BACKGROUND: Optimal antithrombotic management for patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) or coronary artery disease (CAD) remains chal...BACKGROUND: Optimal antithrombotic management for patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) or coronary artery disease (CAD) remains challenging because bleeding and ischemic risks compete. We compared five strategies: de-escalation (short-course dual therapy followed by DOAC monotherapy), VKA triple therapy, VKA dual therapy, DOAC dual therapy, and DOAC triple therapy. METHODS: We searched PubMed, Embase, Web of Science, Scopus, and CENTRAL from inception to 20 December 2025 for randomized controlled trials (RCTs). We performed a frequentist random-effects network meta-analysis (NMA) and reported risk ratios (RRs) with 95% confidence intervals (CIs). Treatments were ranked using P-scores. The primary outcomes were all-cause death and ISTH major or clinically relevant non-major bleeding. RESULTS: Seven RCTs (12,469 participants) were included. For International Society on Thrombosis and Haemostasis (ISTH) major or clinically relevant non-major bleeding (CRNMB), de-escalation reduced bleeding compared with DOAC dual therapy (RR 0.50; 95% CI 0.30-0.82); this estimate is informed by a single Japanese trial (OPTIMA-AF) and should be interpreted cautiously. In contrast, VKA dual therapy (RR 1.33; 95% CI 1.02-1.72) and VKA triple therapy (RR 1.42; 95% CI 1.21-1.66) increased bleeding risk versus DOAC dual therapy; DOAC triple therapy did not differ significantly. There were no significant differences in all-cause death, myocardial infarction, or stent thrombosis among strategies. However, VKA triple therapy increased intracranial hemorrhage (RR 2.95; 95% CI 1.32-6.56) and VKA dual therapy increased stroke (RR 2.72; 95% CI 1.15-6.45) compared with DOAC dual therapy. CONCLUSIONS: In AF patients undergoing PCI, a strategy of short-course dual therapy followed by DOAC monotherapy may reduce bleeding compared with DOAC dual therapy, but evidence is limited and derives from one randomized trial. VKA-based regimens-particularly VKA triple therapy-consistently increased bleeding and intracranial hemorrhage. For ischemic outcomes, event rates were low and confidence intervals were wide; therefore, findings should be interpreted as no statistically detectable differences rather than equivalence.
INTRODUCTION AND AIMS: von Willebrand factor (vWF) is a multimeric plasma glycoprotein synthesized by endothelial cells and megakaryocytes that has an essential role in the primary hemostasis, in fact, the high-molecular...INTRODUCTION AND AIMS: von Willebrand factor (vWF) is a multimeric plasma glycoprotein synthesized by endothelial cells and megakaryocytes that has an essential role in the primary hemostasis, in fact, the high-molecular-weight multimers (HMWMs) of vWF are the most effective in mediating platelet binding to the extracellular matrix. Acquired von Willebrand syndrome (AvWS) is a bleeding disorder characterized by the loss of HMWMs of vWF with consequent impaired vWF binding to platelets. Specific hemodynamic conditions of high vascular shear stress and immunologic diseases are linked to the development of this syndrome. Data on vWF function and its multimeric pattern in maintenance hemodialysis patients are scant and inconsistent. The aim of this study was to investigate the potential development of biochemical markers of AvWS and to preliminarily explore whether the reduction of HMWMs may be associated with an increased risk of bleeding. METHODS: Sodium citrate plasma was collected from 53 hemodialysis patients (HP) and 25 healthy control subjects (C). Plasma levels of von Willebrand factor Antigen (vWF:Ag) were measured, and vWF functional activity was assessed by evaluating its Ristocetin cofactor activity (vWF:Rcof). A vWF:Rcof/vWF:Ag ratio of <0.7 was considered indicative of dysfunctional vWF. von Willebrand Multimers were separated using sodium dodecyl sulfate (SDS)-agarose low-resolution gels and blotted onto a nitrocellulose membrane. Multimer separation was performed based on electrophoretic mobility. Multimers were detected immunologically using rabbit anti-human-vWF antibodies. Densitometric analysis of multimers and quantification of the percentage of different electrophoretic areas were performed using ImageJ software (NIH, USA). Acquired von Willebrand syndrome (AvWS) was diagnosed if the vWF:Rcof/vWF:Ag ratio was below the normal range (<0.7) and densitometric analysis revealed a reduction HMWMs in hemodialysis patients (HP) compared to controls (C). To quantitatively estimate HMWMs loss, a control-derived threshold was established based on the 5th percentile of the control population (9%). Bleeding events in hemodialysis