Clinical and Applied Thrombosis/Hemostasis最新文献

This study investigates the prevalence and risk factors associated with venous thrombotic events in patients receiving (ECMO) support. Systematic review and meta-analysis of case-control and cohort studies. PubMed, Cochrane Library, Embase, CINAHL, Web of Science, Scopus, and ProQuest databases from inception through November 25, 2023.Case-control and cohort studies focusing on the prevalence and risk factors for venous thrombotic events in patients supported by ECMO. Identification of risk factors and calculation of incidence rates. Nineteen studies encompassing 10,767 participants were identified and included in the analysis. The pooled prevalence of venous thrombotic events among patients receiving ECMO support was 48% [95% confidence interval (CI) 0.37-0.60, I²= 97.18%]. Factors associated with increased incidence rates included longer duration of ECMO support (odds ratio [OR] 1.08, 95% CI 1.07-1.09, I²= 49%), abnormal anti-coagulation monitoring indicators (OR 1.02, 95% CI 1.00-1.04, I^2 =84%), and type of ECMO cannulation (OR 1.77, 95% CI 1.14-3.34, I²= 64%). The pooled prevalence of venous thrombotic events in patients with ECMO support is high. Increased risk is associated with extended duration of ECMO support, abnormal anti-coagulation monitoring, and specific types of ECMO cannulation.

Clinical trial registration number: NCT02950168, NCT02951039.

This study aims to identify risk factors for secondary venous thromboembolism (VTE) in stroke patients and establish a nomogram, an accurate predictor of probability of VTE occurrence during hospitalization in stroke patients. Medical Information Mart for Intensive Care IV (MIMIC-IV) database of critical care medicine was utilized to retrieve information of stroke patients admitted to the hospital between 2008 and 2019. Patients were randomly allocated into train set and test set at 7:3. Univariate and multivariate logistic regression analyses were used to identify independent risk factors for secondary VTE in stroke patients. A predictive nomogram model was constructed, and the predictive ability of the nomogram was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). This study included 266 stroke patients, with 26 patients suffering secondary VTE after stroke. A nomogram for predicting risk of secondary VTE in stroke patients was built according to pulmonary infection, partial thromboplastin time (PTT), log-formed D-dimer, and mean corpuscular hemoglobin (MCH). Area under the curve (AUC) of the predictive model nomogram was 0.880 and 0.878 in the train and test sets, respectively. The calibration curve was near the diagonal, and DCA curve presented positive net benefit. This indicates the model's good predictive performance and clinical utility. The nomogram effectively predicts the risk probability of secondary VTE in stroke patients, aiding clinicians in early identification and personalized treatment of stroke patients at risk of developing secondary VTE.

Objective: To investigate the relationship between C-reactive protein and albumin ratios (CAR) and all-cause and cardiovascular disease(CVD)-specific mortality in individuals with coronary heart disease(CHD).

Methods: The data from 1895 patients were extracted from the National Health and Nutrition Examination Survey (NHANES) database from 1999-2010. We used weighted COX regression analyses to explore the association between CAR, all-cause, and CVD-specific mortality. Restricted cubic spline(RCS) regression models and threshold effects analysis were used to analyze nonlinear relationships. Subgroup analyses were also performed to explore these relationships further.

Results: During a mean follow-up of 115.78 months, 61.48% of deaths occurred, and 21.85% were due to CVD. After adjusting for potential confounders, each 1-unit increase in CAR was associated with a 65% increase in all-cause mortality and a 67% increase in CVD-specific mortality. The RCS model revealed a non-linear association between CAR and the risk of all-cause mortality and CVD-specific mortality in CHD patients (all non-linear P < 0.001). Threshold effects analysis identified inflection points in regression models of all-cause mortality (0.04, P < 0.001) and CVD-specific mortality (0.05, P = 0.0024). The interaction tests found sex, smoking and diabetes influenced the association between CAR and all-cause mortality and sex, smoking and HF influenced its association with CVD-specific mortality (all P < 0.05).

Conclusion: There was a nonlinear association between CAR and all-cause mortality and CVD mortality in patients with CHD, with a higher hazard ratio before the inflection point. Sex, smoking, diabetes, and HF might have an effect on the associations between CAR and death risks.

Background: ICU patients have a high incidence of VTE. The American College of Chest Physicians antithrombotic practice guidelines recommend assessing the risk of VTE in all ICU patients. Although several VTE risk assessment tools exist to evaluate the risk factors among hospitalized patients, there is no validated tool specifically for assessing the risk of VTE in ICU patients.

Methods: A retrospective corhort study was conducted between June 2018 and October 2022. We obtained data from the electronic medical records of patients with a variety of diagnoses admitted to a mixed ICU. Multivariable logistic regression analysis was used to evaluate the independent risk factors of VTE. Receiver operating characteristic (ROC) curves were used to analyse the predictive accuracy of different tools.

