Thrombosis Journal最新文献

Background: Rapid diagnosis and treatment of deep vein thrombosis (DVT) reduce morbidity and mortality.

Objective: This study aimed to investigate the time to diagnostic imaging, time to treatment, and outcomes associated with the delayed treatment of DVT.

Methods: We retrospectively investigated 110 patients who were diagnosed with proximal DVT in outpatient clinics in a single academic centre in Thailand from January 2019 to September 2020. We recorded demographic data, clinical presentations, time to diagnostic imaging (ultrasound of the legs), and time to treatment. We recorded outcomes, including death, pulmonary embolism (PE), recurrent DVT, and thrombus resolution 3 months after the diagnosis of DVT.

Results: Of all 110 patients, 42 (38.2%) were male. Median age (IQR) was 68.5 (58-80) years. The median (IQR) time to diagnostic imaging was 7 days (2-27). The median (IQR) interval from the first OPD visit to the initiation of treatment was 14 days (3-31). The delayed diagnosis (more than 7 days from the first clinic visit to diagnostic imaging) was observed in 54 (49%) patients with DVT. The delay in treatment (more than 7 days from the first clinic visit to treatment) was observed in 67 (60.9%) patients. The maximum time to treatment was 160 days. Death and PE occurred in 9% and 33% of patients with delayed treatment, while they occurred in 5% and 20% of those with early treatment, respectively. No recurrent DVT was observed. Among 25 patients who had follow-up imaging, residual thrombus occurred in 71% of patients with delayed treatment and 63% of those with early treatment.

Conclusion: Half of the DVT patients had delays in diagnosis and treatment of proximal DVT. The routine request option was associated with a delayed diagnosis. The importance of early diagnosis and treatment of DVT should be raised among physicians, and improvement strategies are warranted.

Background: Cerebrovascular disease (CVD) remains a leading cause of death in the United States. Although the role of conventional stroke risk factors is well established, the impact of coagulation disorders-both inherited and acquired-on long-term CVD mortality remains underexplored.

Methods: We conducted a cross-sectional analysis using U.S. death certificate data from the CDC WONDER platform (1999-2020). Adults aged ≥ 25 years with CVD as the underlying cause and any coagulation disorder listed as a contributing cause were included. Age-adjusted mortality rates (AAMRs) were calculated per 100,000 population. Joinpoint regression was used to evaluate temporal trends, estimating Annual Percent Change (APC) and Average Annual Percent Change (AAPC) across subgroups.

Results: Between 1999 and 2020, 54,545 CVD-related deaths occurred among adults with coagulation disorders. The overall AAMR was 1.16, with a significant decline over time (AAPC: - 0.58%, 95% CI: - 0.87 to - 0.28; p = 0.0010). Males had higher mortality than females (1.35 vs. 1.01), but females showed greater declines (AAPC: - 0.96% vs. - 0.32%). Black and American Indian individuals experienced the highest rates but also the steepest improvements (AAPCs: - 1.87% and - 2.02%, respectively). In contrast, Hispanic populations showed early declines followed by recent increases. Only the Northeast region had a statistically significant mortality reduction. Rural residents and those in the South had stagnant trends. Mortality rose sharply with age, peaking in adults ≥ 85 years, although older groups also showed significant declines. Most deaths (77%) occurred in inpatient settings.

Conclusions: Although overall CVD mortality declined modestly, widening disparities by sex, race, region, and age group signal critical gaps in prevention and care.

