mutations is recommended in patients with a high suspicion of an inherited disorder of the fibrinolytic pathway.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"227-235"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142294437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical, Laboratory, and Molecular Characteristics of Inherited Vitamin K-Dependent Coagulation Factors Deficiency. 遗传性维生素 K 依赖性凝血因子缺乏症的临床、实验室和分子特征。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-03-01 Epub Date: 2024-11-04 DOI: 10.1055/s-0044-1792031

Salvatore Perrone, Simona Raso, Mariasanta Napolitano

{"title":"Clinical, Laboratory, and Molecular Characteristics of Inherited Vitamin K-Dependent Coagulation Factors Deficiency.","authors":"Salvatore Perrone, Simona Raso, Mariasanta Napolitano","doi":"10.1055/s-0044-1792031","DOIUrl":"10.1055/s-0044-1792031","url":null,"abstract":"Vitamin K-dependent coagulation factors deficiency (VKCFD) is a rare autosomal recessive genetic disease characterized by impaired levels of multiple coagulation factors (II, VII, IX, and X) and natural anticoagulants (proteins C and S). VKCFD is part of familial multiple coagulation factor deficiencies, reporting overall 50 affected families thus far. Disease manifestations are quite heterogeneous, bleeding symptoms may vary, and even, although generally mild, some patients may succumb to fatal outcomes. VKCFD diagnosis may be delayed because the disease phenotype simulates the most frequently acquired deficiencies of vitamin K. First-line coagulation assays, prothrombin time/international normalized ratio (PT/INR) and activated partial thromboplastin time (aPTT), are both prolonged; mixing test typically normalizes the clotting times; and vitamin K-dependent coagulation factors will be variably decreased. Molecularly, VKCFD is associated with mutations in γ-glutamyl-carboxylase (GGCX) or vitamin K epoxide reductase complex subunit 1 (VKORC1) genes. Vitamin K is involved not only in the biosynthesis of coagulation proteins but also in bone metabolism and cell proliferation. Therapeutic options are based on vitamin K supplementation, coagulation factors (prothrombin complex), and fresh frozen plasma, in case of severe bleeding episodes. Two case studies here illustrate the diagnostic challenges of VKCFD: case 1 depicts a woman with a history of bleeding episodes, diagnosed, only in her third decade of life with inherited homozygous GGCX gene mutation. Case 2 shows a man with an acquired vitamin K deficiency caused by Crohn's disease. Better understanding of GGCX and VKORC1 mutations aids in prognosis and treatment planning, with emerging insights suggesting potential limitations in the effectiveness of vitamin K supplementation in certain mutations.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"170-179"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coagulation Abnormalities in Chronic Liver Disease. 慢性肝病的凝血异常。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-02-27 DOI: 10.1055/a-2531-4712

Massimo Franchini, Pier Mannuccio Mannucci

引用次数: 0

Fright of Long-Haul Flights: Focus on Travel-Associated Thrombosis. 长途飞行的恐惧：关注与旅行相关的血栓。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-02-27 DOI: 10.1055/s-0045-1805038

Emmanuel Papadakis, Eleni Gavriilaki, Nikolaos Kotsiou, Antonella Tufano, Benjamin Brenner

{"title":"Fright of Long-Haul Flights: Focus on Travel-Associated Thrombosis.","authors":"Emmanuel Papadakis, Eleni Gavriilaki, Nikolaos Kotsiou, Antonella Tufano, Benjamin Brenner","doi":"10.1055/s-0045-1805038","DOIUrl":"https://doi.org/10.1055/s-0045-1805038","url":null,"abstract":"Travel-related thrombosis (TRT), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), poses a significant health risk associated with long-haul travel. Prolonged immobility, dehydration, and cabin pressure changes during flights contribute to venous stasis, hypoxia, and hypercoagulability, collectively increasing the risk of venous thromboembolism (VTE). While the absolute risk of TRT is relatively low in the population overall, it rises significantly among high-risk groups, including individuals with a history of VTE, thrombophilia, pregnancy, or recent surgery. This review explores the epidemiology, pathophysiology, clinical presentation, and diagnostic evaluation of TRT while highlighting the importance of early recognition and prevention. Risk assessment models can provide guidance for identifying at-risk travelers. Preventive strategies include pharmacological prophylaxis with low-molecular-weight heparin (LMWH) for high-risk individuals and nonpharmacological measures such as compression stockings, intermittent pneumatic compression, mobility exercises, and hydration. Guidelines from international societies recommend tailored interventions based on individual risk profiles, as randomized controlled trials are scarce. Given that long-haul travel dramatically expands, this review critically analyzes the available TRT management strategies in various clinical settings, aiming to increase awareness of this global health issue.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-platelet Factor 4 Antibody-Mediated Disorders: An Updated Narrative Review. 抗血小板因子4抗体介导的疾病：最新的叙事回顾。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-02-19 DOI: 10.1055/a-2528-5425