Results: A total of 566 patients were included, and VTE occurred in 89 patients (15.7%), 62.9% was asymptomatic VTE. A prediction model (the ICU-VTE prediction model) was derived from the independent risk factors identified using multivariate analysis. The ICU-VTE prediction model included eight independent risk factors: history of VTE (3 points), immobilization ≥4 days (3 points), multiple trauma (3 points), age ≥70 years (2 points), platelet count >250 × 10³/μL (2 points), central venous catheterization (1 point), invasive mechanical ventilation (1 point), and respiratory failure or heart failure (1 point). Patients with a score of 0-4 points had a low (1.81%) risk of VTE. Patients were at intermediate risk, scoring 5-6 points, and the overall incidence of VTE in the intermediate-risk category was 17.1% (odds ratio [OR], 11.1; 95% confidence interval [CI], 4.2-29.4). Those with a score ≥7 points had a high (44.1%) risk of VTE (OR, 42.6; 95% CI, 16.4-110.3). The area under the curve (AUC) of the ICU-VTE prediction model was 0.838, and the differences in the AUCs were statistically significant between the ICU-VTE prediction model and the other three tools (ICU-VTE score, Z = 3.723, P < 0.001; Caprini risk assessment model, Z = 6.212, P < 0.001; Padua prediction score, Z = 7.120, P < 0.001).

Conclusions: We identified eight independent risk factors for acquired VTE among hospitalized patients in the ICU, deriving a new ICU-VTE risk assessment model. The model aims to predict asymptomatic VTE in ICU patients. The new model has higher predictive accuracy than the current tools. A prospective study is required for external validation of the tool and risk stratification in ICU patients.

Objective: This study aimed to investigate the associations between total serum bilirubin levels and the incidence of venous thromboembolism (VTE) among patients with influenza infection.

Methods: A retrospective cohort study was conducted among outpatients with laboratory-confirmed influenza using data from the Veterans Affairs Informatics and Computing Infrastructure (VINCI). Propensity score weighting was applied to balance study groups across baseline covariates. Cox proportional hazards models assessed VTE risk by total bilirubin levels, adjusting for important covariates including age, sex, race, comorbidity index, BMI, and smoking status.

Results: A total of 487 patients with total bilirubin levels <0.3 mg/dL, 8608 patients with levels between 0.3-1 mg/dL, and 1148 patients with levels >1 mg/dL were included. Patients with bilirubin <0.3 mg/dL exhibited a 6-fold higher risk of VTE compared to those with levels 0.3-1 mg/dL within 30 days of infection (HR = 6.2, 95% CI = 1.46-26.42). Elevated risks were noted through 90 days post infection (HR = 4.71, 95% CI = (1.42-15.67)).

Conclusions: Serum bilirubin levels, particularly below 0.3 mg/dL, were significantly associated with an increased risk of VTE among individuals with influenza. These findings suggest that lower bilirubin levels may contribute to heightened inflammatory responses and subsequent thromboembolic events in patients with influenza. The underlying mechanisms and potential therapeutic implications for VTE prevention among patients with acute respiratory infection warrants further consideration.

The study aims to evaluate the prognosis and risk factors of sepsis-associated thrombocytopenia (SAT) among patients with coagulopathy, and to provide evidence of the relationship between adverse outcomes and potential risks. Patients with sepsis-associated coagulopathy were included in the study from January 2014 to December 2022. The primary outcome was sepsis-associated thrombocytopenia (platelet count less than 100 *10⁹/L), which was evaluated by logistic regression models adjusted for demographic characteristics and comorbidities. Among patients in the SAT group, 54% developed severe SAT, while 16% of these patients recovered from thrombocytopenia. The in-hospital mortality rate was significantly higher in the SAT group compared to the non-SAT group (31% in SAT group vs 23.9% in non-SAT group, p = 0.029). Even after adjusting for age, gender, Charlson comorbidity, white blood cell, and Sequential Organ Failure Assessment score, the differences in mortality rate persisted (Odds Ratio 0.72, [95% Confidence Interval 0.52-0.92]). Correlation analyses revealed that prothrombin time (r = 0.08, p = 0.50), international normalized ratio (r = 0.08, p = 0.42), prothrombin activity (r = -0.06, p > 0.999), D-dimer (r = -0.02, p > 0.999), and inflammatory parameters such as C-reactive protein (r = -0.11, p = 0.37) were not significantly correlated with platelet counts. According to subgroup analyses, patients with lung infection complicated by SAT had slightly higher mortality (OR 0.66, [95% CI, 0.46 to 0.94]). Sepsis-associated coagulopathy indicates a subset of critical ill patients, with those experiencing thrombocytopenia at greater risk for in-hospital death compared to those without it.

