BackgroundUnfractionated heparin (UFH) is widely used in non-ST-segment elevation myocardial infarction (NSTEMI), but its narrow therapeutic window requires frequent activated partial thromboplastin time (aPTT) monitoring. Data on time in therapeutic range (TTR) in this setting are scarce.MethodsWe analyzed 1,553 consecutive patients with NSTEMI treated with UFH in a tertiary care intensive cardiovascular care unit between July 2019 and December 2025. TTR was calculated by linear interpolation over 72 hours. Associations with complications and 30-day and 1-year mortality were assessed.ResultsAmong them (mean age 67.1 ± 13.8 years, 73.9% male), only 325 (20.9%) reached the therapeutic range. Mean TTR was 12.5 ± 20.2%. An early invasive strategy predominated: 85.5% underwent coronary angiography, approximately 89% of them within 24 hours (mean time to angiography 14.4 ± 10.1 hours). Therapeutic-range attainment was not associated with mortality at 30 days (4.6% vs 4.0%, p=0.614) or 1 year (8.6% vs 9.3%, p=0.710), even after multivariable adjustment (adjusted OR 1.30, 95% CI 0.70-2.40 and 0.98, 95% CI 0.62-1.55, respectively). It was also not associated with in-hospital complications, including re-infarction, stroke, stent thrombosis, or bleeding.ConclusionsTherapeutic aPTT was achieved infrequently, and neither therapeutic-range attainment nor TTR was associated with clinical outcomes. These findings suggest that, using a contemporary approach to NSTEMI with a short time to angiography in the great majority of cases, TTR does not represent an optimal marker of anticoagulation quality, warranting evaluation of alternative strategies. Given the low event rate, confirmation in larger, adequately powered studies is required.

Uncontrolled hemorrhage remains a leading cause of preventable death in trauma patients, and trauma-induced coagulopathy (TIC) is a major determinant of early mortality. Experimental models that reliably recapitulate hemorrhage and associated coagulopathic responses are essential for mechanistic studies and evaluation of targeted interventions. Here, we describe a standardized murine model of profound hemorrhage using reproducible liver laceration (LL) causing hemorrhage, which can be quantified precisely, while also tracking simultaneously systemic coagulopathy, inflammatory markers, and mortality. Mice undergo a standardized midline laparotomy followed by LL, and blood loss is quantified by blood-soaked sponges. Systemic markers of coagulation, fibrinolysis, and inflammation markers are collected by retro-orbital blood draw prior to and at pre-specified, serial intervals post-procedure. LL with blood loss reliably produces TIC (characterized by activated partial thromboplastin time (aPTT) prolongation, thrombin-antithrombin (TAT) complex increase, selective depletion of coagulation factors (F) V and VIII with activation of fibrinolysis). In parallel, inflammatory activation is evidenced by increased interleukin-6 (IL-6). Moreover, the model further allows survival analyses after midline incision repair. As a translational application, rhFVIIa and TXA are used to prove that the model is sensitive to bleed rescue with pharmacologic modulation of coagulation and fibrinolytic parameters. Compared to large-animal models, this murine system offers an economical, versatile, and easily scalable opportunity to study innovative, targeted interventions for traumatic hemorrhage.

BACKGROUND Acquired hemophilia A (AHA) is a rare but potentially life-threatening condition caused by autoantibodies against factor VIII. It often presents in older adults and its presentation can range from isolated lab abnormality of prolonged activated partial thromboplastin time (aPTT) without bleeding to mild bleeding or spontaneous vs disproportionate life-threatening bleeding. Delayed diagnosis is frequent due to the rarity of the condition and propensity to attribute bleeding to other common causes, such as falls. CASE REPORT A 92-year-old woman with recurrent ground-level falls presented with severe right lower extremity pain of several weeks' duration. She was not on any anticoagulant or anti-platelet agent. Computed tomography angiography demonstrated bilateral lower extremity intramuscular hematomas. She had 2 prior admissions for falls within 6 months, including a fall leading to intramuscular hematoma, which was conservatively managed without evaluation of coagulopathy. During current admission, prolonged aPTT prompted further workup, revealing low factor VIII activity of 5% and a high factor VIII inhibitor titer of 15.6 Bethesda Units, establishing the diagnosis of acquired hemophilia A. Bleeding control required sequential bypassing agents, corticosteroids, rituximab, cyclophosphamide, and eventually emicizumab. CONCLUSIONS This case highlights how recurrent or disproportionate intramuscular hematomas following even minor trauma, such as a ground-level fall, in the absence of risk factors such as anticoagulant use, may prompt evaluation for underlying coagulopathy such as AHA. Basic coagulation testing including prothrombin time and aPTT can help screen patients who warrant additional coagulopathy evaluation. Timely diagnosis is critical to avoid life-threatening bleeding complications.

Background/Objectives: Prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT) are routinely used coagulation assays, and analyzer-reagent differences may affect result comparability. This study evaluated analytical comparability between the Sysmex CS-2500 System using Siemens reagents and the Tokra Medical NOVAE II for PT, INR, and aPTT. Methods: Residual routine citrated plasma specimens were measured on both systems. The CS-2500 was designated as the comparator system. Passing-Bablok regression and Bland-Altman analysis were used as the primary method-comparison approaches; Pearson and Spearman correlations and exploratory categorical agreement were secondary analyses. Results: Fifty paired measurements were analyzed for PT and INR and 54 for aPTT. For all three parameters, the 95% confidence interval (CI) for the Passing-Bablok intercept included 0 and the 95% CI for the slope included 1, providing no statistically supported evidence of constant or proportional bias by regression. Mean paired differences (NOVAE II minus CS-2500) were +1.27 s for PT, +0.023 for INR, and +2.32 s for aPTT. The 95% limits of agreement were -0.15 to +2.69 s for PT, -0.112 to +0.159 for INR, and -1.70 to +6.33 s for aPTT. Categorical agreement was influenced by analyzer-specific reference intervals and by the low prevalence of abnormal results. Conclusions: The two analyzer-reagent systems showed positive analytical associations, but the magnitude and dispersion of paired differences varied by assay. Because no clinical equivalence margins were prespecified and markedly pathological or therapeutic-range samples were sparsely represented, these findings support analytical comparison and local verification but do not establish clinical interchangeability.

Chemical sulfation of well-defined, low-molecular-weight, non-animal polysaccharides represents a potential approach to anticoagulants that potently inhibit the intrinsic tenase complex (iFXase) while causing fewer side effects, notably a low risk of bleeding. From Lessonia flavicans, we isolated a 5.5-kDa laminarin (LFP0) with a (1 → 3)-β-D-glucan core and trace branching. LFP0 was sulfated under anhydrous and short-time conditions to afford four derivatives (LFP0-S1-S4) with degrees of substitution (DS, 0.1-1.5), molecular weights (6.2-10.9 kDa), and sulfate contents (5.8%-46.2%). Physicochemical analysis and 2D NMR confirmed an intact structure with predominant C-6-O-sulfation, then C-2/C-4 sulfation. The sulfated laminarins prolonged APTT in proportion to DS and left PT unaltered. LFP0-S4, with high FIXa affinity, surpassed LMWH in iFXase inhibition by 80.6% but showed only 58.7% of its TT prolongation, indicating higher selectivity for intrinsic-pathway inhibition. In mice, LFP0-S4 exhibited potent antithrombotic activity without obvious bleeding risk, and showed no toxicity at doses up to 2000 mg/kg. These findings position L. flavicans laminarin as a promising structural blueprint for developing intrinsically targeted anticoagulants and warrant further investigation of its pharmacological and toxicological profiles.