Bleeding diathesis' diagnosis can be challenging due to the high number of disorders with hemorrhagic symptomatology. Sitosterolemia is a rare disease characterized by increased sterols plasma levels and cardiovascular, cutaneous, articular, and hematological manifestations, including anemia and macrothrombocytopenia. The disorder is caused by ABCG5 and ABCG8 mutations.We present a case of a patient with bleeding diathesis, macrothrombocytopenia, a moderate defect of primary hemostasis and a pathological platelet aggregation analysis, with an initial diagnosis of Bernard-Soulier variant syndrome. After performing a genetic study using an exome analysis, the patient had two ABCG8 gen variants, one pathogenic (NP_071882.1:p.Trp536Ter (NM_022437.2:c.1608G > A) variant, ClinVar ID: 499930) and the other one probably pathogenic (NP_071882.1:p.Leu465Arg (NM_022437.2:c.1394T > G) variant), changing the diagnosis to sitosterolemia, which has its own therapeutic approach.This case report shows the importance of the genetic analysis. Sitosterolemia should be suspected in the presence of macrothrombocytopenia, stomatocytes in the blood smear and hemolytic anemia, performing a genetic study including ABCG5 and ABCG8 gene variants.

Background: Angiogenesis inhibitors are vital in cancer treatment but are increasingly linked to thromboembolic events (TEEs), impacting patient outcomes. Despite extensive clinical trials, real-world data on TEEs associated with these agents remain limited. This study examines real-world TEEs patterns using the FDA Adverse Event Reporting System (FAERS).

Method: A retrospective pharmacovigilance analysis was conducted using FAERS data spanning from 2014 to 2024. Reporting odds ratio (ROR) and Bayesian confidence propagation neural network (BCPNN) was applied to identify significant safety signals. A signal was considered present when the lower limit of the 95% confidence interval for ROR (ROR025) > 1 and that for information component (IC025) > 0, with a minimum requirement of three or more reported cases.

Results: A total of 13,897 TEEs were identified, with 34.9% classified as arterial thromboembolism events (ATEs), 26.5% as venous thromboembolism events (VTEs), and 38.6% as TEEs of unknown origin (other TEEs). Our findings indicate a significant correlation between the use of angiogenesis inhibitors and an increased reporting frequency of TEEs. The disproportionality analysis revealed strong signals for several agents, with the top five drugs being cediranib, aflibercept, ramucirumab, cabozantinib, and sunitinib. The median time-to-onset (TTO) was 32 days (IQR: 6-141), with 48.5% of cases occurring within the first month and 12% persisting beyond one year. Temporal analysis demonstrated a declining incidence pattern, confirmed by Weibull distribution (shape parameter β = 0.63, indicating early failure type). The most frequently reported outcomes of TEEs associated with angiogenesis inhibitors were hospitalization and other serious events.

Conclusion: This study provides a real-world assessment of TEES risk associated with angiogenesis inhibitors. Identifying high-risk agents and temporal patterns underscores the need for early monitoring and highlights their contribution to TEEs in clinical practice.

Background: Majority of people with "kissing carotids", an anatomical variation of the cervical carotid arteries showing tortuosity, kinking or coiling and coming in proximity at the midline are asymptomatic. Less than 1% of the general population have Protein S Deficiency. This report discusses a rare case of a young female with co-existent Protein S deficiency and kissing carotids, who presented with sequential thrombosis in both arterial and venous cerebral circulation systems and further discusses potential mechanisms of arterial thrombosis in Protein S deficiency and medical options for secondary stroke prophylaxis in this context.

Case presentation: A 29-year-old female presented with sudden left hemiparesis and dysarthria. Index Brain MRI revealed acute non-haemorrhagic infarcts in the right middle cerebral artery (MCA) territory. Index brain MRA of cerebral vessels revealed abrupt cut off of the right MCA M1 segment following arterial thrombosis with extracranial kissing internal carotid arteries. Interval imaging of her brain and cerebral vasculature on day 4 of admission following a convulsion revealed left transverse cerebral venous sinus thrombosis. Laboratory workup confirmed low Protein S activity of only 18% (normal 55-123). She was started on rivaroxaban for lifelong secondary arterial stroke prophylaxis.

Conclusions: This is an index sub-Saharan case report of a young female with co-existent Protein S deficiency and kissing carotids phenomenon presenting with sequential cerebral arterial and venous thromboses. Potential mechanisms of arterial thrombosis in Protein S deficiency in which case warfarin may not be a preferred singular option for secondary arterial stroke prophylaxis are discussed.

Objective: This study aims to investigate the effects of gardenia extract (GE) on coagulation function in a rat model of acute myocardial ischemia (AMI).