Plasma-derived von Willebrand factor-containing factor VIII concentrates (pd-VWF/FVIII-C) are the mainstay of treatment in von Willebrand disease (VWD). Real-world data on efficacy and safety of these pd-VWF/FVIII-C are required. To retrospectively evaluate the efficacy and safety of pd-VWF/FVIII-C (Fanhdi® and Alphanate®, Grifols) in clinical practice in Italy. A multicentric, observational, retrospective study at 10 Italian centers was conducted. Eligible patients diagnosed with inherited VWD (ISTH criteria) were treated with either Fanhdi® or Alphanate® for bleeding episodes, prevention of surgical bleeding and secondary long-term prophylaxis (SLTP) according to clinical practice with medical records collected from January 2007 to December 2019. Efficacy/safety of pd-VWF/FVIII-C was assessed according to FDA-agreed objective criteria following regulatory procedures. Fifty-seven patients (M/F: 21/36) were enrolled in the study with the following VWD types: VWD1 (n = 29, 52%), VWD2A (n = 10, 18%), VWD2B (n = 7, 12%), VWD2M (n = 2, 4%), VWD2N (n = 1, 2%), VWD2 unclassified (n = 1, 2%), and VWD3 (n = 7, 12%). These pd-VWF/FVIII-C were used to manage 58 bleeding episodes (n = 24 patients), 100 surgeries (n = 47 patients), and 7 SLTP (n = 6 patients). Global clinical efficacy with these pd-VWF/FVIII-C was reported to be excellent/good in 85% of bleeding episodes, 98% of surgeries, and 100% of SLTP. As far as safety, no adverse-drug-related episodes, immunogenic or thrombotic events were reported. This study confirmed that Fanhdi® and Alphanate® were effective and safe in the management of bleeding episodes, the prevention of bleeding during surgeries and for SLTP in Italian patients with inherited VWD.

Introduction: Essential thrombocythemia (ET) involves the proliferation of megakaryocytes and platelets and is associated with an increased risk of thrombosis. We aimed to evaluate thrombotic risks in patients with epigenetic regulator mutations and generate a model to predict thrombosis in ET.

Materials and methods: This cohort study enrolled patients aged > 15 years diagnosed with ET at the Songklanakarind Hospital between January 2002 and December 2019. Twenty-five targeted gene mutations, including somatic driver mutations (JAK2, CALR, MPL), epigenetic regulator mutations (TET2, DNMT3A, IDH1, IDH2, TET2, ASXL1, EZH2, SF3B1, SRSF2) and other genes relevant to myeloid neoplasms, were identified using next-generation sequencing. Thrombotic events were confirmed based on clinical condition and imaging findings, and thrombotic risks were analyzed using five survival models with the recurrent event method.

Results: Ninety-six patients were enrolled with a median follow-up of 6.91 years. Of these, 15 patients experienced 17 arterial thrombotic events in total. Patients with JAK2 mutation and IDH1 mutation had the highest frequency of thrombotic events with somatic driver mutations (17.3%) and epigenetic regulator mutations (100%). The 10-year thrombosis-free survival rate was 81.3% (95% confidence interval: 72.0-91.8%). IDH1 mutation was a significant factor for thrombotic risk in the multivariate analysis for all models. The Prentice, William, and Peterson (PWP) gap-time model was the most appropriate prediction model.

Conclusions: The PWP gap-time model was a good predictive model for thrombotic risk in patients with ET. IDH1 mutation was significant risk factors for thrombosis; however, further studies with a larger sample size should confirm this and provide more insight.

Objective: DNA methylation, as an epigenetic alteration, plays an essential role in the development of atherosclerosis and venous thrombosis. E-cadherin, a tumor suppressor gene and adhesion molecule, has a crucial function in platelet aggregation and hemostasis. P16, a cell cycle regulator, is involved in venous thrombosis. The aim of this study is to evaluate the DNA methylation patterns and expression levels of the E-cadherin and P16 genes in venous thromboembolism (VTE).

Method: Peripheral blood samples were collected from 32 patients, including those with deep vein thrombosis (DVT, n = 15), pulmonary embolism (PE, n = 8), DVT with PE (n = 4), intestinal thrombosis (IT, n = 3), and cerebral venous sinus thrombosis (CVST, n = 2), as well as from 10 healthy individuals. The DNA methylation patterns and gene expression levels of E-cadherin and P16 were analyzed using methylation-specific PCR (MSP) and Real-Time PCR, respectively.

Results: The promoter of the CDH1 gene was partially methylated in 84.4% of thrombotic patients and unmethylated in 15.6% (P = 0.183). A significantly higher expression level of CDH1 was observed in the patients compared to the controls (P = 0.001). The P16 gene promoter were unmethylated in all control and patient specimens. Compared to normal subjects, the expression level of the P16 was significantly increased in patients (P = 0.000).

Conclusion: Our results indicated that DNA methylation is not the main gene expression regulatory mechanism for E-cadherin and P16 genes in thrombosis. Higher transcription levels of CDH1 and P16 in thrombotic patients may show their crucial roles in the pathogenesis of VTE.