Background/Objectives: Acute carotid tandem lesions (TLs), defined by concurrent cervical internal carotid artery (ICA) stenosis or occlusion and intracranial large vessel occlusion, occur in 10-20% of patients undergoing mechanical thrombectomy (MT) for acute ischemic stroke (AIS). Optimal periprocedural antiplatelet management during emergent carotid artery stenting (eCAS) remains uncertain, particularly regarding the balance between preventing stent thrombosis and avoiding hemorrhagic complications. Methods: A narrative review was conducted using PubMed and Scopus (until 6 March 2026) to identify English-language studies evaluating antiplatelet therapies during eCAS for TLs. We included seven real-world studies and registry analyses. Data on study design, patient characteristics, procedural strategies, angiographic results, functional outcomes, and safety metrics were extracted. Results: No randomized controlled trials (RCTs) were identified. The available evidence is derived exclusively from observational studies. Across these cohorts, glycoprotein IIb/IIIa inhibitors (GPIs), particularly tirofiban, were generally associated with lower rates of in-stent thrombosis and higher reperfusion success, with symptomatic intracranial hemorrhage (sICH) rates that appeared comparable to or lower than those reported with acetylsalicylic acid (ASA). Cangrelor, an intravenous (IV) P2Y12 inhibitor, was associated with improved stent patency and increased likelihood of complete reperfusion, although reported effects on clinical outcomes were inconsistent when compared with GPIs or ASA. Aside from abciximab, potent IV antiplatelet agents did not consistently show an increased sICH signal. Oral dual antiplatelet therapy was also associated with improved technical outcomes without a clear excess in bleeding complications. Conclusions: Current real-world observational data suggest that rapid-acting IV antiplatelet agents-particularly GPIs and, increasingly, cangrelor-may represent feasible periprocedural options during eCAS for TLs, with potential benefits for technical success and no consistent evidence of increased hemorrhagic risk. However, interpretation is limited by study heterogeneity and non-randomized designs. The absence of RCTs highlights the need for prospective comparative studies and standardized periprocedural antiplatelet protocols.

Stent thrombosis remains a critical and fatal complication of angioplasty with stenting, particularly in tandem lesion patients, where the incidence can exceed 20%. A better understanding of the thrombogenicity of clinically used stents could reduce the occurrence of stent thrombosis.We have developed a macrofluidic model mimicking the geometry of the human carotid artery, which is perfectly suited to evaluate the intrinsic thrombogenicity of carotid stents. Real-time video microscopy and scanning electron microscopy were combined to assess the thrombogenicity of three clinically used carotid stents: the laser-cut Protégé RX stent, the braided Casper stent, and Wallstent.The Casper and the Wallstent led to higher rates of platelet adhesion and thrombus formation than the Protégé RX. The thrombi were essentially localized at the intersections of the metal wires in the braided stents, whereas in the laser-cut stent, only more evenly distributed platelet adhesion was observed. Hot spots of thrombosis were identified at the crossings of the stent struts, especially around the external wires of these crossings, which are in contact with the vessel wall. Thrombus formation was effectively prevented in the presence of aspirin or the αIIbβ3 blocker abciximab. Computational fluid dynamics indicated that the wire crossings of braided stents generate a prothrombotic shear environment, with flow recirculation and stagnation regions leading to thrombus formation, as demonstrated by a macroscale in silico simulation.Design plays a major role in thrombus formation on stent wires, with braided stents being more thrombogenic than laser-cut stents.

Variations in thrombus composition significantly influence the efficacy of conventional thrombolytic therapies in acute ischemic stroke. Emerging treatments, designed to target distinct components of the thrombus, are currently under evaluation and offer renewed hope for enhancing clot dissolution and improving clinical outcomes. This review will examine the current evidence surrounding glycoprotein IIb/IIIa inhibitors in the treatment of acute ischemic stroke, drawing on the latest randomised-controlled trials, identifying promising therapeutic candidates and evaluating the clinical contexts in which these agents are most likely to be beneficial.

Mouse models, such as the intravital laser-induced model of thrombus formation, are commonly used for mechanistic and preclinical studies in thrombosis. However, their translational value is limited by species differences. Few in vitro models incorporate laser-induced vascular injury. Here, we developed an endothelialized microfluidic device, the Endo-chip, to model thrombus formation in response to laser injury. Citrated blood was treated with IXA4, an endoplasmic reticulum stress inducer, or with antithrombotic agents including antitissue factor antibody (5G9), antiplatelet drugs (abciximab, aspirin), and anticoagulants (argatroban, heparin). Fluorescently labeled antibodies (to platelets, fibrin, or von Willebrand factor [VWF]), annexin V or the calcium dye Cal520, were added to the blood. After recalcification at 10 mM, blood was perfused through the Endo-chip at a shear rate of 100 s[-1] or 800 s[-1]. Endothelial injury was induced with a 355-nm laser pulse producing a focal 10-μm injury, and phosphatidylserine exposure on endothelial cells within ∼1 cell diameter from the injury site. Annexin V-positive endothelial cells expressed tissue factor and released VWF, supporting localized platelet and fibrin deposition. The thrombus formed a teardrop morphology aligned with flow incorporating VWF with increasing shear. IXA4 enhanced platelet cytoplasmic calcium. Platelet accumulation was inhibited by abciximab but not aspirin, whereas coagulation inhibitors (5G9, argatroban, heparin) markedly reduced thrombus formation. These findings support that the Endo-chip laser-injury model incorporates key features of thrombus formation after endothelial injury, and provides a humanized, in vitro, alternative or auxiliary to mouse models for preclinical studies and antithrombotic drug development.

