Journal of Thrombosis and Thrombolysis最新文献

Thromboembolic events (TE) cause significant morbidity and mortality in SLE patients. Comprehensive data on various types of thromboembolic events and their variation by gender, region, and hospital status are scant. To analyze the epidemiology, morbidity, mortality, and risk factors (e.g., obesity, smoking) of thromboembolic events in SLE. Data from the NIS (2003-2018) were analyzed using ICD-9 and ICD-10 codes to identify patients diagnosed with SLE. SAS-9.4 was used for data analysis. TE variables include DVT, PE, Cerebral venous sinus thrombosis (CVST), Splanchnic thrombosis (ST), and Arterial Thrombosis (AT). Among 513,904 SLE patients, PE, DVT, ST, CVST, and AT were identified in 7,070 (1.38%), 15,800 (3.07%), 6,868 (1.34%), 197 (0.04%), and 1,821 (0.35%) patients, respectively. The prevalence of PE, DVT, ST, and AT is higher in males with SLE. African Americans (29.55% of the cohort) demonstrated a higher prevalence of PE (2,188, 1.6%) and DVT (5,208, 3.46%). The prevalence of obesity was higher in SLE patients with all thrombotic events, except in AT, which had a significantly lower prevalence. A significantly higher all-cause in-hospital mortality, longer LOS, and cost of stay were seen in SLE with thrombotic events (except CVST). Arterial, venous, and atypical thrombosis exert significant morbidity and mortality in patients with SLE. The disparities in thrombotic events within the SLE population underscore the importance of targeted interventions to reduce substantial morbidity and healthcare expenditures.

Post-thrombotic syndrome (PTS) is the most frequent and disabling complication of deep vein thrombosis (DVT). Several studies have evaluated whether direct oral anticoagulants (DOACs) or vitamin K antagonists (VKAs) may reduce the PTS risk over time. Data on patients with inherited thrombophilias (IT) remains scarce. To assess the long-term incidence and severity of PTS in a population of IT patients with proximal DVT of the lower extremity treated with DOACs vs. VKAs. Cases were consecutive IT patients prospectively diagnosed with a first DVT episode at Padova University Hospital, Italy between January 2014 and December 2021, and treated with DOACs. Controls were consecutive IT patients diagnosed with DVT between January 2004 and December 2019, and treated with VKAs. In both groups, the onset and grade of PTS - diagnosed using the Villalta score - was evaluated at 3, 6, 12, 24 and 36 months after DVT diagnosis. We diagnosed PTS in 71 (23.0%) DOACs and 121 (24.3%) VKAs. Crude and adjusted hazard ratios (95% Confidence Interval, CI) for the 3-year cumulative incidence of PTS in cases vs. controls were 0.93 (95% CI, 0.70-1.24) and 0.87 (95% CI, 0.61-1.23), respectively. Severe PTS was observed in 12 (16.9%) cases and 24 (10.8%) controls (p 0.62). The long-term incidence and severity of PTS was comparable between IT patients treated with DOACs or VKAs following a first DVT episode of the lower extremity. Larger more powerful studies are needed to ascertain how to mitigate the risk of developing PTS over time in this subset of patients.

Identifying the underlying etiology of ischemic stroke is crucial for implementing effective stroke prevention measures. In the era of thrombectomy, ischemic stroke thrombus composition has gained considerable interest in the recent years. However, only a limited studies have analyzed the inflammatory milieu of the thrombus in association with stroke etiology. Atrial Fibrillation (AF), a common etiology of large strokes, is difficult to detect, but is known to be an inflammatory disease with a dominance of CD11b cell types (characterizes bone marrow derived myeloid cells such as monocytes, neutrophils, macrophages, and natural killer cells) in the atria. We hypothesized that thrombi from ischemic stroke patients with AF will have increased CD11b cell types as compared to other stroke etiologies. 51 ischemic stroke thrombi were stained for CD11b. The relationship between stroke etiology (TOAST - Trial of ORG 10172 in Acute Stroke Treatment) and number of CD11b positive cells was assessed. Cardioembolic thrombi contained significantly higher number of CD11b positive cells (248.2 ± 137.4, n = 27) as compared to strokes from large artery atherosclerosis (138.3 ± 92.1, n = 11, p = 0.01). Similarly, thrombi from patients with cryptogenic stroke had significantly higher number of CD11b positive cells, when compared to thrombi from patients with strokes from large artery atherosclerosis ((212.1 ± 104.8 vs. 138.3 ± 92.1, p = 0.04). Our study suggests that increased expression of CD11b in ischemic stroke thrombi characterizes strokes from cardioembolic etiology. It elucidates atrial substrate inflammation driven by CD11b positive leukocytes, which leads to thrombogenesis and ischemic stroke. The shared histology of cardioembolic and cryptogenic strokes suggests that many of the cryptogenic strokes may be due to occult AF.

