THE ROLE OF RIVAROXABAN IN THE THERAPY OF ISCHEMIC STROKE COMPLICATIONS: FROM MOLECULAR MECHANISMS TO CLINICAL PRACTICE
DOI:
https://doi.org/10.32782/2411-9164.24.1-4Keywords:
ischemic stroke, rivaroxaban, complications, secondary prevention, hemorrhagic transformation, atrial fibrillation, Factor Xa, PAR-2, neuroinflammationAbstract
Therapy for patients after ischemic stroke (IS) resembles a complex balancing act between two critical threats: early thromboembolic recurrence and hemorrhagic transformation of the ischemic focus. At the center of this clinical dilemma lies rivaroxaban, a direct Factor Xa inhibitor. Despite its status as a key prophylactic tool, the use of this drug in the context of a disrupted blood–brain barrier (BBB) creates a fundamental paradox, which became the focus of our study. The aim of this work was to conduct a comprehensive synthesis of data combining an analysis of the drug’s coagulation-related and pleiotropic mechanisms with the results of large-scale randomized clinical trials (ROCKET AF, NAVIGATE ESUS, COMPASS). Based on a critical review of PubMed, Scopus, and Cochrane Library databases, we identified the dual nature of rivaroxaban’s effects. On one hand, as an anticoagulant, it demonstrated high efficacy in patients with atrial fibrillation, significantly reducing the risk of fatal intracranial hemorrhages compared to warfarin. However, in the heterogeneous group of strokes of undetermined etiology (ESUS), the drug not only failed to outperform aspirin but also increased the risk of bleeding, delineating the boundaries of its use. On the other hand, preclinical analyses revealed a less obvious potential of the molecule: by blocking the FXa/PAR-2 signaling pathway, rivaroxaban is capable of exerting neuroprotective effects, reducing neuroinflammation, and stabilizing the BBB. In conclusion, in real-world clinical practice (“in vivo”), these pleiotropic effects are often offset by systemic anticoagulation, particularly in severe strokes. Therefore, modern neurology should move away from rigid consensus-based therapy initiation schemes (the “1-3-6-12 days” rule) in favor of a flexible, biomarker-guided strategy that considers the individual pathogenesis of each patient.
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