Introduction: Plasma donation is generally considered a safe procedure, and most reported adverse events are related to venipuncture or transient volume loss. Arterial thrombotic events, including acute myocardial infarction, are exceedingly rare but have been described after source plasma donation performed by plasmapheresis. We report a young man without traditional cardiovascular risk factors who presented with acute ST-elevation myocardial infarction after plasma donation. Case presentation: A 27-year-old man with eczema and intermittent cannabis use presented with chest pain approximately 12 hours after plasma donation. Electrocardiography demonstrated anterolateral ST-segment elevation, and coronary angiography showed a large proximal left anterior descending (LAD) artery thrombus with TIMI 1 flow. Aspiration thrombectomy restored TIMI 3 flow, although residual stenosis persisted. A repeat angiogram performed two days later showed persistent proximal LAD thrombus. When the patient returned several days later for completion of the evaluation, repeat angiography demonstrated a contained proximal LAD dissection without residual thrombus; based on the initial angiographic appearance and interval development after thrombectomy, this finding was considered most consistent with a procedural complication rather than the primary cause of presentation. Transthoracic echocardiography showed new severe left ventricular systolic dysfunction with an ejection fraction of 20%–25% and extensive apical akinesis. Conclusion: Plasma donation may rarely be followed by arterial thrombosis, including ST-elevation myocardial infarction. In this case, plasma donation was considered a plausible trigger for coronary thrombosis, while cannabis use represented a potential additional contributing factor. Persistent ischemic symptoms after donation warrant prompt evaluation for acute coronary syndrome.

Quercetin targeted NF-κB to regulate platelet activation and prevent arterial thrombosis.

Although patent foramen ovale (PFO) is common in the general population, it is notably more prevalent among patients with cryptogenic stroke (CS). The optimal management of PFO remains uncertain, with ongoing debate over the effectiveness of medical therapy compared to closure procedures. Medical treatments typically include antiplatelet drugs such as aspirin, clopidogrel, and dipyridamole, which aim to prevent arterial thrombus by inhibiting platelet aggregation, or anticoagulants like warfarin and direct oral anticoagulants (DOACs), which work on the coagulation cascade to reduce venous thrombus formation and embolic risk. In contrast, closure techniques aim to eliminate the anatomical conduit for emboli. Transcatheter closure using devices such as Amplatzer or Gore has demonstrated high success and safety rates, with evidence from trials including RESPECT, CLOSE, and REDUCE supporting reduced risk of recurrent CS. However, atrial fibrillation remains a common early complication. To address concerns about implants or nickel allergies, the NobleStitch EL suture system offers a promising device-free alternative. Patient selection for closure relies on risk stratification tools such as the RoPE and PASCAL scores, while contraindications include cardiac thrombus, endocarditis, or other potential embolic sources. Overall, current evidence indicates that closure may benefit carefully selected patients, yet medical therapy remains crucial, especially when closure is contraindicated or patient preference guides the decision. Further research is required to refine selection criteria, weigh long-term safety against efficacy, and clarify the comparative benefits of medical versus closure strategies. This review aims to synthesize the available evidence.

Dysfunction of pulmonary artery endothelial cells (PAECs) contributes to the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH). However, the role of mitochondrial metabolism in this process remains unclear. The present study evaluated whether the tetrameric form of pyruvate kinase muscle isoform 2 (PKM2) regulates PAEC mitochondrial metabolism through peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1alpha) and mitochondrial transcription factor A (mtTFA), thereby influencing arterial intimal remodeling in CTEPH. A CTEPH rat model was established by repeated injections of autologous thrombi. Activation of PKM2 tetramer expression was achieved through synthetic pyruvate kinase M2 activator (TEPP-46) administration. Pulmonary artery pressure (PAP), thrombus pathology, and protein expression levels of PKM2, mtTFA, and PGC-1alpha were assessed. Plasma lactate concentrations and tumor necrosis factor alpha (TNF-alpha) levels were measured. Rats with CTEPH demonstrated thrombotic obstruction, elevated PAP, and reduced expression of the PKM2 tetramer, mtTFA, and PGC-1alpha. Treatment with TEPP-46 was associated with a reduction in thrombus burden, lower PAP, and restoration of mitochondrial protein expression, accompanied by decreased lactate concentrations and TNF-alpha levels. In the CTEPH rat model, increased inflammation and elevated lactate concentrations were observed, along with decreased expression of mtTFA and PGC-1alpha in the pulmonary artery intima, which is indicative of mitochondrial dysfunction. The PKM2 tetramer may play a role in modulating PAEC mitochondrial function, reducing pulmonary artery pressure, and improving pulmonary arterial intimal remodeling in CTEPH. Key words Chronic thromboembolic pulmonary hypertension " Lactic acid " Mitochondrial transcription factor A " Peroxisome proliferator-activated receptor gamma coactivator 1alpha " Pyruvate kinase muscle.