Trauma-induced coagulopathy (TIC) is a dynamic process that contributes to early mortality following injury, with dysregulated fibrinolysis playing a central role in its pathophysiology. Tranexamic acid (TXA), a potent antifibrinolytic agent, is widely used in trauma and surgical settings for hemorrhage management. Its effectiveness is dependent on appropriate timing and patient selection, as indiscriminate use may increase the risk of thromboembolic events. As a result, real-time monitoring of coagulation status is essential to guide TXA therapy. Conventional coagulation tests (CCTs), such as the International Normalized Ratio (INR) and Activated Partial Thromboplastin Time (aPTT), are inadequate in trauma care, as they provide static snapshots of coagulation status. By contrast, viscoelastic testing (VET) platforms, including thromboelastography (TEG) and rotational thromboelastometry (ROTEM), allow for real-time assessments of coagulation status. More recently, tissue plasminogen activator-augmented VET (tPA-VET) has been developed to more effectively distinguish between fibrinolysis phenotypes. This review explores the pathophysiology of TIC, current approaches to hemorrhage management including the use of TXA, the role of VET in guiding TXA therapy, the diagnostic value of tPA-VET, and future directions in implementing VET-guided trauma resuscitation protocols.

This commentary explores the evolving landscape of United States healthcare policy and its global implications, specifically in cardiovascular and thrombosis associated conditions. Recent legislative and executive actions have introduced sweeping reforms to federal programs such as Medicaid, Medicare, and drug pricing (Medicare Drug Price Negotiation, Medicaid Drug Rebate, Federal Supply Schedule) threatening access and affordability for millions of Americans-many already vulnerable and at risk for life threatening and life altering events. These changes reverberate internationally, influencing research collaborations, supply chains, accessibility, and the cost of care. This commentary advocates for evidence-based policy, multi-level collaboration, increased international education directives, and an unwavering commitment to broad-based healthcare access worldwide.

Despite timely primary percutaneous coronary intervention (pPCI), the no-reflow phenomenon (NRP) continues to adversely affect myocardial perfusion and outcomes in ST-segment elevation myocardial infarction (STEMI). While multiple mechanisms are implicated, reliable biomarkers for early prediction remain limited. Platelet-derived growth factor-BB (PDGF-BB), a cytokine involved in vascular inflammation and remodeling, is elevated in acute coronary syndromes. This study aimed to assess whether pre-procedural PDGF-BB levels could predict NRP in STEMI patients undergoing pPCI. In this prospective observational study, 80 STEMI patients undergoing pPCI were grouped by post-procedural TIMI flow: NRP(+) (TIMI ≤2; n=33) and NRP(-) (TIMI 3; n=47). Serum PDGF-BB levels were measured before angiography, and clinical, angiographic, and laboratory variables were compared. PDGF-BB levels were significantly higher in the NRP group (168.5 ± 177.3 vs. 65.5 ± 43.1 pg/mL; p=0.004), along with lower baseline TIMI flow (p=0.002), greater stent diameter (p=0.013), and more total occlusions (p=0.015). PDGF-BB remained an independent predictor in multivariate analysis (p=0.01). ROC analysis showed a cutoff of 89.99 pg/mL predicted NRP with 51.5% sensitivity and 87.2% specificity (AUC=0.688; p=0.004). Elevated pre-procedural PDGF-BB levels are independently associated with NRP in STEMI patients. Although its diagnostic performance is moderate, its high specificity may aid in identifying high-risk patients. Further validation and integration into risk models are warranted.

