Seminars In Thrombosis And Hemostasis[JOURNAL]
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200 papers
Mortality from Pulmonary Embolism in Patients with Post-Coronavirus Disease Syndrome.
Lippi G, Mattiuzzi C, Favaloro EJ
Semin Thromb Hemost · 2025 Oct · PMID 40154505 · Publisher ↗
Abstract loading — click title to view on PubMed.
Hemostatic Manifestations of Invasive Fungal Infections: A Comprehensive Review of Pathophysiological Mechanisms in Sepsis-Induced Hemostatic Disturbances, with a Focus on the Neonatal Population.
Lianou A, Tsantes AG, Piovani D … +6 more , Bonovas S, Lapaj IM, Gounari EA, Tsantes AE, Iacovidou N, Sokou R
Semin Thromb Hemost · 2025 Jun · PMID 40127884 · Publisher ↗
Sepsis is a life-threatening condition that has challenged many clinicians over the years. The immune and hemostatic systems are the primary pillars of sepsis pathogenesis. Dysregulation of these intricate mechanisms sig...
Sepsis is a life-threatening condition that has challenged many clinicians over the years. The immune and hemostatic systems are the primary pillars of sepsis pathogenesis. Dysregulation of these intricate mechanisms significantly worsens the prognosis. Coagulopathy is a critical aspect of sepsis, with the degree of hemostatic impairment being a key determinant of poor outcomes. Although the concept of sepsis caused by bacteria has been well investigated, the fungal impact in the complexity of sepsis-related hemostatic derangement is not yet fully unraveled. In addition, sepsis occurs in patients across all age groups, with a particular concern for neonates, whose immature and vulnerable systems amplify the challenges. Notably, despite the high incidence of fungal septicemia in neonatal intensive care units (NICUs), along with its significant morbidity, mortality, and adverse neonatal outcomes, the impact of fungal sepsis on the neonatal hemostatic system-an essential determinant of prognosis-remains largely unexplored. The present review delves into the pathophysiologic mechanisms of sepsis-induced coagulopathy attributed to fungal infection, the mechanisms of fungal involvement in the hemostatic derangement, and attempts to contextualize this knowledge within the unique neonatal population. Finally, it aims to raise awareness of the critical need for a deep understanding of this hazardous condition to guide the development of optimal therapeutic strategies.
Unlocking the Potential of MicroRNA Expression: Biomarkers for Platelet Reactivity and Coronary Artery Disease.
Nissen PH, Pedersen OB
Semin Thromb Hemost · 2025 Nov · PMID 40074010 · Publisher ↗
Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide, with platelet reactivity playing a central role in its pathogenesis. Recent research has identified microRNAs (miRNAs; miRs) as poten...
Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide, with platelet reactivity playing a central role in its pathogenesis. Recent research has identified microRNAs (miRNAs; miRs) as potential biomarkers for CAD, due to their ability to regulate platelet function and reactivity. This review focuses on four key miRNAs-miR-223, miR-126, miR-21, and miR-150-known to influence platelet reactivity and their implications in CAD. miR-223, which is highly expressed in platelets, has shown associations with CAD and myocardial infarction, while miR-126 has been linked to thrombus formation and vascular health. Additionally, miR-21 and miR-150 have also emerged as important players, with roles in platelet reactivity and cardiovascular outcomes. However, despite their potential, the use of miRNAs as clinical biomarkers faces several challenges, including variability in reported results across studies. These inconsistencies often arise from differences in sample material, preanalytical conditions, and normalization strategies. Furthermore, the influence of antiplatelet therapy on miRNA expression adds another layer of complexity, making it difficult to determine whether observed changes in miRNA levels are due to disease states or therapeutic interventions. This review therefore highlights the need for standardization in miRNA research to enhance the reliability of findings. By addressing these methodological challenges, miRNAs could become powerful tools in personalized medicine, aiding in the development of tailored therapeutic strategies for CAD patients and ultimately improving clinical outcomes.