The aim of this study was to assess the safety and effectiveness of abciximab (ReoPro®), a glycoprotein-IIb/IIIa receptor antagonist, in the management of thromboembolic complications during endovascular treatment of intracranial aneurysms.

Abdominal aortic aneurysm (AAA) is a non-communicable disease (NCD) with high morbidity and mortality, commonly observed worldwide. Understanding its molecular mechanisms and identifying potential therapeutic targets are crucial for disease screening, diagnosis, and treatment. In this study, we conducted a meta-analysis of multiple genome-wide association studies (GWASs) to identify genetic variants associated with AAA and explored the functional implications of these variants in disease pathology. We identified differentially expressed genes (DEGs) based on significant single nucleotide polymorphisms (SNPs) from expression quantitative trait loci (eQTL) and transcriptome-wide association study (TWAS) analyses. Using these DEGs, we constructed an AAA-related protein-protein interaction (PPI) network and prioritized key genes for further analysis. Furthermore, we performed drug repurposing by identifying drug-gene and drug-protein interactions in existing databases and validated potential candidates through molecular docking. Our findings reveal 42 novel disease-associated SNPs and 52 previously unreported disease-related genes. Some residual confounding factors cannot be fully ruled out and may represent a limitation of our study. However, it is worth noting that only a minority of SNPs exhibited heterogeneity. Functional pathways analysis highlighted key processes, including lipid and cholesterol metabolism, tissue remodeling, and acetylcholine activation. We identified 74 DEGs through eQTL and TWAS analyses, with PPI network analysis highlighting CD40 and LRP1 as key proteins. Drug repurposing and molecular docking suggested abciximab and paclitaxel as potential therapeutic agents targeting CD40, while ivermectin emerged as a strong candidate for LRP1 binding. In conclusion, our integrative bioinformatics frameworks links genomics and transcriptomics with network biology and structural modeling, providing valuable insights into the molecular mechanisms of AAA and potential therapeutic strategies.

A robust, rapid, and highly sensitive LC-MS/MS method was developed and validated for the simultaneous quantification of atezolizumab and bevacizumab in rat plasma, with potential applications in pharmacokinetic studies. The mobile phase comprised water with 0.1% formic acid (mobile phase A) and acetonitrile with 0.1% formic acid (mobile phase B) in an isocratic ratio of 30:70, providing optimal separation on an Agilent Eclipse XDB column (250 mm × 4.6 mm, 5 μm). The selected peptides for atezolizumab (IYPTNGYTR) and bevacizumab (LTVLHQDWLNGK) yielded parent ions at m/z 579.78 and 686.38, and daughter ions at 746.36 and 859.44, respectively. The internal standard, abciximab, used the peptide VQWLQAGK with parent and daughter ions at m/z 471.26 and 590.32, respectively. Atezolizumab and bevacizumab were validated over linear ranges of 3.00-120 ng/mL and 1.25-50.00 ng/mL, showing excellent correlation coefficients (r2 = 0.999). Method accuracy for atezolizumab ranged from 96.76% to 99.55%, with precision (%CV) between 0.09% and 2.45% across quality controls, while bevacizumab demonstrated accuracy from 97.05% to 99.82% with precision (%CV) ranging from 0.09% to 8.82%. Matrix effects at low and high QC levels confirmed consistency, with accuracy and precision for atezolizumab and bevacizumab exceeding ICH guidelines. This optimized method offers a valuable tool for pharmacokinetic profiling of atezolizumab and bevacizumab in rat plasma, providing insights for therapeutic monitoring and drug development.

Platelet-driven blood clot contraction (retraction) is important for hemostasis and thrombosis. Red blood cells (RBCs) occupy approximately half of the clot volume, but their possible active contribution to contraction is unknown. The work was aimed at elucidating the ability of RBCs to promote clot shrinkage. To distinguish the effects of platelets and RBCs, we formed thrombin-induced clots from reconstituted human samples containing platelet-free plasma and platelet-depleted RBCs, followed by tracking the clot size. The clots before and after RBC-induced shrinkage were analyzed using histology and scanning electron microscopy. Tension developed in the RBC-containing plasma clots was measured with rheometry, and theoretical modeling was used to elucidate the clot shrinkage mechanisms. Platelet-depleted clots formed in the presence of RBCs exhibited >20% volume shrinkage within one hour. This process was insensitive to blebbistatin, latrunculin A, and abciximab. At a higher RBC count, clot shrinkage increased, whereas in the absence of RBCs no plasma clot shrinkage was observed. At low platelet counts, RBCs stimulated clot contraction proportionately to the platelet level. Inside the shrunken clots, RBCs formed aggregates. The average tensile force per 1 RBC was ∼120 ± 100 pN. Clots from purified fibrinogen formed in the presence of RBCs did not change in size, but underwent shrinkage in the presence of osmotically active dextran. Blood clot shrinkage can be caused by RBCs alone, and this effect is because of the RBC aggregation driven mainly by osmotic depletion. The RBC-induced clot shrinkage may reinforce platelet-driven blood clot contraction and promote clot compaction when there are few and/or dysfunctional platelets.