Cardiac surgery is considered to be a hypercoagulable state with an increased incidence of thromboembolic events. To evaluate the connection between hypercoagulability and mesenteric ischemia (Me-Is), we investigated hemostatic parameters in patients with diagnosed Me-Is. Out of a cohort of 500 consecutive cardiac surgery patients, 25 patients with hyperinflammatory indicators (interleukin-6 > 600 ng/l) and metabolic acidosis (lactate > 4 mmol/l) were retrospectively matched 1:4 into Me-Is (n = 5) and control (n = 20) groups. Blood samples collected before surgery, on intensive care unit (ICU) admission, and 12 h after ICU admission were assessed for hemostatic parameters, including fibrinogen, D-dimer, thrombin-anti-thrombin complex (TAT), and prothrombin fragments 1 + 2 (F1.2). Thrombin generation assays were conducted on all samples, and intestinal fatty acid-binding protein (I-FABP) was assessed as a marker for Me-Is. Baseline levels of hemostatic markers were similar between the two groups. TAT levels were significantly higher in the Me-Is group 12 h after ICU admission (54.20 ± 10.49 vs. 22.18 ± 12.43 ng/ml, p = 0.010). In contrast, at ICU admission, absolute F1.2 values were higher in the control group (1.19 ± 0.04 vs. 0.49 ± 0.47 ng/ml, p = 0.047). However, increase of F1.2 values of the Me-Is group (394.2 ± 231.6%) vs. the control group (114.7 ± 144.9%) 12 h after ICU admission were 3.9- vs. 1.1-fold compared to baseline (p = 0.046). Postoperatively, higher levels of I-FABP and of D-dimers were observed in the Me-Is group at ICU admission (17116.2 ± 18185.4 vs. 2252.3 ± 1582.7 pg/ml; p = 0.006; and 5.3 ± 1.3 vs. 3.0 ± 2.1 µg/ml; p = 0.043; respectively) and 12 h after ICU admission (16998.2 ± 20346.3 vs. 1030.8 ± 1100.0 pg/ml; p = 0.030; and 3.7 ± 1.8 vs. 1.2 ± 0.8 µg/ml; p = 0.005; respectively) compared to the control group. No significant differences were observed for parameters of thrombin generation (TGA, peak value, ETP) between the two groups. Our findings suggest that TAT and F1.2 levels are promising candidates as markers of coagulability after cardiac surgery. High levels of activation markers suggest a temporary stage of hypercoagulability immediately after surgery in Me-Is patients. Nevertheless, the serial assessment of thrombotic profiles offers valuable mechanistic insights, although these exploratory findings require confirmation in larger cohorts.

Following percutaneous coronary intervention (PCI), dual antiplatelet therapy (DAPT) is standard to reduce thrombotic complications. However, the optimal monotherapy after DAPT remains debated. Clopidogrel may offer better protection than aspirin. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing clopidogrel versus aspirin monotherapy after DAPT in PCI patients. Searches were performed in MEDLINE, Embase, Scopus, CENTRAL, and ClinicalTrials.gov up to April 12, 2025. Outcomes included stroke, myocardial infarction (MI), all-cause mortality, and cardiovascular (CV) death. Hazard ratios (HRs) were pooled using random-effects models. Four RCTs comprising 19,554 patients (clopidogrel: 9,846; aspirin: 9,708) were included. Clopidogrel was associated with a significantly lower risk of stroke (HR: 0.69; 95% CI: 0.51-0.94; p = 0.02; I² = 28%) and MI (HR: 0.71; 95% CI: 0.51-0.99; p = 0.05; I² = 48%) compared with aspirin. There was no significant difference between clopidogrel and aspirin in terms of all-cause mortality (HR: 0.99; 95% CI: 0.78-1.25; p = 0.92; I² = 55%), CV death (HR: 0.87; 95% CI: 0.70-1.08; p = 0.22; I² = 0%), coronary revascularization (HR: 0.95; 95% CI: 0.83-1.09; p = 0.44; I² = 0%), major bleeding (HR: 0.97; 95% CI: 0.70-1.35; p = 0.87; I² = 57%), or stent thrombosis (HR: 0.66; 95% CI: 0.38-1.15; p = 0.15; I² = 0%). Clopidogrel monotherapy post-DAPT after PCI reduces stroke and MI risk compared to aspirin, without increasing mortality or bleeding. These findings support clopidogrel as a favorable alternative for monotherapy.

It is generally accepted that higher phospholipid concentrations generate shorter clotting times. Phospholipid-dependent lupus anticoagulants (LA) assays such as dilute Russell's viper venom time (dRVVT) and silica clotting time (SCT) have therefore been developed. However, cases have been observed where LA confirming tests (concentrated phospholipid) generates longer clotting times than screening tests (diluted phospholipid). This study investigates the underlying cause of this paradox and assess its implications. With different phospholipid concentrations, Russell's viper venom and/or silica-induced clotting times were assayed in normal pooled plasmas (NPPs), factor deficient plasmas, cirrhotic patients' plasmas (CPPs), LA positive plasmas (LPPs). Additionally, routine LA assays were performed in LPPs with or without factor deficiency. In NPPs and factor deficient plasmas, higher phospholipid concentrations resulted in shorter clotting times, however, this effect was more evident with low-middle phospholipid than with higher phospholipid (a U shape curve). In CPPs, clotting time was increasing along with increasing phospholipid from the beginning (right part of a U shape curve). In LPPs, clotting time was shortening along with increasing phospholipid at the beginning, but changeless thereafter (left part of a U shape curve). Compared to LPPs without factor deficiency, LPPs with factor deficiency demonstrated a smaller correction of screening by confirming (dRVVT, 25.9% versus 15.1%, SCT, 28.6% versus 4.1%), leading to a possibility of LA misdiagnosis. Increasing phospholipid could induce "hook effect" in coagulation assays, therefore, phospholipid-dependent clot-based coagulation assays such as LA assays need careful interpretation, especially among patients suffering coagulation factor deficiency.