Journal of Thrombosis and Thrombolysis最新文献

In this review, we aimed to evaluate Sonothrombolysis when combined with primary percutaneous coronary intervention (pPCI) in STEMI patients with regard to improving cardiac function and clinical outcomes. This study primarily assesses short-term efficacy outcomes, while long-term impacts, such as mortality, were not evaluated. Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we searched four electronic databases (PubMed, Scopus, Cochrane Library, and Web of Science) to identify eligible studies reported up to November 2024. Four studies, with a total population of 252 participants, were included. The sonothrombolysis group demonstrated an overall greater improvement in left ventricular ejection fraction compared to the control group (MD = 3.07, 95% CI [1.20 to 4.94], p = 0.001), with no heterogeneity (p = 0.44, I² = 0%). When subgrouped according to the follow-up period, there was no significant difference between the two groups (MD = 2.56, 95% CI [-0.35 to 5.46]) after 2 to 6 months. Infarction size, microvascular obstruction, left ventricular end-diastolic volume, and left ventricular end-systolic volume showed no statistically significant difference between the two groups. Sonothrombolysis following pPCI is associated with better left ventricular ejection fraction, emphasizing the potential role of sonothrombolysis as an adjunctive therapy to pPCI in the management of STEMI.

Hereditary thrombophilia testing is frequently ordered after venous thromboembolism (VTE), despite little evidence of clinical utility and most guidelines cautioning against testing. We conducted a retrospective, observational study of inpatient hereditary thrombophilia testing ordered during a hospital admission for acute VTE between 2019 and 2024. We aimed to characterize patterns of testing results, and costs, and to evaluate whether younger patients and those with unprovoked VTE were more likely to test positive for hereditary thrombophilia. A total of 835 hereditary thrombophilia tests - including those for factor V Leiden, prothrombin_G20210A, deficiencies of protein S, protein C, and antithrombin, hyperhomocysteinemia, and plasminogen activator inhibitor-1 excess - were ordered in 220 patients. Overall, 19.6% of results were abnormal, and 45.0% of patients had at least one abnormal result. There was no difference in the rate of positive results among patients with provoked vs. unprovoked VTE (30.7% vs. 34.5%, p = .554) nor patients < 50 vs. ≥ 50 years of age (33.1% vs. 32.4%, p = .912). Only 4/99 (4.0%) patients with an abnormal result had their clinical management clearly changed due to the result. The tests totaled $385,161 USD in institutional charges and $26,029 USD in Medicare fees. Inpatient hereditary thrombophilia testing during admission for acute VTE is low yield, with frequent abnormal results, many of which likely represented false positives, and minimal impact on clinical management with high costs.

To investigate the prevalence of FV Hong Kong(p.Arg306Gly) variant in patients with thrombotic disorders in South China, and to explore the association between FV Hong Kong and thrombosis according to genotype and clinical manifestations of the patients. A total of 367 patients with thrombotic disorders and 555 healthy volunteers in South China were screened by exon sequencing to identify FV Hong Kong variant carriers. Acquired risk factors for thrombosis of all subjects were also recorded. Among 367 thrombosis patients, 10 (2.72%) carried heterozygous FV Hong Kong mutations. In contrast, 9 of 555 healthy controls (1.62%) harbored the heterozygous mutation. There is no significant differences in the prevalence rate between patients and healthy controls. Among patients with the FV Hong Kong mutation, 90% exhibited concurrent predisposing factors. The FV Hong Kong variant demonstrates a high prevalence in the South Chinese population, with a similar rate in thrombosis patients and healthy population. The variant, when co-occurring with genetic or acquired risk factors, may synergistically elevate thrombotic risk. Further investigations are warranted to elucidate the clinical implications in thrombotic disorders.

