SEMINARS IN THROMBOSIS AND HEMOSTASIS血栓与止血研讨会
SEMINARS IN THROMBOSIS AND HEMOSTASIS(英文缩写 SEMIN THROMB HEMOST),ISSN 0094-6176,eISSN 1098-9064,中文译名:血栓与止血研讨会 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.415 | Q1 |
| 2022 | 5.700 | Q1 |
| 2023 | 3.600 | Q1 |
| 2024 | 4.100 | Q1 |
| 2025 | 4.200 | Q1 |
SEMINARS IN THROMBOSIS AND HEMOSTASIS 最新收录文献
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1. Hemostasis in Exercise and the Athlete Part II, Plus An Additional Mini-Compilation.
PMID:日期:2026-10-01该文献暂无摘要。
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3. Blood Flow Restriction Training in Athletes: Endothelial Phenotype, Thromboembolism Risk, and Tailored Safety Protocols.
PMID:日期:2026-10-01Low-load blood flow restriction (LLBFR) training has gained traction as a rehabilitation and performance tool, offering muscle strength and hypertrophy adaptations comparable to high-load resistance training while minimizing joint and tissue stress. However, its application in athletes at risk for venous thromboembolism, post-thrombotic syndrome (PTS), inherited thrombophilia, and special populations (pregnant competitive female athletes and paralympic athletes with spinal cord injury) raises safety concerns. This narrative review synthesizes evidence on LLBFR's hemodynamic and endothelial effects, highlighting pressure-dependent basal lamina thickening, impaired flow-mediated dilation, and transient elevations in peripheral venous pressure. It emphasizes the importance of pre-exercise risk stratification, genetic screening for factor V Leiden and prothrombin mutations, and assessment of cardiovascular and coagulation markers. For athletes with confirmed deep vein thrombosis, PTS, or multiple risk factors, LLBFR should be contraindicated. In paralympic athletes with spinal cord injury, stringent exclusion criteria (e.g., severe autonomic dysreflexia, pressure ulcers) are essential, whereas female athletes may require individualized monitoring of coagulation changes during oral contraceptive use and pregnancy. Although LLBFR shows promise for preserving muscle function when traditional loading is impractical, robust, large-scale studies measuring thrombogenesis and fibrinolysis markers are urgently needed. Tailored protocols that balance musculoskeletal benefits against thrombotic risks will ensure safe, effective implementation across diverse athlete populations.
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4. Integrating Next-Generation Sequencing into von Willebrand Disease Diagnostics: Insights from the PCM-EVW-ES Multicenter Project.
PMID:日期:2026-10-01Von Willebrand disease (VWD) is the most common inherited bleeding disorder, caused by quantitative or qualitative defects in von Willebrand factor (VWF). Diagnosis is challenging and requires integrating bleeding history, VWF antigen and activity measurements, FVIII assays, and specialized phenotyping. Genetic testing is increasingly recognized as a key component. Here, we review current concepts in VWD diagnostics and highlight the Spanish Clinical and Molecular Profile of von Willebrand Disease (PCM-EVW-ES) project as a model for genomics-enabled precision medicine. PCM-EVW-ES is a multicenter initiative involving 48 hospitals, centralized phenotypic testing, and next-generation sequencing of the coding region, enabling definitive classification in 730 individuals with VWD to date. Harmonized recruitment criteria and standardized workflows improve subtype assignment, uncover complex genotypes, refine genotype-phenotype correlations, and facilitate the identification of asymptomatic carriers. The PCM-EVW-ES variant spectrum highlights recurrent disease-causing variants in Spain and underscores the value of coordinated national registries for variant curation. Building on these data, we propose a diagnostic algorithm in which bleeding assessment and first-line VWF/FVIII assays, combined with, early molecular testing increases diagnostic accuracy and guides targeted second-line investigations to confirm and refine VWD subtype classification. We also outline persisting challenges, including the interpretation of variants of uncertain significance and patients without identifiable pathogenic variants, and future directions integrating third-generation sequencing, expanded gene panels, functional studies, and artificial-intelligence-driven multiomic approaches. Together, these advances illustrate how robust multicenter studies can bridge the gap between complex diagnostics and clinical practice in VWD.