patients were retrospectively collected from the initiation of dialysis and classified according to ISTH criteria. Corresponding HMWMs levels and vWFRcof/vWF:Ag ratio values were analyzed by means of binary logistic regression. Statistical analysis was performed using MedCalc software (MedCalc Software Ltd., Ostend, Belgium). The alpha value for statistical significance was set at 0.05. RESULTS: vWF:Ag levels were higher in HP compared to controls 169.3% (77.9-238.0) vs. 120.8% (82.3-141.6); p = 0.017. Hemodialysis patients (HP) exhibited also lower vWF:Rcof values to Controls, but this difference was not statistically significant 88.7% (30-148.2) vs. 105.2% (96.1-113.6); p = 0.167. The mean vWF:Rcof/vWF:Ag ratio was notably lower in HP than in controls 0.51 (0.38-0.70) vs. 0.88 (0.74-1.24); p < 0.0001, indicating a dysfunctional vWF profile in HP. vWF:Rcof/vWF:Ag ratio values were all above 0.7 in Controls. Densitometry analysis revealed a reduction in high molecular weight multimers, HMWMs 9.5% (3.1-14.1) vs. 12.5% (9.4-17.7); p = 0.016 and an increase in low molecular weight multimers (LMWMs) 49% (46.4-53.1) vs. 45.9% (38.7-49.2); p = 0.008 in HP compared to Controls. Among HP patients 47.2% exhibited HMWMs values below the control-derived cut-off. In contrast 8% of controls met this criterion; p < 0.001. Electrophoretic analysis confirmed a reduction in HMWMs and a greater representation of LMWMs in HP relative to Controls. In HP binary logistic regression showed that higher HMWMs levels were significantly associated with a reduced risk of bleeding OR = 0.71 [95% CI 0.57-0.89] p = 0.003, with a 29% decrease in bleeding odds per 1% increase in HMWMs. No significant association was observed between the vWF:Rcof/vWF:Ag ratio and bleeding risk. CONCLUSIONS: Among hemodialysis patients, our data confirm the presence of the biochemical markers of AvWS which involve dysfunctional plasma vWF, as indicated by the low vWF:RCo/vWF:Ag ratio. Loss of HMWMs, defined using a control-derived cut-off, was identified in 47.2% of hemodialysis patients, and exploratory binary logistic regression suggests that this condition may be associated with an increased bleeding risk. Larger and prospective studies are needed to validate HMWMs as a potential biomarker of bleeding risk in this population.
Sato T, Ogihara Y, Yamashita Y
… +31 more, Morimoto T, Muraoka N, Shioyama W, Chatani R, Shibata T, Nishimoto Y, Doi K, Oi M, Shiga T, Sueta D, Kim K, Tanabe Y, Koitabashi N, Takada T, Ikeda S, Nakagawa H, Tsukahara K, Shoji M, Sakamoto J, Hisatake S, Ogino Y, Fujita M, Nakanishi N, Dohke T, Hiramori S, Nawada R, Kaneda K, Ono K, Kimura T, Dohi K, ONCO PE Trial Investigators
Sheikh MM, Attar H, Book D
… +12 more, Corrao K, Cunningham A, Field JJ, Foy P, Harrington AM, Janssen J, Jung B, Kolinski J, Ledeboer N, McIntosh J, Singh S, Baumann Kreuziger L
BACKGROUND: Platelet hyperreactivity and in vivo platelet activation, effectors of increased cardiovascular risk, have been associated with both type 2 diabetes (T2DM) and obesity, however, whether T2DM and obesity when...BACKGROUND: Platelet hyperreactivity and in vivo platelet activation, effectors of increased cardiovascular risk, have been associated with both type 2 diabetes (T2DM) and obesity, however, whether T2DM and obesity when combined further enhance platelet activation has not been explored. MATERIALS AND METHODS: We assessed several parameters of platelet reactivity and in vivo platelet activation, VWF activity and adipokine levels in 40 well characterized obese subjects without T2DM (metabolically healthy obese, MHO), non obese T2DM patients (metabolically unhealthy normal weight, MUNW), obese and T2DM patients (metabolically unhealthy obese, MUO) and age and sex-matched healthy controls (metabolically healthy normal weight, MHNW). RESULTS: Both MUNW and MHO subjects showed enhanced platelet thrombus formation, increased response to collagen and ADP at light transmission aggregometry, raised urinary 11-dehydro-TxB, higher production of platelet reactive oxygen species and impaired platelet nitric oxide formation compared to MHNW, which were further significantly worsened in MUO. VWF activity and resistin levels were significantly higher in MUO patients compared to the other groups. CONCLUSIONS: Our data show that the concomitant presence of T2DM and obesity exert a significant additive effect on platelet hyperreactivity and in vivo platelet activation compared with only one of these risk factors, and suggest that enhanced VWF and resistin levels in MUO subjects play a pathogenic role in the modulation of the platelet response to stimuli leading to a strong platelet hyperreactivity and in vivo platelet activation, in turn favoring enhanced cardiovascular risk.