Angela Napolitano, Luca Spiezia, Marta Biolo, Claudia Maria Radu, Serena Toffanin, Elena Campello, Paolo Simioni

{"title":"Anti-platelet Factor 4 Antibody-Mediated Disorders: An Updated Narrative Review.","authors":"Angela Napolitano, Luca Spiezia, Marta Biolo, Claudia Maria Radu, Serena Toffanin, Elena Campello, Paolo Simioni","doi":"10.1055/a-2528-5425","DOIUrl":"10.1055/a-2528-5425","url":null,"abstract":"Anti-platelet factor 4 (PF4) antibody-mediated disorders are a heterogeneous group of diseases characterized by the presence of highly pathogenic immunoglobulins G directed against PF4 and/or PF4/heparin complexes. These antibodies are able to activate platelets, neutrophils, and monocytes, thus resulting in thrombocytopenia and a hypercoagulable state. Five different forms of anti-PF4 antibody-mediated disorders have been identified: (1) classic heparin-induced thrombocytopenia (HIT) mediated by heparin and certain polyanionic drugs; (2) autoimmune HIT characterized by the presence of anti-PFA/polyanion antibodies that can strongly activate platelets even in the absence of heparin; (3) spontaneous HIT characterized by thrombocytopenia and thrombosis without proximate exposure to heparin, with two subtypes: (a) post-total knee arthroplasty and cardiac surgery using cardiopulmonary bypass or extracorporeal membrane oxygenation and (b) postinfections; (4) vaccine-induced immune thrombotic thrombocytopenia (VITT) characterized by thrombocytopenia, arterial and venous thrombosis, or secondary hemorrhage after receiving adenoviral vector vaccines for coronavirus disease 2019; (5) VITT-like disorders triggered by adenoviral infections. Although extremely rare and largely unknown, there has been growing interest in the VITT syndrome in recent years due to its clinical relevance. Timely detection of these antibodies is crucial for the diagnosis and treatment of anti-PF4 antibody-mediated disorders, via anti-PF4 antibody immunoassays using several antibody capture systems (e.g., enzyme-linked immunosorbent assay-based, particle gel, turbidimetry) and functional assays (e.g., serotonin release assay or heparin-induced platelet activation). We aimed to present the latest on laboratory findings, clinical characteristics, and therapeutic approaches for anti-PF4 antibody-mediated disorders.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Monitoring Hemostatic Function during Cardiac Surgery with Point-of-Care Viscoelastic Assays: A Narrative Review. 监测心脏手术中的止血功能与护理点粘弹性分析：叙述性回顾。

IF 3.6 2区医学

Seminars in thrombosis and hemostasis Pub Date : 2025-02-12 DOI: 10.1055/s-0045-1802573

Brandon Jin An Ong, Hui Xin See Tow, Alyssa Tze Wei Fong, Ryan Ruiyang Ling, Kiran Shekar, Kristine Teoh, Lian Kah Ti, Graeme MacLaren, Bingwen Eugene Fan, Kollengode Ramanathan

{"title":"Monitoring Hemostatic Function during Cardiac Surgery with Point-of-Care Viscoelastic Assays: A Narrative Review.","authors":"Brandon Jin An Ong, Hui Xin See Tow, Alyssa Tze Wei Fong, Ryan Ruiyang Ling, Kiran Shekar, Kristine Teoh, Lian Kah Ti, Graeme MacLaren, Bingwen Eugene Fan, Kollengode Ramanathan","doi":"10.1055/s-0045-1802573","DOIUrl":"https://doi.org/10.1055/s-0045-1802573","url":null,"abstract":"Bleeding is a well-known and severe complication of cardiac surgery. Cardiopulmonary bypass, along with heparinization and hemodilution, is thought to affect all pathways of the hemostatic process, leading to excessive bleeding and worsened morbidity and mortality. The traditionally used standard laboratory tests (SLTs) were not designed for the surgical setting, have long turnaround times, and are poor predictors of bleeding. This review aims to give an overview of viscoelastic assays (VEAs), compare VEAs to conventional testing methods, and summarize the evidence for VEAs in cardiac surgery. A search of Medline via Pubmed, Scopus, and Embase yielded 2,868 papers, which we reviewed and summarized the key findings. VEAs such as rotational thromboelastometry and thromboelastography provide a quick turnaround, graphical, global impression of hemostasis in whole blood. VEAs allow for the analysis of specific contributors to the coagulation process and may facilitate cause-oriented hemostatic treatment and the development of treatment algorithms. VEAs have been found to have a high specificity and high negative predictive value for coagulopathic bleeding. Patients treated with VEA-based algorithms have been shown to have lower rates of bleeding, transfusion requirements, and exposure to allogeneic blood products. However, VEA-based algorithms have not demonstrated a mortality benefit and evidence for outcomes such as surgical re-exploration and hospital length of stay remains equivocal. In conclusion, VEAs have been shown to be comparable if not superior to SLTs in cardiac surgery. Further large-scale studies are needed to better evaluate the impact of VEAs on clinical outcomes.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143410312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0