Dysfunction of pulmonary artery endothelial cells (PAECs) contributes to the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH). However, the role of mitochondrial metabolism in this process remains unclear. The present study evaluated whether the tetrameric form of pyruvate kinase muscle isoform 2 (PKM2) regulates PAEC mitochondrial metabolism through peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA), thereby influencing arterial intimal remodeling in CTEPH. A CTEPH rat model was established by repeated injections of autologous thrombi. Activation of PKM2 tetramer expression was achieved through synthetic pyruvate kinase M2 activator (TEPP-46) administration. Pulmonary artery pressure (PAP), thrombus pathology, and protein expression levels of PKM2, mtTFA, and PGC-1α were assessed. Plasma lactate concentrations and tumor necrosis factor alpha (TNF-α) levels were measured. Rats with CTEPH demonstrated thrombotic obstruction, elevated PAP, and reduced expression of the PKM2 tetramer, mtTFA, and PGC-1α. Treatment with TEPP-46 was associated with a reduction in thrombus burden, lower PAP, and restoration of mitochondrial protein expression, accompanied by decreased lactate concentrations and TNF-α levels. In the CTEPH rat model, increased inflammation and elevated lactate concentrations were observed, along with decreased expression of mtTFA and PGC-1α in the pulmonary artery intima, which is indicative of mitochondrial dysfunction. The PKM2 tetramer may play a role in modulating PAEC mitochondrial function, reducing pulmonary artery pressure, and improving pulmonary arterial intimal remodeling in CTEPH.

The mechanisms driving spatial heterogeneity of arterial thrombus and its three-stage dynamics are poorly understood. To investigate the potential principles regulating the size of the thrombus core and shell we developed a 3D continuum computational model that describes thrombus heterogeneity, thrombin-induced platelet dense granule secretion and clot propagation through thrombin and ADP-induced platelet activation. The continuum model predicted that spatial confinement of the thrombus core was a result of thrombin transport and a threshold-like dependence of platelet activation on thrombin concentration. This new model recapitulated three-stage dynamics observed in vivo and explained it with a burst-like ADP concentration dynamics due to the confinement of thrombus core propagation and rapid dense granule pool depletion within the core. The maximal shell size in silico was regulated by the transport of ADP and the kinetics of thrombin-dependent dense granules secretion. Simulations also predicted that partial propagation of thrombin inside the thrombus shell caused irreversible platelet activation by the low-dose thrombin and defined the residual shell size. Moreover, our results provided an explanation for the reduced size of a thrombus core observed in the mouse models of Hermansky-Pudlak syndrome. The continuum model was then applied to describe a FeCl3-induced thrombosis in macrocirculation, and described the thrombin-flux-depending switch between occlusive and non-occlusive thrombosis scenarios in mouse carotid artery. Finally, our simulations reinforced the hypothesis suggesting the importance of the large ADP-dependent thrombus shell for sealing the breach in case of a penetrating injury. Taken together, our results suggest a novel mechanism that may regulate arterial thrombus dynamics and offer several insights and сlarification to the core-and-shell model of arterial thrombus organization, as well as a possible role of the large thrombus shell in hemostasis.