BACKGROUND: People living with post-pulmonary embolism syndrome (PPES) commonly experience persistent dyspnoea, fatigue, reduced exercise tolerance, anxiety, and fear of recurrence. When symptoms continue beyond three mo...BACKGROUND: People living with post-pulmonary embolism syndrome (PPES) commonly experience persistent dyspnoea, fatigue, reduced exercise tolerance, anxiety, and fear of recurrence. When symptoms continue beyond three months after effective anticoagulation, quality of life can be substantially impaired. Although healthy lifestyle behaviours may improve PPES symptoms, little is known about the barriers and facilitators influencing behaviour change from the perspective of those affected. AIM: To explore patients' perceived barriers and facilitators to adopting healthy lifestyle behaviours following PE, in order to inform the future development of rehabilitation interventions for people with PPES. METHODOLOGY: A purposive sample of adults with PPES took part in semi-structured interviews informed by the Theoretical Domains Framework (TDF) and the Capability, Opportunity, Motivation-Behaviour (COMB) model. Interviews were transcribed and analysed using a framework approach with inductive and deductive coding. Codes were grouped into categories and mapped to the 14 TDF domains and six COM-B constructs to identify behavioural influences and key barriers and facilitators. FINDINGS: Thirty-one participants (18 women, 13 men; aged 25-67 years) were interviewed. Ninety-eight codes were identified and organised into 35 categories, which were mapped to TDF and COM-B domains. The most frequently represented domains were Knowledge, Beliefs about Capabilities, Beliefs about Consequences, and Emotion. Key barriers and facilitators included pain, dyspnoea, healthcare professional knowledge and training, financial resources, and access to education and rehabilitation services. CONCLUSIONS: Engagement in healthy lifestyle behaviours after PE is shaped by interacting physical, emotional, socioeconomic, and environmental factors. These findings highlight the need for comprehensive, theory-informed rehabilitation strategies that address both individual and contextual influences on behaviour change in people with PPES.
Intermediate-high-risk pulmonary embolism (PE) is characterized by broad clinical, physiologic, and hemodynamic parameters, but its prognostic trajectory is poorly described by current risk stratification tools. New clin...Intermediate-high-risk pulmonary embolism (PE) is characterized by broad clinical, physiologic, and hemodynamic parameters, but its prognostic trajectory is poorly described by current risk stratification tools. New clinical scoring systems and echocardiographic indices have gained attention for their improved capacity to anticipate disease progression and predict clinical decompensation, particularly within the first 72 h or up to 7 days of diagnosis despite systemic anticoagulation. This growing evidence-base underscores the importance of clinical phenotype to determine the management approach, as well as early referral to specialized centers with access to pulmonary embolism response teams (PERTs) and the capacity to provide advanced reperfusion strategies, including systemic thrombolysis, catheter-directed therapy, surgical embolectomy, and mechanical circulatory support when indicated. This review provides a critical appraisal of the literature regarding the management of intermediate-high-risk PE, highlighting prognostic factors, phenotype-driven therapeutic approaches, emerging biomarkers, and existing gaps in evidence, to gain perspective on the spectrum of clinical trajectories for such patients.