Alterations in the Blood-Brain Barrier in Mood Disorders and Neurodegenerative Diseases.
Conejero I, Chea M, Courtet P … +2 more , Bouvier S, Pereira F
Semin Thromb Hemost · 2025 Jun · PMID 40058364 · Publisher ↗
Depressive disorders and suicidal behaviors represent major causes of health loss. Modifications of brain microvasculature, and specifically alterations of the blood-brain barrier have been supposed to participate in the...
Depressive disorders and suicidal behaviors represent major causes of health loss. Modifications of brain microvasculature, and specifically alterations of the blood-brain barrier have been supposed to participate in the vulnerability to those disorders along with cognitive impairment, especially in the older adults. In this article, we addressed evidence linking blood-brain barrier impairments with mood disorders and suicide. Secondly, we investigated their relationship with depression in old age, and with neurodegenerative processes. Particular attention was drawn toward the potential interactions between the coagulation processes and the blood-brain barrier dysfunctions, as innovative treatment strategies may emerge from research in those fields. Overall, the studies reviewed highlight the implication of multiple dysfunctions of the blood-brain barrier in mood disorders and suicide. Impairments of the blood-brain barrier show relationships with altered expression of endothelial cell junction proteins. These modifications also implicate receptors of the extracellular matrix, the vascular endothelial growth factor, changes in perivascular astrocytes, and has links with local and systemic inflammatory processes. Dysfunctions of the blood-brain barrier underly chronic stress and participate in psychiatric diathesis in old age. In addition, we outline that coagulation processes are likely to interact with the blood-brain barrier and further contribute to neurodegenerative disorders. In conclusion, new pathophysiological models offer perspectives toward detecting new biomarkers in mood disorders and suicide. In parallel, these models open avenues for developing innovative therapeutic agents, although further considering their potential risks and eventual benefits is needed.
Nebulized Heparin in 2025: at the Interface between Promising Benefits and the Need for Further Research.
Lippi G, Favaloro EJ
Semin Thromb Hemost · 2025 Oct · PMID 40049605 · Publisher ↗
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Neutrophil Extracellular Traps: At the Interface of Thrombosis and Comorbidities.
Varjú I, Tanka-Salamon A, Kolev K
Semin Thromb Hemost · 2025 Oct · PMID 40020757 · Publisher ↗
Since their discovery in 2004, neutrophil extracellular traps (NETs) have been at the center of multidisciplinary attention. Although a key tool in neutrophil-mediated immunity, these filamentous, enzyme-enriched DNA-his...
Since their discovery in 2004, neutrophil extracellular traps (NETs) have been at the center of multidisciplinary attention. Although a key tool in neutrophil-mediated immunity, these filamentous, enzyme-enriched DNA-histone complexes can be detrimental to tissues and have been identified as an underlying factor in a range of pathological conditions. Building on more than 20 years of research into NETs, this review places thrombosis, the pathological formation of blood clots, in the spotlight. From this point of view, we discuss the structure and formation of NETs, as well as the interaction of their components with the hemostatic system, dissecting the pathways through which NETs exert their marked effect on formation and the dissolution of thrombi. We pay distinct attention to the latest developments in the research of a key player in NET formation, peptidyl-arginine-deiminase (PAD) enzymes: their types, sources, and potential cross-play with the hemostatic machinery. Besides these molecular details, we elaborate on the link between pathological thrombosis, NETs, and widespread conditions that represent a debilitating public health burden worldwide, such as sepsis and neoplasms. Finally, future implications on the treatment of thrombosis-related conditions will be discussed.
Use of Oral Anti-Xa Inhibitor in Prosthetic Mechanical Aortic Valve with Warfarin Hypersensitivity Due to the FIX p.(Ala37Thr) Propeptide Variant: Case Report and Literature Review.