Patients with high-risk pulmonary embolism complicated by cardiac arrest frequently require V-A ECMO support; however, the traditional peripheral catheterization pathway may be obstructed in patients who have already had an inferior vena cava (IVC) filter implanted. This article aims to investigate alternative ECMO establishment strategies. A 68-year-old female patient with acute myeloid leukemia experienced sudden cardiac arrest due to high-risk pulmonary embolism. Due to contraindications to thrombolysis, emergency pulmonary artery thrombus aspiration and IVC filter implantation were performed. However, after repeated episodes of cardiac arrest, conventional femoral vein catheterization proved challenging. Consequently, the "top-in, bottom-out" strategy was employed: a 21Fr porous venous drainage catheter was inserted through the right internal jugular vein under DSA guidance, with the tip positioned at the opening of the IVC, effectively bypassing the filter. The arterial perfusion catheter was placed in the left femoral artery. V-A ECMO was successfully established, leading to improved spontaneous circulation without further cardiac arrests. Nevertheless, the patient ultimately succumbed to disseminated intravascular coagulation (DIC) within 10 hours. For high-risk pulmonary embolism patients who have already had an IVC filter implanted, positioning the drainage catheter at the opening of the IVC via the right internal jugular vein offers a viable and effective method for establishing V-A ECMO. This approach provides a novel technical route for critically ill patients where traditional catheterization is limited.

This study evaluates radiomics correlation with mortality and suitability as prognostic indicator for troponin for pulmonary embolism to enhance prognostic accuracy and guide personalized treatment strategies with the help of machine learning. We conducted an initial study focusing on texture information of the arterial thrombus. Computed tomography (CT) of the lung from 86 patients with pulmonary embolism was used. As target variables, we used patients 30-day mortality and troponin results. Each arterial thrombus was manually segmented. After the extraction of their radiomics features and the reduction via correlation analysis and 12 feature selection methods, these and the target variables were given to 12 different classification methods to record the accuracies (Acc.), F1-scores (F1) and ROC curve areas under the curve (AUC) for comparison and evaluation. The resulting accuracy achieved was 0.967, the F1-score 0.973 for class 0 and 0.967 for class 1 and the AUC around 0.9686. The feature selection methods which resulted in the highest results were ReliefF (RF), Logistic Regression (LOR) and CART Classification (CARTC). For the classification methods, Support Vector Machines (SVM), eXtreme Gradiant Boosting (XGB) and Ensemble Bagged Trees (EBT) lead to the highest results. Firstorder, Shape and gray-level co-occurrence matrix (GLCM) were the most selected radiomics feature classes. Within this study, we conducted radiomics feature extraction within a medical image data analysis pipeline with subsequent correlation analysis and training of classifiers for patients with pulmonary lung embolism. We could show that the radiomics features correlated with patient's morphology as well as troponin range with an accuracy of 0.967 and 0.9302, respectively, yield high potential for prognosis and treatment strategy of pulmonary embolism patients in the future.

Mechanisms of Symptomatic Lower Extremity Artery Disease in Femoropopliteal Arteries Assessed by Optical Frequency Domain Imaging.

USP25-mediated talin-1 stabilization in platelets: a novel mechanism of hyperreactivity and thrombosis risk during aging.

Aortotomy-induced acute mural thrombosis progresses to saccular aneurysm formation.

An adolescent female with a prior diagnosis of Kawasaki disease (KD) presented with systemic inflammatory symptoms, including periorbital swelling, odynophagia and transient fever following initiation of statin therapy. Several months earlier, she experienced a prolonged febrile illness with unilateral neck pain and a desquamating rash, but without classic KD features. Imaging later revealed significant progression of coronary artery aneurysms and thrombus formation, raising concern for KD recurrence. Extensive autoimmune and infectious evaluations were largely unremarkable, apart from a primary Epstein-Barr virus infection. She was treated with intravenous immunoglobulin, corticosteroids and anticoagulation. This case highlights the diagnostic challenges posed by atypical presentations in a condition associated with rare recurrence rates. It underscores the need for long-term cardiovascular surveillance in patients with previous KD, even into adolescence.

