Keeping prior anticoagulation treatment in the acute phase of ischaemic stroke: the REKOALA study

Rigual R, Rodríguez-Pardo J, Lorenzo-Diéguez M et al. J Neurol. 2024 Apr 5. doi: 10.1007/s00415-024-12204-8. Epub ahead of print. PMID: 38578495

Introduction; A consensus on the management of anticoagulated patients in the acute phase of ischaemic stroke has not yet been established. We aimed to evaluate clinical outcomes in such patients based on the continuation or discontinuation of anticoagulation.
Methods: Retrospective study of patients with acute ischaemic stroke and cardioembolic source receiving anticoagulant therapy is done. Patients were classifed based on the continuation or discontinuation of anticoagulation at admission. Clinical outcomes, haemorrhagic and ischaemic events were assessed. Multivariate logistic regression analysis, propensity score matching (PSM) analysis and a sub-analysis of patients with severe ischaemic stroke at admission (NIHSS score≥15) were performed.
Results: Anticoagulation was continued in 147 (78.8%) of 186 patients. Patients continuing anticoagulant had lower NIHSS (median 5 vs 18, p<0.001). There were no diferences in haemorrhagic or ischaemic events. In the multivariate analysis, good functional outcome at discharge was higher in the continuation group, OR (CI95%) 3.77 (1.2–11.2). PSM analysis adjusted for potential confounders such as NIHSS had higher rates of good functional outcomes at discharge (80% vs 36%, p=0.004) and at 90 days (76% vs 44%, p=0.042) in the continuation group. Patients with severe stroke in this group had lower 90-day mortality (34.6% vs 62.5%, p=0.045) and higher rates of good clinical outcome at discharge (33.3% vs 8.3%, p=0.032). No diferences were observed in 90-day haemorrhagic or ischaemic events.
Conclusion: Continuation of anticoagulation in patients with acute ischaemic stroke and cardioembolic source did not increase the risk of intracranial haemorrhage and may be associated with better functional outcomes.

Funding: Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. This work was supported by RICORS network under Grant RD21/0006/0012.

The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review

Fernández-Pérez I, Macias-Gómez A, Suárez-Pérez A et al. Int J Mol Sci. 2024 Mar 19;25(6):3433. doi: 10.3390/ijms25063433. PMID: 38542406

Abstract: This comprehensive review explores the emerging field of epigenetics in intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (aSAH). Despite recent advancements, the high mortality of aSAH needs an understanding of its underlying pathophysiology, where epigenetics plays a crucial role. This review synthesizes the current knowledge, focusing on three primary epigenetic mechanisms: DNA methylation, non-coding RNA (ncRNA), and histone modification in IA and aSAH. While DNA methylation studies are relatively limited, they suggest a significant role in the pathogenesis and prognosis of IA and aSAH, highlighting differentially methylated positions in genes presumably involved in these pathologies. However, methodological limitations, including small sample sizes and a lack of diverse population studies, temper these results. The role of
ncRNAs, particularly miRNAs, has been more extensively studied, but there are still few studies focused on histone modifications. Despite methodological challenges and inconsistent findings, these studies underscore the involvement of miRNAs in key pathophysiological processes, including vascular smooth muscle regulation and the inflammatory response. This review emphasizes methodological challenges in epigenetic research, advocating for large-scale epigenome-wide associationnstudies integrating genetic and environmental factors, along with longitudinal studies. Such research could unravel the complex mechanisms behind IA and aSAH, guiding the development of targeted therapeutic approaches.

Funding: This research was supported in part by Spain’s Ministry of Health (Instituto de Salud Carlos III, Fondos FEDER, (RICORS-ICTUS/RD21/0006/0021)).