Tufano A, Fierarossa C, Cirillo F … +10 more , Miele C, Capasso F, Mazzaccara C, Micale L, Vecchione G, Castori M, Frangipane I, Mocerino L, Cimino E, Di Minno M
Semin Thromb Hemost · 2025 Jun · PMID 40015335 · Publisher ↗
Bleeding is the most common side effect during treatment with vitamin K antagonists (VKAs). Sometimes, VKA use causes bleeding episodes due to rare variants in the factor IX (FIX) propeptide that modify the affinity of F...
Bleeding is the most common side effect during treatment with vitamin K antagonists (VKAs). Sometimes, VKA use causes bleeding episodes due to rare variants in the factor IX (FIX) propeptide that modify the affinity of FIX propeptide to the binding of γ-glutamyl carboxylase. We report on a 51-year-old patient who presented with recurrent spontaneous and severe intramuscular and cutaneous bleedings during VKA (warfarin) treatment for the presence of a prosthetic mechanical aortic valve. Laboratory evaluation revealed INR within the therapeutic range with markedly prolonged aPTT and a large reduction of FIX levels. Laboratory parameters significantly improved when warfarin was switched with low-molecular-weight heparin. Next-generation sequencing analysis revealed the variant p.(Ala37Thr) in the F9 gene, which has been previously associated with VKA sensitivity. As an alternative to warfarin, apixaban 5 mg twice daily and aspirin 100 mg daily were started, with no thrombosis or recurrence of hemorrhage and normalization of INR, aPTT, and FIX levels, at 12-month follow-up. We also performed a literature search across PubMed and Scopus, until January 2025. The analysis evidenced five case reports and two case series. The mechanisms of this rare VKA hypersensitivity have also been reviewed. In conclusion, while VKA hypersensitivity is a rare phenomenon, awareness of this complication and the current accessibility to molecular testing make it important to identify patients at risk. The efficacy/safety of direct thrombin or factor Xa inhibitors in patients with a mechanical heart valve and VKA hypersensitivity due to the F9 p.(Ala37Thr) variant deserves more attention and further investigation.
Factor Inhibitor Testing: An Update from Australasia/Asia-Pacific.
Favaloro EJ, Arunachalam S
Semin Thromb Hemost · 2025 Sep · PMID 40015334 · Publisher ↗
Factor VIII (FVIII) inhibitors represent antibodies that develop against coagulation FVIII and reduce FVIII functional activity. FVIII inhibitors may develop in patients with congenital hemophilia A (CHA) in response to...
Factor VIII (FVIII) inhibitors represent antibodies that develop against coagulation FVIII and reduce FVIII functional activity. FVIII inhibitors may develop in patients with congenital hemophilia A (CHA) in response to infused FVIII (allo-antibodies) or in patients without CHA in a variety of situations (auto-antibodies; acquired hemophilia A). We report updated findings for FVIII inhibitor testing in our geographic region using recent data (testing for the past 5 years; 2020-2024 inclusive) from the RCPAQAP (Royal College of Pathologists of Australasia Quality Assurance Program), an international external quality assessment (EQA) program, with over 80 enrolments for the FVIII inhibitor module. Four samples are assessed each year, with these comprising both FVIII inhibitor negative samples and FVIII inhibitor positive samples with various inhibitor titers. This EQA data largely evidences favorable findings in FVIII inhibitor testing in our jurisdiction, with >99% of test results interpreted correctly by participants for the presence ("detected") or absence ("not detected") of FVIII inhibitors in assessed samples. Moreover, most errors in interpretation appear to be transcription or data entry errors rather than analytic errors. The coefficient of variation (CV) values for FVIII inhibitor samples were moderately high, ranging from 25 to 40%, irrespective of the inhibitor titer (range: 3-64 Bethesda units [BU]/mL) or the method (i.e., Bethesda vs. Nijmegen). In conclusion, most laboratories were able to correctly identify the presence versus absence of FVIII inhibitors, although laboratory-reported titers varied moderately.
Fright of Long-Haul Flights: Focus on Travel-Associated Thrombosis.
Papadakis E, Gavriilaki E, Kotsiou N … +2 more , Tufano A, Brenner B
Semin Thromb Hemost · 2025 Jun · PMID 40015328 · Publisher ↗
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 pressur...