Thrombolytic therapy alleviates pulmonary embolism (PE) symptoms rapidly but increases bleeding risk, with no consistent consensus on acute intermediate-high risk PE. This study evaluated the efficacy and safety of low-dose prolonged infusion thrombolysis for acute intermediate-high risk PE to provide a safer clinical option. A total of 120 patients were collected and divided into anticoagulant (Group A, n = 58) and thrombolytic (Group B, n = 62) groups. Efficacy outcomes included pulmonary artery thrombus clearance rate, 30-day all-cause mortality, and 3-6 month pulmonary hypertension incidence; the primary safety outcome was treatment-related bleeding. Both groups showed improved SBP, DBP, SpO₂, and RV/LV ratio (all p < 0.05) with no inter-group differences, but Group B had higher thrombus clearance rate ([64.85 ± 17.47]% vs. [41.65 ± 16.19]%, p < 0.001), with similar 30-day mortality (1.61% vs. 5.17%, p = 0.278). At 1 day, post-treatment, Group B had higher D-dimer (26.78 ± 16.57 μg/mL vs. 7.60 ± 7.23 μg/mL) and FDP (91.45 ± 97.37 μg/mL vs. 18.60 ± 26.34 μg/mL, all p < 0.001) but comparable FIB (p = 0.091); these differences persisted until discharge (all p < 0.05 for D-dimer/FDP). Although the incidence of bleeding events in group B was numerically higher than that in group A (17.74% vs. 6.90%, p = 0.073), the difference between the two groups was not statistically significant. No fatal bleeding, intracranial hemorrhage, or recurrent pulmonary embolism occurred in either group. Group B had lower 3-6 month pulmonary artery systolic pressure (PASP) (30.70 ± 9.70 vs. 34.44 ± 10.04 mmHg, p = 0.045) and pulmonary hypertension incidence (27.87% vs. 54.55%, p = 0.004). Thrombus clearance rate correlated with treatment group (r = 0.57, p < 0.001), and D-dimer (r = 0.42) and FDP (r = 0.32) levels at 1 day post-treatment (both p < 0.001). Low-dose prolonged infusion can effectively clear pulmonary artery thrombi in patients with acute intermediate-high-risk PE, which may be associated with a reduced incidence of pulmonary hypertension. Patients in the thrombolysis group showed significant dynamic changes in D-dimer and FDP levels, which were significantly correlated with a higher thrombus clearance rate.

Compared with an arterial thrombus (AT) or a venous thrombus (VT), there is limited knowledge about arteriovenous thrombus (AVT). AVT develops in 69% of arteriovenous fistulae (AVF) and 50% of arteriovenous grafts (AVG) within 1 year. Thrombosis remains one of the major complications after creation of a vascular access often resulting in failure of the access.To characterize and differentiate AVT from VT or AT.An AVT model was established by a needle puncture through the aorta to the inferior vena cava (IVC) in wild type mice and different reporter mice and compared with a mouse venous thrombus (VT) model using IVC ligation. AVT was also examined under defined arteriovenous flow conditions. AVT was examined by gross view, histology, immunofluorescence, and scanning electron microscopy.AVT occurs immediately at the juxta-anastomotic area (JAA) after successful arteriovenous flow was established, with platelets being a major component of early AVT. Reduced injury to the endothelium resulted in smaller AVT, whereas local delivery of rapamycin to inhibit cell proliferation failed to decrease the volume of the AVT. Incomplete reendothelialization of the peri-fistula exit area correlated with growth of the AVT. AVT universally presents at the JAA in other arteriovenous models.We provide the first detailed histopathological characterization of AVT induced by AVF. AVT originates from the injured vessel wall and is more similar to AT than VT. This model provides a valuable tool to characterize AVT. Both this AVT model and our data have potential for clinical translation.

The conventional transcranial approach for treating lower basilar artery aneurysms is challenging because the deep and narrow surgical field limits surgical maneuvering for clipping. We report a case of a 77-year-old female who presented with right hemiparesis caused by a partially thrombosed giant aneurysm in her lower basilar artery. We performed neck clipping and thrombus debulking using a combined transcranial and endonasal approach. This approach enabled us to secure the parent artery from the endonasal side, which is difficult to achieve with the transcranial approach alone. It also allowed for early thrombus removal, thereby widening the surgical field on the transcranial side. Additionally it compensated for the transcranial blind spot by observing the clip tip from the endonasal side. After surgery, the patient required 3 months of rehabilitation for residual right hemiparesis before being discharged. Follow-up imaging revealed a reduction in the size of the partially thrombosed aneurysm. To our knowledge, this is the first report of a combined transcranial and endonasal approach for the treatment of a basilar artery aneurysm. For lower basilar artery aneurysms, this combined approach may offer advantages in achieving safe parent artery control, thrombus debulking, and neck clipping.