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5. Redefining Fibrinolytic Insufficiency in Sepsis-Associated DIC.
PMID:日期:2026-10-01Sepsis disrupts the physiological balance between coagulation and fibrinolysis, resulting in a state in which fibrin formation exceeds fibrin removal and drives microvascular thrombosis, organ failure, and mortality. Although an early burst of endothelial tissue-type plasminogen activator (t-PA) may transiently increase plasmin generation, this phase is rapidly eclipsed by sustained upregulation of plasminogen activator inhibitor-1 (PAI-1), dysregulated activation of thrombin-activatable fibrinolysis inhibitor, depletion of endogenous anticoagulants, and progressive endotheliopathy. Beyond inhibitor excess, emerging evidence indicates that a quantitative defect in plasminogen is a central contributor to fibrinolytic insufficiency. Neutrophil extracellular traps (NETs) contain elastase, which cleaves plasminogen into inactive fragments, reducing functional plasminogen availability and impairing fibrin-bound plasmin generation. When functional plasminogen falls below rate-limiting levels, fibrin surfaces cannot efficiently support plasmin formation, resulting in persistent microvascular fibrin deposition despite elevated D-dimer concentrations. This NET-plasminogen axis links immunothrombosis to the "fibrinolytic insufficiency phenotype observed in sepsis-induced coagulopathy and overt disseminated intravascular coagulation (DIC)." Clinically, hypofibrinolysis is characterized by high D-dimers, elevated PAI-1, reduced plasmin generation, and low fibrinolytic activity on viscoelastic testing. Multimodal assessment integrating biomarker panels and viscoelastic assays, including t-PA- or urokinase-challenged protocols, may improve risk stratification. Therapeutic strategies largely targeted coagulation; however, persistent hypofibrinolysis limits their effectiveness. Translational data demonstrate that plasminogen supplementation restores functional plasminogen levels and normalizes plasmin generation in septic patients and in experimental DIC, providing proof of concept for fibrinolysis-directed therapy. Future progress requires standardized definitions, functional fibrinolytic phenotyping, and phenotype-guided clinical trials to restore the coagulo-fibrinolytic balance in sepsis.
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6. Neonatal Sepsis-Induced Coagulopathy: An Evolving Frontier at the Crossroads of Inflammation and Hemostasis.
6. 新生儿败血症引起的凝血病：炎症和止血十字路口的一个不断发展的前沿PMID:日期:2026-10-01Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host immune response to an infection. Sepsis is often associated with significant hemostatic disorders that may lead to extensive intravascular thrombosis, disseminated intravascular coagulation (DIC), multi-organ dysfunction syndrome (MODS), and increased mortality. Sepsis-induced coagulopathy (SIC) is currently recognized as an early distinct phase of hemostatic derangement caused by sepsis, and a prodrome of overt DIC. SIC is characterized by endovascular clotting activation, hypercoagulability, and consumption of clotting factors and platelets. DIC, traditionally considered the final stage of this process, is now recognized as a part of a continuum of pathophysiological dysregulation with a distinct clinical significance. Despite being extensively studied in the adult population, SIC remains poorly defined in neonates. The distinct characteristics of neonatal hemostasis, coupled with immunological immaturity, pose significant challenges to the direct application of adult diagnostic approaches of SIC in this population. This review focuses on the pathophysiological mechanisms of SIC and the unique characteristics of neonatal hemostasis, summarizes current knowledge regarding the underlying mechanisms of neonatal SIC, and explores the developmental interplay between inflammation and hemostasis. By integrating current evidence, the review aims to establish a conceptual framework that will guide future experimental and clinical studies directed toward improving the management and outcomes of neonates who develop coagulopathy during sepsis.
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7. How Do Muscles Protect Joints in Hemophilia? Integrating Mechanical, Neural, and Endocrine Mechanisms.