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.
Monitoring Hemostatic Function during Cardiac Surgery with Point-of-Care Viscoelastic Assays: A Narrative Review.
Ong BJA, See Tow HX, Fong ATW … +7 more , Ling RR, Shekar K, Teoh K, Ti LK, MacLaren G, Fan BE, Ramanathan K
Semin Thromb Hemost · 2026 Jun · PMID 39938563 · Publisher ↗
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 b...
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.
Coagulation Abnormalities in Chronic Liver Disease.
Franchini M, Mannucci PM
Semin Thromb Hemost · 2026 Apr · PMID 39904369 · Publisher ↗
Chronic liver disease is a frequently encountered disorder and a major concern worldwide with a complex pathophysiology, which often affects the hemostatic system. Such alterations, which affect both primary and secondar...
Chronic liver disease is a frequently encountered disorder and a major concern worldwide with a complex pathophysiology, which often affects the hemostatic system. Such alterations, which affect both primary and secondary hemostasis, are heterogenous, including prohemorrhagic (i.e., decreased coagulation factors, increased fibrinolysis, thrombocytopenia, and platelet dysfunction) and prothrombotic (i.e., decreased natural anticoagulants) changes. As a consequence of this unstable balance, patients with liver cirrhosis may experience both hemorrhagic complications and venous thromboembolic events, which are often unpredictable and whose management is particularly challenging for clinicians. This narrative review will address the most recent advances in the pathophysiology of key derangements of hemostasis in patients with chronic liver disease, focusing on their clinical implications and management.
Anti-platelet Factor 4 Antibody-Mediated Disorders: An Updated Narrative Review.
Napolitano A, Spiezia L, Biolo M … +4 more , Radu CM, Toffanin S, Campello E, Simioni P
Semin Thromb Hemost · 2025 Jun · PMID 39884292 · Publisher ↗
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...
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.
Inflammation and Coagulation in Neurologic and Psychiatric Disorders.
Khoury R, Chapman J
Semin Thromb Hemost · 2025 Jun · PMID 39848256 · Publisher ↗
Coagulation factors are intrinsically expressed in various brain cells, including astrocytes and microglia. Their interaction with the inflammatory system is important for the well-being of the brain, but they are also c...
Coagulation factors are intrinsically expressed in various brain cells, including astrocytes and microglia. Their interaction with the inflammatory system is important for the well-being of the brain, but they are also crucial in the development of many diseases in the brain such as stroke and traumatic brain injury. The cellular effects of coagulation are mediated mainly by protease-activated receptors. In this review, we sum up the role of the coagulation cascade in the development of different diseases including psychiatric disorders. In inflammatory diseases such as multiple sclerosis, fibrinogen activates microglia and suppresses the differentiation of oligodendrocytes, leading to axonal damage and suppression of remyelination. In ischemic stroke, thrombin activity is associated with the size of infarction, and the inhibition of either thrombin- or protease-activated receptor 1 promotes neuronal survival and reduces the size of infarction. Patients suffering from Alzheimer's disease express higher levels of thrombin, which in turn damages the endothelium, increases blood-brain barrier permeability, and induces cell apoptosis. In major depressive disorder, a positive correlation is present between prothrombotic states and suicidality. Moreover, both protein S deficiency and antiphospholipid antibodies are associated with schizophrenia and there is an effect of warfarin on psychosis-free intervals. Studying the coagulation in the brain could open a new door in understanding and treating neurological and psychiatric disorders, and extensive research should be conducted in this field.
Inherited or Immunological Thrombocytopenia: The Complex Nature of Platelet Disorders in 22q11.2 Deletion Syndrome.
Urbański B, Urbańska Z, Bąbol-Pokora K … +3 more , Subocz E, Młynarski W, Janczar S
Semin Thromb Hemost · 2025 Nov · PMID 39805292 · Publisher ↗
22q11.2 deletion syndrome (22q11.2DS) is one of the most common congenital malformation syndromes resulting from disrupted embryonic development of pharyngeal pouches. The classical triad of symptoms described by Angelo...