Antiphospholipid syndrome (APS) is an acquired coagulation disorder with an unclear pathogenesis, diagnosed in the presence of thrombotic events, obstetric complications, or non-thrombotic manifestations, alongside persi...Antiphospholipid syndrome (APS) is an acquired coagulation disorder with an unclear pathogenesis, diagnosed in the presence of thrombotic events, obstetric complications, or non-thrombotic manifestations, alongside persistently detectable antiphospholipid antibodies. aPLs seroconversion, defined as the transition from persistent antibody positivity to sustained antibody negativity, is typically confirmed by at least two negative tests ≥12 weeks apart and maintained for over one year. This phenomenon is distinct from seronegative APS (SNAPS), in which patients present with APS-like clinical features but never fulfill laboratory criteria. Thrombotic risk remains significant in APS, particularly in patients with prior events or persistently elevated aPLs titers. Immunomodulatory therapies, such as hydroxychloroquine, rituximab, eculizumab, sirolimus, or other agents, may reduce antibody levels and contribute to improved outcomes, though evidence is limited. Among these, hydroxychloroquine is the most established agent, particularly in refractory or recurrent thrombotic cases, and is recommended as adjunctive therapy alongside anticoagulation in high-risk thrombotic and obstetric APS. While these therapies may allow cautious adjustments in anticoagulation for low-risk patients, anticoagulants should not be discontinued solely based on seroconversion or adjunctive treatment. Overall, immunomodulatory drugs should be considered strictly as adjuncts, with patient selection guided by clinical phenotype, thrombotic risk, and available evidence.
Anticoagulation use is common in persons with cancer (PWC) due to a high prevalence of venous thromboembolism (VTE) and atrial fibrillation (AF). These PWC often require central venous catheters (CVC) for administration...Anticoagulation use is common in persons with cancer (PWC) due to a high prevalence of venous thromboembolism (VTE) and atrial fibrillation (AF). These PWC often require central venous catheters (CVC) for administration of chemotherapy, intravenous fluids, and blood products however the ideal peri-procedural anticoagulation management strategy for tunneled and port CVC insertion is unknown. Peri-procedural anticoagulation interruption is the de facto standard of care strategy for general procedures in the general population, however may not apply to tunneled and port CVC insertion in PWC as these are specialized low risk radiologically guided procedures but conducted in a high risk population. Alternatively, peri-procedural anticoagulation continuation, as conducted in the procedurally similar cardiac device insertion may be the strategy of choice given its simplicity and potentially equal or lower risk of complications. Improper peri-procedural anticoagulation management may expose PWC to bleeding and thrombotic risks, with the risks higher in those on anticoagulation for VTE compared to those on anticoagulation for AF. Despite the limited data available, guidelines regarding non-tunneled CVC insertion are consistent, endorsing peri-procedural anticoagulation continuation. Guidelines regarding peri-procedural anticoagulation for tunneled and port CVC insertion however are conflicting, with some endorsing interruption, and others continuation. With the incidence of cancer, thrombosis, and CVC use increasing, peri-procedural anticoagulation management for CVC insertion is expected to continue to become more frequent over time. High-quality data regarding peri-procedural anticoagulation management for tunneled and port CVC insertion in PWC are needed to standardize practice, streamline care, and mitigate complications in this high-risk population.
PURPOSE: To study COVID-19-associated coagulopathy and the clinical outcomes across different COVID-19 pandemic waves. METHODS: We retrospectively analyzed n 344 patients hospitalized for acute COVID-19 to Padova Univers...PURPOSE: To study COVID-19-associated coagulopathy and the clinical outcomes across different COVID-19 pandemic waves. METHODS: We retrospectively analyzed n 344 patients hospitalized for acute COVID-19 to Padova University Hospital between March 2020-March 2023, grouped by variants: Wild-type (G1, n 155; March 2020-January 2021), Alpha (G2, n 79; February-May 2021), Delta (G3, n 50; May-December 2021), and Omicron (G4, n 60; December 2021-March 2023). We compared traditional coagulation tests, thromboelastometry and impedance aggregometry. Clinical outcomes were also considered. RESULTS: Factor VIII decreased progressively from G1 (195%, IQR 149-227) to G4 (156%, IQR 128-197; p < 0.05), as did von Willebrand factor (343%, IQR 244-407 to 235%, IQR 216-247; p < 0.05). Thromboelastometry showed a significantly and progressively: i) prolonged INTEM and EXTEM clot formation time (p < 0.05 in all comparisons); ii) reduced INTEM, EXTEM and FIBTEM maximum clot firmness (p < 0.05 in all comparisons). Platelet aggregation significantly decreased from G1 to G4 (p < 0.05 in all comparisons). VTE occurred in 18.1% of G1 and 19.0% of G2 patients vs. 6.0% and 6.7% in G3 and G4, respectively (p < 0.05 in all comparisons). The 28-day mortality was 15.5% in G1 and 15.2% in G2 vs. 4.0% and 1.7% in G3 and G4, respectively (p < 0.05 in all comparisons). CONCLUSIONS: We observed a significant and progressive decrease in hypercoagulability across the four COVID-19 variants. A parallel decline in VTE incidence and 28-day mortality was also observed. Larger studies are needed to ascertain the pathophysiological mechanisms underlying the changes in coagulative profiles and their clinical implications.