Optimal systolic blood pressure (SBP) targets after endovascular therapy (EVT) for stroke in older adults (≥ 65 years) remain undefined. This study assessed age-stratified associations between early post-EVT SBP (first 6 h) and outcomes. Post hoc analysis of two trials. Patients were stratified by age (18-64 vs. ≥ 65 years) and SBP (≤ 120, 120-140, > 140 mmHg). Primary outcome was 90-day functional status (modified Rankin Scale, mRS). Inverse probability treatment weighting (IPTW) and multivariable regression adjusted for confounders. Post-EVT SBP data were available for 267 young and 395 old patients. IPTW analysis revealed that sustained SBP below 120 mmHg during the first 6 h post-EVT significantly enhanced functional independence in elderly patients (common OR: 2.00; 95% CI: 1.18-3.39). Among young cohorts, maintenance of SBP ≤ 120 mmHg (cOR, 2.89; 95% CI, 1.45-5.82) and 120-140 mmHg (cOR, 3.18; 95% CI, 1.58-6.47) were associated with a better outcome. sICH incidence demonstrated no statistically significant association with systolic blood pressure (SBP) levels (P = 0.21; 95% CI: 0.93-1.35). During the initial 6-h window post-EVT, younger patients with SBP ≤ 140 mmHg and elderly patients with SBP ≤ 120 mmHg were associated with favorable outcome. These results suggest that stricter blood pressure control may be particularly beneficial for older adults in the early post-EVT phase.Trial Registration: The DEVT registration: URL: http://www.chictr.org.cn ; Chinese Clinical Trial Registry: ChiCTR-IOR-17013568, and the RESCUE BT registration: URL: http://www.chictr.org.cn ; ChiCTR-INR-17014167.

Protein carbonylation (PC), a marker of oxidative stress, was shown to be elevated in both hyperthyroid and hypothyroid disorders. These conditions are associated with unfavorable fibrin clot properties. We sought to investigate whether elevated PC is associated with prothrombotic markers in hyperthyroid and hypothyroid individuals before and following effective therapy. We studied 31 hyperthyroid, 29 hypothyroid patients, and 29 sex- and age-matched controls. Along with plasma total PC content, we measured fibrin clot properties (fibrin clot permeability, K_s; clot lysis time, CLT), fibrinolysis proteins, and thrombin generation before and after 3-month successful therapy. Hyperthyroid patients had a tendency to higher PC (+ 9.1%; p = 0.05), while hypothyroid individuals had 17.2% higher PC (p = 0.01) compared with controls, without any difference between the patient groups. Pre-treatment PC inversely correlated with K_s in both hyper- (R=-0.425, p = 0.017) and hypothyroid (R=-0.510, p = 0.005) individuals, while solely in hyperthyroid patients PC was associated with CLT (R = 0.556, p = 0.001), but not with fibrinolysis inhibitors, or other hemostatic markers. On-treatment PC, which decreased by 19.6% (p < 0.001) in hyperthyroid and by 23.4% (p < 0.001) in hypothyroid patients reaching the control levels, was associated with K_s (R=-0.401, p = 0.031) and CLT (R = 0.537, p = 0.003) only in the hypothyroid group. In hyper- and hypothyroid patients elevated PC may contribute to formation of more compact fibrin clot networks with impaired fibrinolysis in the former group. Reduced PC following thyroid hormone normalization maintained its impact on fibrin clot properties solely in hypothyroid patients, which indicates complex effects of oxidative stress on blood coagulation.

During the alpha wave of SARS-CoV-2 (SCA), the number of ICU-hospitalized COVID-19 patients was high. In a dynamic co-evolution, the virulence of the virus changed during the Omicron wave (SCO). Initial findings of COVID-19 indicate that infection with SARS-CoV-2 leads to endothelial dysfunction through inflammatory pathways, oxidative stress, and alterations in vascular homeostasis. Upregulation of adhesion molecules (ICAM-1 and VCAM-1) in response to pro-inflammatory cytokines helps immune cell migration and vascular inflammation. Furthermore, oxidative stress disrupts the balance between the oxidant and antioxidant systems. Excessive NOX2 activity promotes ROS production and Nrf2 suppression, leading to endothelial dysfunction. Also, alterations in vascular homeostasis and increased vWF secretion heightens the risk of thrombosis, while dysregulated iNOS contributes to further endothelial damage. Considering that endothelial cell dysfunction can promote various disease processes, including thrombosis and atherosclerosis, this study evaluates the main changes in the host lung endothelium in COVID-19 during this co-evolution. The direct effects of SCA and SCO on endothelial function were investigated in bronchoalveolar lavage fluid (BALF) samples obtained from leftover specimens of COVID-19 patients, which were compared to the control group. In the BALF samples of patients, key endothelial molecules involved in immune cell recruitment, such as iNOS, Nrf2, NOX2, vWF, ICAM-1, and VCAM-1, were evaluated using RT-qPCR and Western blotting. In severe COVID-19, ICAM-1 and VCAM-1 were upregulated compared to the control group. Furthermore, vWF expression was also upregulated. A significant increase in iNOS gene expression was observed during the Omicron wave. Although NOX2 expression increased during the SCA and SCO waves, Nrf2 expression was downregulated in both SARS-CoV-2 waves. Overall, during the co-evolution of the virus and host, disruption of endothelial cell function can affect selective immune cell recruitment and, in the late phase, lead to local vascular dysfunction and severe outcomes such as hospitalization. Targeting key endothelial molecules for therapy can not only alter immune cell recruitment but also prevent endothelial dysfunction throughout the body.

