LIPOPROTEIN (a) IN STROKE: FROM PATHOPHYSIOLOGY TO EMERGING THERAPEUTIC POSSIBILITIES

Background: Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein increasingly recognized as an independent cardiovascular risk factor. Its role in ischemic stroke has gained attention, although its clinical relevance remains incompletely defined. Objective: To summarize current evidence on the role of Lp(a) in stroke pathophysiology, its diagnostic value, and therapeutic possibilities. Materials and Methods: A systematic review of literature published between 2016 and 2026 was conducted using PubMed, Web of Science, and Google Scholar. Meta-analyses, cohort studies, clinical trials, and guideline-based publications addressing Lp(a) and stroke were included. Results: Elevated Lp(a) levels are associated with an increased risk of ischemic stroke, supported by observational studies and meta-analyses. This relationship is largely driven by proatherogenic, proinflammatory, prothrombotic, and antifibrinolytic mechanisms. Lp(a) levels are strongly genetically determined, primarily by LPA gene variants. Evidence does not support a significant association between Lp(a) and hemorrhagic stroke. Therapeutic options remain limited, as standard lipid-lowering therapies have minimal impact on Lp(a). PCSK9 inhibitors provide modest reductions, while novel RNA-based therapies show substantial Lp(a) lowering, though their clinical benefit in stroke prevention is yet to be confirmed. Conclusions: Lp(a) is an important but underutilized marker of ischemic stroke risk. Further studies are needed to establish the clinical effectiveness of targeted therapies and to refine its role in routine risk assessment.