INTRODUCTION: Patients with traumatic spinal injuries face a high risk of venous thromboembolism (VTE); however, the optimal timing of VTE prophylaxis to most effectively reduce VTE rates remains unclear. This study aims...INTRODUCTION: Patients with traumatic spinal injuries face a high risk of venous thromboembolism (VTE); however, the optimal timing of VTE prophylaxis to most effectively reduce VTE rates remains unclear. This study aims to assess the association between thromboprophylaxis timing and clinical outcomes in patients with traumatic spinal injuries. METHODS: This retrospective cohort study used the ACS-TQIP database (2017-2023) to evaluate the timing of VTE prophylaxis in adult trauma patients (≥18 years) with isolated acute spinal cord injuries (SCI). Patients were stratified by prophylaxis type, management strategy, and spinal injury area. The primary outcomes were the odds of deep vein thrombosis (DVT) and pulmonary embolism (PE). Secondary outcomes included in-hospital mortality, complication rates, transfusion requirements, and ICU length of stay (ICU-LOS). RESULTS: Among severe spinal trauma patients, very early prophylaxis was associated with significant reductions in the odds of DVT (aOR: 0.387, p < 0.001, SE = 0.159) and PE (aOR: 0.342, p < 0.001, SE = 0.249) without increasing mortality or other complications. In patients undergoing operative management, only very early prophylaxis was associated with decreased odds of VTE (DVT: aOR: 0.506, p = 0.016, SE: 0.283; PE: aOR: 0.271, p = 0.035, SE: 0.620). CONCLUSION: Very early VTE prophylaxis resulted in a significant reduction in VTE rates without increasing adverse outcomes in patients with severe spinal trauma, regardless of spinal region, management strategy, and prophylaxis type.
BACKGROUND: Sepsis-induced coagulopathy (SIC) is a life-threatening complication characterized by high heterogeneity and mortality. Current prognostic models relying solely on clinical indices often fail to capture compl...BACKGROUND: Sepsis-induced coagulopathy (SIC) is a life-threatening complication characterized by high heterogeneity and mortality. Current prognostic models relying solely on clinical indices often fail to capture complex molecular pathophysiology, limiting precise risk stratification. This study aimed to unveil the molecular landscape of SIC via multi-omics integration and develop a robust machine learning (ML) predictive model. METHODS: We conducted a comprehensive study of 878 SIC patients. A discovery cohort of 626 patients underwent blood transcriptomic profiling (RNA-seq) and a subset of 214 patients was analyzed for proteomic validation. Weighted Gene Co-expression Network Analysis (WGCNA) and Gene Set Enrichment Analysis (GSEA) were used to identify survival-associated modules and pathways. An ensemble ML framework was developed to integrate the clinical features with transcriptomic signatures for survival prediction. RESULTS: Clinical analysis identified age, lung infection, higher SOFA scores, and lactate levels as significant independent risk factors for mortality. Transcriptomic profiling revealed that elevated expression of GABARAPL1, PHLPP1, and KLF6 was strongly associated with an increased risk of death, whereas elevated expression of genes, including TSN, NUP155, and TTC39C, was associated with better outcomes. Functionally, GSEA enrichment analysis revealed the suppression of oxidative phosphorylation and ribosome biogenesis along with the activation of hypoxia, heme metabolism, and inflammatory pathways in non-survivors. Proteomic analyses validated the mechanistic findings. The integrated ensemble machine learning survival model (Clinical + Transcriptomics) achieved a C-index of 0.735, which significantly outperformed the clinical-only model (C-index: 0.694). Stratification based on the model successfully distinguished high-risk patients with significantly lower survival rates (p = 0.00057). CONCLUSION: Our multi-omics analysis highlights metabolic reprogramming, hypoxia, and dysregulated heme metabolism as the key molecular features of SIC. The developed ensemble ML model, which integrates molecular and clinical features, offers a superior tool for early risk stratification and precision management of septic coagulopathy.
