The retrieval of an inferior vena cava (IVC) filter is essential for preventing complications related to the filter. Surgically induced suture fixation is an extremely rare cause of filter entrapment and presents unique technical challenges. This case describes a balloon-assisted radial release within the filter frame followed by snare retrieval to successfully address this condition. We report a rare case of successful retrieval of a surgically suture-fixed inferior vena cava filter via femoral venous access using a balloon-assisted radial release technique combined with snare retrieval, which has not been previously reported. An endovascular strategy of “release first, then retrieval” was adopted. Sequential balloon dilations were performed to achieve controlled radial expansion and mechanical release at the fixation site. Following controlled strut fracture and resolution of the external constraint, the filter was completely retrieved using a snare technique under large-sheath protection. The balloon-assisted radial release technique may provide a minimally invasive solution for the retrieval of inferior vena cava filters fixed by surgical sutures.
Direct oral anticoagulants (DOACs) are widely used for treating venous thromboembolism (VTE). However, uncertainty remains regarding their use among individuals diagnosed with sickle cell disease (SCD), as this population was primarily excluded from pivotal trials establishing DOAC safety and therapeutic success. We evaluated the clinical utility and safety profile of DOACs in patients with SCD. PubMed, Scopus, and the Cochrane Library were searched without language restrictions. Quantitative synthesis was carried out utilizing MetaXL and Review Manager version 5.4. Primary outcomes of interest were the clinical success and safety profile of DOAC therapy for individuals with SCD. Odds ratios (ORs) were used as measures of effect, and statistical variance was evaluated via the I-squared metric, where values exceeding 50
Vascular calcification and coagulation disorders are highly prevalent in patients with chronic renal failure (CRF); however, whether a causal relationship between these two exist is not clear. This study investigated the role of the coagulation factor von Willebrand factor (vWF) in the pathogenesis of vascular calcification in CRF. RNA sequencing was used to detect changes in gene expression involved in coagulation cascades in human umbilical vascular endothelial cells (HUVECs) treated with Na2HPO4 and NaH2PO4, reaching a final total phosphate concentration of 3 mM. A rat model of vascular calcification was generated by feeding rats a diet containing 0.5
Acquired hemophilia A (AHA) is a rare autoimmune bleeding disorder caused by neutralizing autoantibodies against coagulation factor VIII (FVIII). It usually develops in older adults or during the postpartum period and often presents with new extensive subcutaneous, soft-tissue, muscular, mucosal, or internal bleeding in a person without a previous bleeding history. Diagnostic delay and treatment-related infection remain important causes of avoidable morbidity and mortality. This narrative review integrates international recommendations, registry data, prospective studies, and contemporary real-world evidence published through June 2026. A structured diagnostic pathway begins with recognition of an isolated prolonged activated partial thromboplastin time, exclusion of anticoagulant and pre-analytical effects, an immediate and incubated mixing study, measurement of FVIII activity, and confirmation of a FVIII inhibitor. Acute clinically significant bleeding requires prompt treatment with recombinant activated factor VII, activated prothrombin complex concentrate, or recombinant porcine FVIII; drug selection should reflect bleeding site, thrombosis risk, access, and monitoring capacity. Emicizumab, a subcutaneous bispecific FVIIIa-mimetic antibody, has emerged as effective bleed-prevention therapy while inhibitor eradication is pending. Prospective and real-world studies show substantial reductions in recurrent bleeding and may permit de-escalation or temporary postponement of intensive immunosuppression in selected frail patients. Nevertheless, emicizumab is not an acute rescue agent and does not eradicate the inhibitor. Immunosuppressive therapy therefore remains necessary for immunological remission in most patients, but its intensity should be individualized according to FVIII activity, inhibitor titer, frailty, infection, malignancy, and competing treatment risks. Laboratory monitoring during emicizumab exposure requires assay-specific planning. Modern AHA care should integrate rapid hemostatic control, early bleed prevention, and risk-adapted inhibitor eradication rather than applying a uniform treatment sequence. Clear laboratory communication, explicit definitions of remission, and coordinated follow-up at an experienced hemophilia center are essential to reduce both bleeding-related and treatment-related harm.