Methods: Healthy male SD rats were randomly divided into five groups: Sham, AMI, GE-L (low-dose GE), GE-M (medium-dose GE), and GE-H (high-dose GE). Two weeks later, echocardiography was performed to assess cardiac function, including left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD), and left ventricular end-systolic diameter (LVESD). Hematoxylin-eosin (HE) staining and TUNEL staining were implemented to observe myocardial pathological changes and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) was employed to measure serum levels of inflammatory factors and oxidative stress markers. Coagulation function was evaluated using an automatic coagulation analyzer, with parameters including prothrombin time (PT), thrombin time (TT), prothrombin time ratio (PTR), international normalized ratio (INR), and fibrinogen level (FIB).

Results: Compared with the Sham group, the AMI group exhibited myocardial injury, coagulation dysfunction, impaired cardiac function, and significantly increased levels of inflammation, oxidative stress, and PTR. In contrast, all GE dose groups showed elevated TT, PT, FIB, and INR compared to the AMI group.

Conclusion: GE can reverse the cardiac function, inflammatory and oxidative stress indicators, as well as coagulation function in AMI model rats, thereby improving AMI.

Background: While anti-Xa assays are increasingly used to monitor rivaroxaban therapy, evidence supporting specific thresholds for bleeding risk remains limited.

Objective: To determine predictive thresholds of peak and trough anti-Xa levels for bleeding complications in patients with nonvalvular atrial fibrillation (NVAF) receiving rivaroxaban.

Methods: In this prospective multicenter cohort study conducted at four tertiary care hospitals in Damascus, Syria, we enrolled 70 NVAF patients receiving rivaroxaban (20 mg/day; 15 mg/day if eGFR < 50 mL/min). Anti-Xa levels were measured at peak (1-3 h post-dose) and trough (pre-dose). Patients were followed for 6 months for bleeding events.

Results: Twenty-five patients (35.7%) experienced bleeding (8 major, 17 minor). Bleeding patients demonstrated significantly higher anti-Xa levels (peak: 399 ± 78 vs. 206 ± 67 ng/mL, p < 0.0001; trough: 41 ± 14 vs. 20 ± 10 ng/mL, p < 0.0001). ROC analysis identified optimal predictive thresholds of 298 ng/mL for peak levels (AUC = 0.985, sensitivity 89.5%, specificity 93.3%) and 27.5 ng/mL for trough levels (AUC = 0.887, sensitivity 86.4%, specificity 76.3%).

Conclusion: Anti-Xa levels strongly predict bleeding risk in rivaroxaban-treated NVAF patients. The identified thresholds may guide clinical decision-making regarding dose adjustment, particularly in high-risk patients. However, it is important to acknowledge limitations, including the modest sample size and the exclusion of patients on antiplatelet therapy, which may affect generalizability.

Background: Venous thromboembolism (VTE), which includes Pulmonary embolism (PE) and Deep vein thrombosis (DVT), is a complex vascular disorder with poorly understood pathological mechanisms. Emerging research highlights the potential involvement of immune cells in the pathogenesis of VTE, although their causal relationship remains unproven.

Methods: To systematically assess the causal relationships between 731 immune phenotypic traits and VTE, PE, and DVT, this study employed a bidirectional, two-sample Mendelian randomization (MR) approach. In the forward MR analysis, immune cell characteristics were treated as the exposure, while VTE, DVT, and PE were the outcomes. In the reverse MR analysis, VTE, DVT, and PE were considered exposures, with immune cell characteristics as the outcomes. To ensure the robustness, heterogeneity, and control for potential confounding factors in the study results, we performed a sensitivity analysis. Furthermore, we applied the False discovery rate (FDR) method to account for statistical bias arising from multiple comparisons.

Results: After FDR correction, we identified potential causal associations between four immune cell types and VTE, six types and PE, and three types and DVT.

Conclusion: This study demonstrates that specific immune cell types are causally linked to VTE, DVT, and PE, providing valuable insights for future clinical research.