Optimal lead-in duration of apixaban following a period of therapeutic parenteral anticoagulation for venous thromboembolism (VTE) has become controversial, and truncated lead-in periods accounting for parenteral therapy have been proposed in recent studies. Results from previous studies cannot be generalized to many subpopulations of interest, including patients with obesity. This study characterized recurrent VTE in patients with obesity within 6 months of apixaban initiation based on full versus truncated lead-in times following parenteral anticoagulation. This single-center, multi-site, retrospective cohort study within the West Virginia University Medicine enterprise among adult patients with obesity, defined as body mass index (BMI) of 30 kg/m² or greater, diagnosed with VTE who received apixaban following at least 48 h of parenteral anticoagulation. Truncated lead-ins were uncommon (10%). There were no significant differences in recurrent thrombosis between full and truncated lead-in cohorts [10 (4.5%) vs. 2 (8.0%); p = 0.771]. The truncated lead-in cohort was associated with longer length of stay and extended duration of parenteral anticoagulation. A truncated lead-in strategy may be reasonable for patients with obesity. Larger studies should be conducted to identify patient factors that support the use of a truncated lead-in strategy. 1) Previous studies investigating truncated lead-in times cannot be generalized to subpopulations of interest such as patients with obesity 2)Safety and efficacy outcomes are variable among the general population within previous studies 3) In clinical practice, truncated lead-in regimens are chosen for patients with longer durations of parenteral anticoagulation 4)Recurrent thrombosis rates within subpopulations who are at higher of thrombosis requires further evaluation regarding the truncated lead-in.

Tyrosine kinase inhibitors (TKIs) have revolutionised cancer therapy, significantly impacting survival and outcomes by targeting specific signalling pathways that are necessary for tumour survival. Despite their clinical efficacy, TKIs exhibit a complex toxicity profile. Many of the signalling pathways that are targeted by TKIs are shared with normal homeostatic processes, including those responsible for modulating thrombosis and bleeding. The risk profile of thrombosis and bleeding associated with TKIs varies considerably across agents. Multi-kinase inhibitors, particularly those targeting the breakpoint cluster regio-abelson murine leukaemia 1 gene mutation (BCR-ABL) (i.e., nilotinib and ponatinib), significantly elevate arterial thrombotic events. This thrombosis risk is driven by endothelial dysfunction, accelerated atherosclerosis, platelet hyper-reactivity, and impaired fibrinolysis. Similarly, vascular endothelial growth factor (VEGF) pathway inhibition contributes markedly to thrombotic vascular complications by reducing vasodilators like nitric oxide and promoting pro-thrombotic endothelial environments. TKIs targeting the VEGF receptor (VEGFR-TKIs) (i.e., sunitinib and regorafenib) and brutons tyrosine kinase (BTK) inhibitors (i.e., ibrutinib), increase bleeding risk through platelet dysfunction, thrombocytopenia, and interactions affecting coagulation pathways. Optimal management of these medications encompasses careful baseline cardiovascular and bleeding risk assessments, proactive modification of modifiable risk factors, and vigilant patient monitoring. Prophylactic antithrombotic therapy necessitates cautious individualised evaluation and comprehensive patient monitoring strategies. TKIs exemplify the advancements in precision oncology but necessitate nuanced management of their complex vascular toxicities. A multidisciplinary cardio-oncology approach involving detailed patient education, robust risk stratification, and collaborative clinical management is essential. Future research should aim to clarify TKI-specific haemostatic mechanisms and develop predictive biomarkers, enabling tailored therapeutic strategies to optimise clinical outcomes and reduce adverse events..