22q11.2 deletion syndrome (22q11.2DS) is one of the most common congenital malformation syndromes resulting from disrupted embryonic development of pharyngeal pouches. The classical triad of symptoms described by Angelo DiGeorge is frequently accompanied by hematological and immune disorders. While it is well-established that patients with 22q11.2DS have an increased risk of recurrent autoimmune cytopenias, including immune thrombocytopenia, the platelet abnormalities in this population are more complex and multifaceted. Given this issue, we conducted a comprehensive literature review on platelet disorders in 22q11.2DS using accessible databases (PubMed and Scopus). We aimed to outline previous studies limitations and most urgent challenges concerning thrombocytopenia in these patients. One characteristic finding frequently observed in 22q11.2DS is mild macrothrombocytopenia caused presumably by the loss of one allele, encoding the element of the GPIb-IX-V complex. This structure plays a central role in thrombocyte adhesion, aggregation, and subsequent activation. Recent studies suggest that defective megakaryopoiesis and impaired vasculogenesis may strongly influence platelet and hemostasis disorders in 22q11.2DS. Furthermore, the phenotypic manifestation may be modulated by epigenetic factors and gene expression modifiers located outside the deletion region. Although the final hemorrhagic phenotype is typically mild, these patients may require more frequent transfusions following major surgical procedures. Despite the risk of thrombocytopenia and thrombocytopathy, there is a lack of large-scale research on hematological anomalies in 22q11.2DS, and the available results are often inconclusive. Given the complexity of hemostatic disorders, it is essential to establish specific recommendations for perioperative management and autoimmune cytopenias treatment within this population.
Venous Thromboembolism Occurrence and Association with Gastrointestinal Disorders in Children with Cystic Fibrosis: An Analysis from the TriNetX Research Network Global Multicenter Real-World Dataset.
Trocchia C, Ashour D, Mosha M … +4 more , Hamner B, Betensky M, Goldenberg N, Khalaf R
Semin Thromb Hemost · 2025 Oct · PMID 39805291 · Publisher ↗
The purpose of this study is to (1) estimate and compare the prevalence of venous thromboembolism (VTE) in children (age 0 to ≤21) with versus without cystic fibrosis (CF); (2) investigate putative associations between s...
The purpose of this study is to (1) estimate and compare the prevalence of venous thromboembolism (VTE) in children (age 0 to ≤21) with versus without cystic fibrosis (CF); (2) investigate putative associations between specific gastrointestinal (GI) manifestations and the development of VTE among children with CF. This was a multicenter case-control analysis among patients aged 0 to ≤ 21 years between 2010 and 2020, using the TriNetX Research Network. Data queries included ICD-9/10 (International Classification of Diseases-9th/10th Revision) diagnosis codes. Bivariate associations with VTE among CF patients were compared using Chi-square testing for categorical variables and Student's -test for continuous variables. We used multivariable logistic regression to test for independent associations of GI manifestations with VTE among children with CF, with adjustment for other salient covariates. There was a total of 7,689 children with and 22,327,660 without CF. The frequency of occurrence of VTE was increased nearly 20-fold among those with, as compared with without CF (130 vs. 7 per 10,000 patients). Acute pancreatitis (adjusted odd ratio [aOR] = 3.80, [95% confidence interval, CI: 2.00-7.22]), biliary disease (aOR = 2.17 [95% CI: 1.17-4.03]), gastrostomy status (aOR = 2.01 [95% CI: 1.27-3.18]), and malabsorption/malnutrition (aOR = 2.41 [95% CI: 1.52-3.82]) were each associated with a higher likelihood of VTE among children with CF. In conclusion, we found a significantly increased frequency of VTE occurrence and association of specific GI diseases as independent risk factors for VTE among children with CF compared with those without.
Recent Advances in Thrombosis and Hemostasis-Part XI.