Sepsis-associated disseminated intravascular coagulation (DIC) is a severe and rapidly progressive complication that markedly increases mortality. Because DIC lacks specific clinical manifestations in its early stage and conventional coagulation parameters show only limited changes at disease onset, early prediction in clinical practice remains challenging. Inflammatory responses, infectious burden, and aberrant activation of the complement system are recognized as key pathological mechanisms underlying coagulation imbalance in sepsis. However, the potential value of multidimensional combined indicators for the early prediction of DIC has not been fully elucidated. In this retrospective cohort study, 133 adult patients with Sepsis-3–defined sepsis were enrolled and classified into DIC (n = 47) and non-DIC (n = 86) groups according to ISTH criteria. Admission clinical data, inflammatory markers (CRP, PCT, IL-6), and complement components (C3, C4) were collected. Logistic regression, ROC curve analysis, and decision curve analysis (DCA) were used to assess predictive performance, with internal validation of the combined model performed by bootstrap resampling. Patients in the DIC group had significantly higher SOFA scores and 28-day mortality than those in the non-DIC group (p < 0.001). Serum levels of PCT and IL-6 were markedly elevated in the DIC group, whereas complement components C3 and C4 were significantly reduced (p < 0.001). Multivariable analysis identified IL-6, PCT, C3, and C4 as independent predictors of DIC (p < 0.05). The combined model incorporating all four biomarkers achieved an AUC of 0.915 (95
Ischemic stroke is increasingly understood not as a purely thromboembolic event but as a thromboinflammatory disease in which innate immune and hemostatic pathways interact. Neutrophil extracellular traps (NETs) have emerged as potentially important mediators and biomarkers within this broader immunothrombotic network. Experimental studies provide mechanistic evidence that NETs can stabilize thrombi, impair fibrinolysis, obstruct the microcirculation, and promote neurovascular injury, whereas human studies predominantly demonstrate associations between NET burden, reperfusion difficulty, and adverse clinical outcomes. This review critically synthesizes mechanistic, translational, observational, and emerging interventional evidence linking NETs to ischemic stroke. We distinguish established experimental mechanisms from human associations, place NETs within reciprocal interactions involving platelets, endothelial cells, monocytes/macrophages, complement, coagulation, and inflammatory mediators, and examine current controversies and barriers to therapeutic translation. We further consider DNase-mediated NET degradation, PAD4 inhibition, biomarker-guided patient selection, high-resolution multiomic and spatial technologies, and imaging-based thrombus characterization. This evidence-calibrated framework identifies where NET biology is most strongly supported and where causal and clinical uncertainty remains.
Argatroban and bivalirudin may interfere with routine coagulation and antithrombin assays through direct thrombin inhibition. However, the magnitude of interference differs across analytical platforms owing to distinct assay principles and reagent formulations. This study aimed to characterize the specific impacts of argatroban and bivalirudin on results of routine coagulation and antithrombin tests on three widely utilized coagulation analytical platforms. Pooled normal human plasma was spiked with clinically relevant concentrations of argatroban (0–2.0 µg/mL) or bivalirudin (0–20 mg/L). Antithrombin (AT) activity, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), and Clauss fibrinogen (FIB) were measured simultaneously on all three analytical platforms. Corresponding antigen concentrations of AT and ClaussFIB were quantified via immunoturbidimetric assays to discriminate analytical interference from genuine biological alterations. On Stago and Sysmex platforms, AT activity increased concentration‑dependently with both DTIs, whereas no significant change was observed on Werfen. Fibrinogen levels decreased markedly with argatroban only on Werfen, and with bivalirudin across all three platforms. PT, APTT, and TT were prolonged dose‑dependently on all platforms, though TT frequently exceeded the detection limit at low DTI concentrations. Inter‑platform agreement assessed by intraclass correlation coefficients was poor to moderate for most parameters. Antigen levels remained unchanged, confirming that the observed discrepancies were due to analytical interference. Argatroban and bivalirudin produce significant platform-dependent interference in coagulation testing, particularly in thrombin-based fibrinogen and AT activity assays. Such interference may lead to falsely decreased fibrinogen activity and falsely elevated AT activity. Platform-specific validation and confirmatory testing are essential for accurate interpretation of coagulation results during direct thrombin inhibitor therapy.