ABSTRACT Platelets play a crucial role in arterial thrombus formation, offering potential for new antiplatelet therapies with reduced bleeding risk. Here, we investigated the role of the renin-angiotensin system (RAS) in human platelets and explored its potential link to COVID-19 coagulopathy. Experiments were performed ex vivo on healthy human platelets. The expression of RAS receptors (Mas, MrgD, ACE, ACE2, AT1 and AT2) was evaluated using western blot and immunofluorescence. Platelets were incubated in vitro with either Captopril or different RAS peptides including Alamandine, Angiotensin-I, Angiotensin-II, Angiotensin-(1–7), and Angiotensin-(1–9). Platelet adhesion was measured by spectrophotometry using BCECF fluorescence. Platelet activation and aggregation were analyzed using aggregometry after stimulation with extracellular matrix proteins. ACE and ACE2 activity were assessed using Fluorescent Peptides (FPS). We demonstrated that healthy human platelets express all the tested RAS receptors. However, RAS peptides did not modulate platelet adhesion or aggregation despite a wide range of concentrations tested. ACE activity was detected in platelet lysates, but it was not inhibited by Captopril, while ACE2 activity was undetectable. Our findings suggest that while RAS receptors are expressed in platelets, RAS peptides do not impact platelet function, at least in our experimental setting. COVID-19 coagulopathy may occur independently of the RAS.

Pulmonary embolism (PE) is a major cause of cardiovascular morbidity and mortality. Current risk stratification tools have limitations in predicting short-term outcomes. Radiological parameters such as thrombus density, measured in Hounsfield Units (HU) on computed tomography pulmonary angiography (CTPA), may provide additional prognostic information. This study aims to assess the association between pulmonary artery thrombus density on CTPA and 30-day mortality in patients with intermediate-risk PE. This retrospective cohort study included patients diagnosed with acute PE by contrast-enhanced CTPA in the emergency department of a single tertiary center between January 1, 2022, and December 31, 2024. Only patients classified as intermediate-risk according to European Society of Cardiology guidelines were included. HU values were measured from predefined pulmonary artery locations. The primary outcome was 30-day all-cause mortality. Multivariate logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors and assess discriminative ability. A total of 121 patients (mean age: 70 ± 14.5 years; 58.5% male) were analyzed. The 30-day mortality rate was 26.4%. Thrombus HU values were significantly higher in deceased patients compared to survivors (median 76 vs. 56, p = 0.001). In multivariate analysis, HU value (OR: 1.03; 95% CI: 1.001-1.06; p = 0.04) and sPESI score (OR: 1.70; 95% CI: 1.04-2.78; p = 0.03) were independent predictors. AUCs were 0.702 for HU and 0.731 for sPESI. Thrombus density on CTPA was independently associated with 30-day mortality in intermediate-risk PE. HU measurement may serve as a practical imaging biomarker for early prognostic assessment.

ABSTRACT Xanthone, a naturally occurring oxygenated heterocyclic compound from the Garcinia family with known anti-cancer, antimicrobial, antioxidant, anti-inflammatory, and antiviral properties, has an unclear role in platelet function. This study investigated its effects by incubating human platelets with xanthone at doses of 0, 5, 10, and 20 μM for 1 hour to analyze platelet aggregation, granule release, activation, receptor expression, spreading, and clot retraction, while also administering xanthone (10 mg/kg) to mice to evaluate its impact on hemostasis, arterial, and venous thrombosis. Our findings demonstrated that xanthone dose-dependently reduced platelet aggregation and granule release induced by collagen-related peptide (CRP) or thrombin without altering the surface expression of receptors αIIbβ3, GPIbα, and GPVI; it also significantly inhibited platelet spreading on collagen or fibrinogen, thrombin-mediated clot retraction, and decreased phosphorylation of c-Src and PLCγ2 in treated platelets. In vivo, xanthone-administered mice exhibited prolonged tail bleeding time and impaired arterial and venous thrombosis. Mechanistically, xanthone inhibited NF-κB activation, phosphorylation of ERK1/2 and p38, calcium mobilization, and platelet procoagulant activity. These findings indicate that xanthone impairs platelet activation and both arterial and venous thrombus formation, suggesting its potential as a novel agent for treating thrombotic or cardiovascular diseases.

Brachial Artery Entrapment in a Professional Athlete.

Transient build-up of a mural thrombus promotes intrathrombus coagulation reactions.