PMID:日期:2026-10-01People with hemophilia (PwH) face persistent joint damage risk despite prophylactic factor replacement therapies. Although muscles are recognized as biomechanical stabilizers, their broader protective mechanisms remain poorly understood. This review provides an integrative theoretical framework that examines how muscles protect joints in PwH through three interconnected dimensions: (1) mechanical-via joint stabilization and force absorption; (2) neuromuscular control; and (3) biochemical regulation through exercise-induced myokines (exerkines). Muscle contractions provide joint stabilization and attenuate mechanical impacts via eccentric actions and muscle-tendon buffering, thereby reducing joint loading during daily activities. Neuromuscular control maintains joint stability through coordinated muscle activation, though excessive co-contraction in arthropathy can paradoxically increase joint stress. Critically, the endocrine function of skeletal muscle, producing anti-inflammatory and cartilage-protective exerkines including interleukin-6, irisin, and lubricin (among others), represents an underexplored yet crucial protective mechanism. Physical inactivity and intramuscular fat accumulation impair these protective functions, accelerating joint degeneration. This integrative theoretical perspective offers a comprehensive framework for understanding how muscles protect joints in hemophilia. Understanding these integrated mechanisms is essential for developing targeted rehabilitation strategies and guiding future research to optimize joint health in PwH.
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8. Impact of Exercise/Sport on Well-Being in von Willebrand Disease and Other Congenital Bleeding Disorders: An Update.
PMID:日期:2026-10-01Worldwide, one in four adults and three in four children fail to meet the physical activity targets recommended by the World Health Organization (WHO). Patients with chronic diseases and disabilities represent some of the least active populations. WHO guidelines encourage regular physical activity for individuals with disabilities, considering functional capacity and clinical status. Recommended interventions include moderate-to-vigorous activity, muscle-strengthening exercises at least twice weekly, and functional balance training at least three times per week, with specialist consultation as needed. Data on physical activity and sports participation in patients with chronic conditions such as inherited bleeding disorders are very limited. This narrative review updates the literature, focusing on von Willebrand disease and rare coagulation defects and highlighting the need for individualized, multidisciplinary recommendations to promote safe physical activity and optimize health outcomes.
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9. Physical Activity in People with Hemophilia.
PMID:日期:2026-10-01Hemophilia is a rare inherited bleeding disorder associated with recurrent musculoskeletal bleeding, chronic pain, and functional decline. Advances in prophylactic therapies, including extended half-life factors, non-factor therapies like emicizumab, and gene therapies, have fundamentally transformed care, enabling a paradigmatic shift from activity restriction to promotion. This review synthesizes recent evidence to examine the multifaceted role of physical activity (PA) in people with hemophilia (PwH), current challenges, and strategies to optimize health outcomes. PA confers substantial benefits for PwH, improving muscle strength, coordination, bone density, cardiovascular fitness, mental health, and quality of life. It modulates chronic pain through neuroplastic, anti-inflammatory, and neuroendocrine mechanisms, while exercise-derived molecules (exerkines) may directly influence cartilage health. With individualized prophylaxis and structured programming, both resistance and aerobic exercise can be prescribed safely using evidence-based risk stratification (categories I-III) and comprehensive monitoring approaches, including accelerometers, questionnaires, and subjective effort scales. Persistent barriers include chronic pain, fear of injury, insufficient professional guidance, and treatment inequities, while facilitators encompass enjoyment, social support, and adequate prophylactic coverage. Therapies providing continuous hemostatic protection have further expanded safe PA opportunities, supporting participation in previously restricted activities. In this new therapeutic era, PA should be recognized as a fundamental pillar alongside medical care. Not only for musculoskeletal preservation, but also as a strategy promoting metabolic and mental health. Ensuring access for all patients to both advanced therapies and tailored PA prescription, supported by education, enabling policies, and multidisciplinary care, is essential for democratizing active lifestyles within the global hemophilia community.
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10. Resistance or Resilience? Hemostatic Balance in an FV Leiden Elite Athlete.
PMID:日期:2026-10-01该文献暂无摘要。