Atrial fibrillation (AF) is a leading cause of cardioembolic ischemic stroke, accounting for approximately 20–30
Abstract Background Acidosis is common in critically ill patients and is associated with coagulopathy. The impact of different acids on coagulation remains poorly understood. Hydrochloric acid has often been used without critical evaluation. We aimed to investigate the influence of different acids and their concentrations on rotational thromboelastometry (ROTEM). Methods In this observational study ten, blood samples were treated with hydrochloric acid (HCl), lactic acid (C₃H₆O₃), phosphoric acid (H₃PO₄), or dihydrogen phosphate (H₂PO₄⁻) to achieve defined pH levels (7.2–6.9). Respiratory acidosis was simulated by incubation in a 20% CO₂ atmosphere. Five additional samples were exposed to varying acid concentrations. Samples were analyzed using the ROTEM EXTEM assay. Clotting time (CT), clot formation time (CFT), α-angle, maximum clot firmness (MCF), and maximum lysis (ML) were assessed. Results All acids exhibited concentration-dependent effects on EXTEM parameters. HCl caused significant reductions in MCF and prolonged CFT, indicating impaired clot firmness and propagation. C 3 H 6 O 3 induced moderate changes, with elevated fibrinolysis at intermediate concentrations. H₃PO₄ reduced MCF and increased ML, while H₂PO₄⁻ primarily delayed clotting initiation and markedly inhibited fibrinolysis. CO₂-induced acidosis (pH ≈ 7.1) led to reduced fibrinolytic activity without affecting CT or MCF. Across acid types, increasing acidity consistently impaired clotting dynamics. Conclusion The type of acid inducing acidosis was associated with distinct alterations in ROTEM parameters in vitro. The choice of acid should be carefully considered in experimental models and taken into account when interpreting data. Whether such effects occur in vivo remains uncertain.
Vancomycin-induced immune thrombocytopenia (VIIT) is a rare but potentially life-threatening adverse drug reaction characterized by profound platelet destruction. Diagnosis is challenging in critically ill patients, and optimal management beyond drug cessation remains poorly defined. A 54-year-old female admitted to the ICU for severe community-acquired pneumonia developed profound, refractory thrombocytopenia 12 days after the initiation of vancomycin. Blood, sputum, and pleural fluid cultures were negative. Vancomycin was continued due to the severity of the pneumonia, a fluctuating clinical course with recurrent fevers and progressive infiltrates, a complicated parapneumonic effusion requiring drainage and surgical consultation, and infectious disease service recommendations. The patient presented with gross hematuria and a rapid decline in platelet count to 6,000/µL. Following the exclusion of alternative etiologies—including sepsis-associated coagulopathy and heparin-induced thrombocytopenia (HIT)—vancomycin was discontinued. The patient required intravenous immunoglobulin (IVIG) and corticosteroids in addition to drug cessation to achieve platelet recovery. This case underscores the critical importance of early recognition of VIIT. Our literature review reveals that while discontinuation of the offending agent is the cornerstone of therapy, severe cases (platelets < 20,000/µL) often require adjunctive immunomodulatory treatment. VIIT should remain a primary differential diagnosis in patients presenting with unexplained thrombocytopenia during vancomycin therapy.