Schulman S
Semin Thromb Hemost · 2025 Apr · PMID 39706222 · Publisher ↗
Abstract loading — click title to view on PubMed.
Recurrent Thromboembolism in Pediatric Congenital Heart Disease: Cumulative Incidence and Prognostic Factors.
Kiskaddon AL, Giglia TM, Betensky M … +9 more , Do NL, Witt DM, Stock AC, Amankwah EK, Fierstein JL, Ashour D, Ignjatovic V, Quintessenza JA, Goldenberg NA
Semin Thromb Hemost · 2025 Apr · PMID 39694044 · Publisher ↗
Congenital heart disease (CHD) is a risk factor for thromboembolism (TE). Data describing the rate of, and risk factors associated with, recurrent TE in children with CHD are limited. We prospectively evaluated TE recurr...
Congenital heart disease (CHD) is a risk factor for thromboembolism (TE). Data describing the rate of, and risk factors associated with, recurrent TE in children with CHD are limited. We prospectively evaluated TE recurrence risk in children with CHD and acute TE and investigated clinical risk factors associated with recurrent TE. Patients < 21 years of age with CHD and acute TE were enrolled in a single-institutional prospective inception cohort study (July 2013-April 2024). Descriptive statistics summarized variables including CHD and thrombus characteristics, antithrombotic regimens, bleeding, and recurrent TE. Multivariable logistic regression determined risk factors for recurrent TE. Among 40 children with CHD and acute TE, 13 (33%) developed ≥ 1 recurrent TE (arterial = 1 [6%], venous = 15 [83%], venous + arterial = 2 [11%]) at a median time of 86 (interquartile range, 45-112) days postdiagnosis of the index TE. One-year cumulative incidence of recurrent TE was 38%. Twelve (67%) recurrent TE events were central venous catheter (CVC)-related. In univariable analyses, immobility (46% vs. 7%, = 0.01), the presence of a CVC (69% vs. 30%, = 0.02), and lower extremity index venous TE (89% vs. 41%, = 0.04) were associated with TE recurrence. After adjustment for other potential risk factors via multivariable logistic regression, immobility (adjusted odds ratio [OR] 13.2, 95% confidence interval [CI] 1.16-151.3, = 0.04) and the presence of a CVC (adjusted OR 5.28, 95% CI 1.03-27.1, = 0.05) remained as independent risk factors for recurrent TE. The 1-year risk of TE recurrence was high among pediatric patients with CHD and acute TE. Immobility and the presence of CVC were independent risk factors for recurrent TE. Multicenter prospective cohort studies are warranted to substantiate and expand upon these important findings.
Hereditary Hemorrhagic Telangiectasia: On the Brink of a New Treatment Era?
Cerrone A, Buscarini E, Berté R … +5 more , Alicante S, Bertolazzi S, Moreschi O, Griffanti P, Manfredi G
Semin Thromb Hemost · 2025 Feb · PMID 39694043 · Publisher ↗
Hereditary hemorrhagic telangiectasia (HHT) is an inherited vascular disorder with highly variable penetrance, affecting up to 1 in 5,000 individuals. It is characterized by the presence of abnormal blood vessels that ca...
Hereditary hemorrhagic telangiectasia (HHT) is an inherited vascular disorder with highly variable penetrance, affecting up to 1 in 5,000 individuals. It is characterized by the presence of abnormal blood vessels that can lead to excessive bleeding-most frequently recurrent nosebleeds (epistaxis), skin and mucosal telangiectasias (small, dilated blood vessels), as well as arteriovenous malformations (AVMs) that can form in various organs, particularly the lungs, liver, and brain. HHT is caused by loss-of-function mutations in the BMP9-10/ENG/ALK1/SMAD4 signaling pathway, an important mediator of vascular quiescence. HHT possesses significant challenges for affected individuals, as the complications can range from mild to life-threatening events, depending on the severity and location of the vascular abnormalities. Despite this bleeding disorder being not uncommon, nowadays no specific treatment is as yet available for HHT and most current therapies include repurposed drugs. The aim of this review was to show therapeutic advances on the basis of recent promising clinical trials for HHT.