The pathological hypercoagulable state and associated risk of thrombosis in colorectal cancer (CRC) persist throughout the disease course. Accurate identification of patients at high risk of venous thromboembolism (VTE)...The pathological hypercoagulable state and associated risk of thrombosis in colorectal cancer (CRC) persist throughout the disease course. Accurate identification of patients at high risk of venous thromboembolism (VTE) and judiciously applying drug or mechanical prevention measures can significantly reduce the incidence of VTE. The review details a range of biomarkers, including platelet count, soluble P-selectin, D-dimer, and vascular endothelial growth factor (VEGF), which have been shown to correlate with increased VTE risk in CRC patients. In addition to the biomarker analysis, the review makes important recommendations for the routine monitoring of these biomarkers in CRC patients, especially those at higher risk for VTE. Furthermore, it discusses the integration of these biomarkers into clinical VTE risk prediction models, advocating for personalized and targeted thromboprophylaxis strategies. The review also explores future research directions, emphasizing the potential of antiplatelet and anticoagulant therapies in improving the prognosis of CRC patients by reducing thromboembolic events. This narrative review not only deepens our understanding of the molecular mechanisms driving cancer-associated thrombosis but also paves the way for novel therapeutic interventions aimed at preventing VTE in CRC patients.
BACKGROUND: Congenital fibrinogen deficiency is a rare inherited coagulation disorder characterized by partial or total lack of plasma fibrinogen (hypo- or afibrinogenemia), or expression of dysfunctional fibrinogen (dys...BACKGROUND: Congenital fibrinogen deficiency is a rare inherited coagulation disorder characterized by partial or total lack of plasma fibrinogen (hypo- or afibrinogenemia), or expression of dysfunctional fibrinogen (dysfibrinogenemia), which may cause plasma level reduction (hypodysfibrinogenemia). Loss of functional fibrinogen causes bleeding disposition. In case of trauma or surgical intervention, supplementation of human fibrinogen is required to stop or prevent extensive bleeding events. STUDY DESIGN: A prospective, open-label, uncontrolled, multi-center phase I/III trial was performed to investigate pharmacokinetics, efficacy and safety of single and/or repetitive intravenous infusions of a human fibrinogen concentrate (BT524) for on-demand prophylaxis (ODP) and/or on-demand treatment (ODT) of bleeding events in patients with congenital fibrinogen deficiency. PATIENTS: In the phase III part of the trial reported here, 36 patients (3 children <6 years, 9 children 6-12 years, 4 adolescents and 20 adults) were treated with BT524 for 175 bleeding events, either for ODP or ODT. RESULTS: Fibrinogen concentrate infusion substantially improved maximum clot firmness (MCF). The overall hemostatic response was rated as good or excellent in 98.9% of bleedings. Loss of blood was considered normal in the majority of surgical interventions, and wound healing was also positively assessed. Additional evaluations, including blood product consumption and adverse events, further supported the efficacy and confirmed the favorable safety profile of the novel fibrinogen product. CONCLUSION: BT524 represents a novel human fibrinogen concentrate provenly efficacious and safe both for the treatment of bleeding and for peri-operative bleeding prophylaxis in patients with congenital fibrinogen deficiency of all ages.
Essential Thrombocythemia (ET) is a myeloproliferative neoplasm driven by JAK2V617F, CALR, and MPL mutations, characterized by persistent thrombocytosis and hypercoagulability. Cerebral Venous Sinus Thrombosis (CVST) rep...Essential Thrombocythemia (ET) is a myeloproliferative neoplasm driven by JAK2V617F, CALR, and MPL mutations, characterized by persistent thrombocytosis and hypercoagulability. Cerebral Venous Sinus Thrombosis (CVST) represents a severe complication of ET, yet the underlying mechanisms remain unclear. Genetically, the JAK2V617F mutation activates the JAK-STAT pathway, inducing platelet hyperactivation, neutrophil extracellular trap formation, and the release of platelet-derived microparticles, which alter blood rheology and promote thrombosis. Mutations in CALR and MPL accelerate megakaryopoiesis, while erythrocyte dysfunction exacerbates hyperviscosity. Anatomical variations in the cerebral venous sinuses synergize with these abnormalities to create a prothrombotic microenvironment. Diagnostically, MRI/MRV is the first choice, with the primary challenge being the differentiation of venous sinus hypoplasia from thrombosis in ET patients, combined with the detection of the JAK2 mutation for confirmation. This review summarizes the genetic and cellular mechanisms linking ET to CVST, discusses tailored diagnostic strategies and therapies (JAK inhibitors, anticoagulants), and highlights the need for further research to clarify the interplay between molecular abnormalities and vascular factors, aiming to optimize clinical management.