Venous thromboembolism (VTE) carries substantial global morbidity and mortality, with 50
The incidence of deep venous thrombosis (DVT) is higher for severe pneumonia patients hospitalized in respiratory intensive care unit (RICU). Currently, no validated risk assessment tool specifically exists for evaluating DVT risk in this population. This study aimed to develop a screening tool to estimate the risk of in-hospital DVT in patients with severe pneumonia admitted to the RICU. In this retrospective cohort study, least absolute shrinkage and selection operator (LASSO) regression was used to identify candidate predictors of in-hospital DVT. We then developed two prediction models, a support vector machine (SVM) algorithm and a nomogram model, to predict DVT risk in patients with severe pneumonia in the RICU. We included 368 patients with severe pneumonia admitted to the RICU. DVT occurred in 124 patients (33.7
Motoric cognitive risk syndrome (MCR), defined by subjective cognitive complaints and slow gait in individuals without dementia, is a clinically relevant pre-dementia phenotype. Platelets are increasingly linked to inflammation, endothelial dysfunction, and neurovascular signaling, but the prospective association between platelet count and MCR remains unclear. To examine whether baseline platelet count is associated with incident MCR among older Chinese adults. We analyzed 2,246 participants aged 60 years or older from the China Health and Retirement Longitudinal Study who were free of MCR at baseline in 2011 and had platelet count and follow-up MCR data in 2013. Platelet count was modeled as a continuous variable per 100 × 10⁹/L increase and by quintiles, with the middle quintile as the reference. Multivariable logistic regression models were adjusted for sociodemographic characteristics, lifestyle factors, adiposity indicators, depressive symptoms, and major chronic diseases. Restricted cubic spline analysis was used to evaluate the dose-response pattern. Subgroup analyses and a sensitivity analysis excluding participants with baseline stroke were also conducted. During the 2-year follow-up, 264 participants (11.8
Peripherally inserted central catheter (PICC)-related thrombosis (CRT) is a critical complication in cancer patients. However, the impact of vascular morphological parameters on the risk of this complication remains poorly understood. This study aimed to identify independent risk factors associated with vascular morphology and develop a nomogram for predicting CRT. Cancer patients who underwent placement of a PICC at a tertiary hospital between 2021 and 2023 were retrospectively identified. Vascular parameters (vessel depth, vessel diameter, arm circumference) and procedural factors (cannulation/attempts, catheter tip position) were assessed by ultrasonography. Independent risk factors for CRT were identified by multivariate logistic regression and Cox proportional hazards models. A nomogram was constructed using the rms package in R. Discrimination was evaluated via the area under the curve and calibration by the Hosmer–Lemeshow goodness-of-fit test. A PICC was placed in 2,183 cancer patients during the study period. CRT occurred in 102 (4.7
Abstract In recent years, establishing multidisciplinary pulmonary embolism response teams (PERTs/EXPERT-PE) has become more prevalent. A survey was conducted to assess the availability and structure of PERTs in German and European hospitals. A survey was circulated among German hospital centers with cardiovascular expertise to obtain data on their current PE treatment approaches, the existence and features of PERTs, their activation methods, and their structural organization. Additionally, data regarding PE treatment priority relative to acute coronary syndrome and the availability of outpatient PE follow-up programs was gathered. Results were compared with those of European PE reference centers. Overall, 65 hospitals participated at this German survey with most PERTs available at university hospitals (63%), especially in West (63%) and Southern (62%). Although 61.5% of the German centers handle over 40 PE cases annually, only 52.3% of those hospitals already implemented a PERT, which is low in comparison to a European Survey among PE reference centers (80.8%). In 86% cases, PERT is led by Cardiology, followed by Angiology (6.9%), Pulmonology (4.6%), and Critical Care Medicine (2.3%). Regarding advanced treatment the majority of hospitals performed catheter-directed thrombolysis (72.2%) and catheter-based thrombectomy/aspiration (74.1%). A follow-up program for patients with PE is considerable higher in European reference centers opposed to German hospitals. This survey demonstrated that among large German cardiovascular centers PERTs are markedly less often present compared to European PE reference centers. Additionally, in German centers, PE follow-up programs are not widely implemented. This emphasizes the pressing need for awareness campaigns for acute and chronic PE.