Comprehensive Mendelian Randomization Analysis of Smoking and Its Effects on Venous Thromboembolism.
Li Y, Tong L, Zhang Y … +2 more , Huang B, Zhu L
Semin Thromb Hemost · 2025 Apr · PMID 39689867 · Publisher ↗
An increasing number of Mendelian randomization (MR) studies have evaluated the causal link between smoking and venous thromboembolism (VTE). However, previous studies often rely on single genetic variants related to smo...
An increasing number of Mendelian randomization (MR) studies have evaluated the causal link between smoking and venous thromboembolism (VTE). However, previous studies often rely on single genetic variants related to smoking quantity and exhibit various other shortcomings, making them prone to pleiotropy and potentially leading to imprecise causal estimates. Thus, the deeper causal mechanisms remain largely unexplored. This MR study reassessed the causal relationship between smoking and VTE, including its subtypes-deep vein thrombosis (DVT) and pulmonary embolism (PE). Data on VTE were sourced from the FinnGen consortium with nonoverlapping sample sizes. The smoking phenotypes analyzed included smoking initiation, lifetime smoking, the number of cigarettes smoked per day by both current and former smokers (CigDay), and total pack-years of smoking in adulthood. The primary analytical method was inverse-variance-weighted (IVW), supplemented by multiple verification methods to ensure robust results. Statistical rigor was ensured through LDtrait pruning and Steiger filtering for reverse causation, with comprehensive sensitivity analyses including RadialMR confirming the findings' robustness. After Bonferroni correction, this study demonstrates significant causal evidence linking lifetime smoking with the incidence of VTE (odds ratio [OR] = 1.50, 95% confidence interval [CI] 1.21-1.85, = 1.75 × 10) and PE (OR = 1.69, 95% CI 1.25-2.28, = 6.55 × 10), and suggestive evidence with DVT, consistent in direction with previous studies but showing considerable differences in effect sizes and significance. Additionally, CigDay (past and current) increases the risks of VTE and DVT, while no causal link was found between smoking initiation and VTE or its subtypes ( < 0.05), both directly contradicting previous conclusions. Furthermore, our study is the first to suggest a causal link between pack-years and an increased risk of VTE. This MR study employed rigorous statistical pruning of its instrumental variables, using the most comprehensive smoking phenotype to date. It successfully mitigated biases such as winner's curse, yielding causal effect results distinct from previous studies.
The Overlooked Risk of Venous Thromboembolism in Psychiatric Patients: Epidemiology, Pathophysiology, and Implications for Clinical Care.
Jacob G, Ocytil Y, Brenner B
Semin Thromb Hemost · 2025 Jun · PMID 39672190 · Publisher ↗
Psychiatric patients face a significantly shorter life expectancy than the general population due to a complex interplay of medical, behavioral, and social factors. Venous thromboembolism (VTE), encompassing both pulmona...
Psychiatric patients face a significantly shorter life expectancy than the general population due to a complex interplay of medical, behavioral, and social factors. Venous thromboembolism (VTE), encompassing both pulmonary embolism and deep vein thrombosis, is an underrecognized yet critical contributor to morbidity and mortality in this population. Evidence suggests a two to three times higher prevalence of VTE in psychiatric patients compared to the general population, with incidence rates up to 4.5 per 1,000 person-years. This elevated risk is attributed to a hypercoagulable-hypofibrinolytic state. It is influenced by metabolic abnormalities, pro-inflammatory pathways, antipsychotic medications, and genetic factors. Health care biases and reduced treatment compliance further exacerbate the burden. This review explores the epidemiology, pathophysiology, and mechanistic underpinnings of VTE in psychiatric populations, emphasizing the role of metabolic syndrome and antipsychotic therapy. To mitigate mortality and enhance outcomes for these high-risk individuals, it is imperative to address this issue through improved risk stratification and preventive strategies.
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