The relationship between obstructive sleep apnea syndrome (OSAS) and pulmonary embolism (PE) remains inadequately characterized, and prospective data obtained with objective sleep testing in confirmed PE patients are scarce. We aimed to determine the prevalence of OSAS in patients with radiologically confirmed PE and to compare clinical, laboratory, and polysomnographic features according to OSAS status. In this single-center prospective observational study, 45 patients with confirmed PE (thoracic computed tomography pulmonary angiography or ventilation/perfusion scintigraphy) underwent portable polysomnography (WatchPAT 200®) within two weeks of diagnosis. OSAS was defined as an apnea–hypopnea index (AHI) ≥ 5 events/hour. Group comparisons used the Mann–Whitney U test and chi-square or Fisher’s exact test; associations with AHI were assessed by Spearman’s rank correlation. OSAS was identified in 31 patients (68.9
Persistent inflammation, immunosuppression, and catabolism syndrome (PIICS) is a post-critical illness characterized by sustained inflammation, immune suppression, and hypercatabolism, the mechanisms of which remain unclear. Coagulopathy, which frequently accompanies critical illness, has been suggested to be associated with PIICS; however, few studies have directly investigated this relationship. We hypothesized that the timing of onset of disseminated intravascular coagulation (DIC), a representative form of coagulopathy, is associated with the development of PIICS and aimed to clarify their relationship. This study included 100 patients admitted to the intensive care unit (ICU) for ≥ 15 days. PIICS was defined as meeting at least two of the following: elevated C-reactive protein (CRP) level, decreased serum albumin (Alb) level, and decreased lymphocyte count. The primary outcome was the association between the timing of DIC and PIICS development. For each ICU day (days 1–15), risk ratios (RRs) for PIICS were calculated using 2 × 2 contingency tables comparing DIC-positive and DIC-negative patients, and statistical significance was assessed using Fisher’s exact test. Multivariable logistic regression analysis was performed to estimate adjusted associations with PIICS development. Statistical analyses were performed via R software. Variables for logistic regression were selected based on previous literature and clinical relevance, with significance level set at p < 0.05. From approximately day 8 onward, the RR of PIICS in patients with DIC showed an increasing trend. In multivariable analysis, age, cumulative CRP level, and cumulative SOFA score were independently associated with PIICS development. The logistic regression model demonstrated good discrimination (AUC of 0.80). DIC occurring after approximately day 8 of ICU admission may be associated with an increased risk of PIICS development. These findings suggest that persistent coagulopathy during the middle phase of ICU stay may contribute to the pathogenesis of PIICS.
Atherosclerosis is the main pathological basis of cardiovascular events. Urinary 11-dehydrothromboxane B 2 (11-dhTXB2), as a stable metabolite of Thromboxane (TX) A2, may reflect platelet activity and plaque stability, but its mechanism is not clear. A total of 160 patients with atherosclerosis were enrolled in this study. The correlation between urinary 11-dhTXB2 level and plaque morphology and inflammation index was detected. The effects of 11-dhTXB2 on macrophage polarization and endothelial barrier function were investigated by THP-1 macrophage and HUVEC co-culture model and ApoE−/− mouse model, and the intervention effects of curcumin and aspirin were evaluated. High levels of urinary 11-dhTXB2 were significantly associated with thinner fibrous cap and increased inflammatory markers, especially in diabetic patients with atherosclerosis and aspirin resistance. Cell experiments showed that activation of the TXA2 pathway (as indicated by elevated urinary 11-dhTXB2) promoted macrophage M1 polarization and impaired endothelial connexin expression. The combination of curcumin and aspirin can synergistically reduce urinary 11-dhTXB2, reduce plaque area and improve plaque stability. Notably, urinary 11-dhTXB2 serves as a stable metabolite reflecting in vivo TXA2 production and platelet activation, but is not itself a functional ligand acting on macrophages or endothelial cells. Urinary 11-dhTXB2 can be used as a dynamic monitoring biomarker for the risk of atherosclerotic thrombosis. Elevated TXA2 pathway activity aggravates plaque instability by promoting inflammation and endothelial dysfunction. Curcumin combined with aspirin has the potential for synergistic intervention and provides a new strategy for individualized prevention and treatment. Not applicable.
Portal vein thrombosis (PVT) is a rare but clinically significant condition often associated with myeloproliferative neoplasms (MPNs). Diagnosing MPNs in acute PVT may be difficult, particularly in the absence of overt hematologic abnormalities. We retrospectively analyzed 93 patients with acute PVT from January 2009 to June 2024, excluding those with chronic thrombosis or previously established systemic diseases. MPNs were identified in 23 patients (24.7
Clinical practice guidelines of venous thromboembolism prophylaxis for acutely ill hospitalized medical patients recommend intermittent pneumatic compression (IPC) devices as a mechanical thromboprophylaxis option for those at high risk for bleeding. However, supporting evidence focusing on this patient population is limited. This case–cohort study used a university hospital–based retrospective cohort to assess the association between IPC use and lower-extremity deep vein thrombosis (DVT) development within 30 days of admission among inpatients in Japan. The parental cohort included 3876 consecutive acutely ill patients aged 15 years and older admitted to a general internal medicine department between July 2016 and July 2021. Weighted multivariable survival models and analyses that additionally accounted for time-varying covariate effects and competing risks were employed. In total, 52 patients who developed lower-extremity DVT within 30 days (9/52 [17
