ArticleJournal of thrombosis and haemostasis : JTH2024
A multitrait genetic study of hemostatic factors and hemorrhagic transformation after stroke treatment.
Article in Journal of thrombosis and haemostasis : JTH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Advances in genetics and multi-omics for ischemic stroke: from pathogenesis to clinical translation.Frontiers in genetics · 2026Review
- AI prediction model for endovascular treatment of vertebrobasilar occlusion with atrial fibrillation.NPJ digital medicine · 2025Article
- The differences of fibrinogen levels in various types of hemorrhagic transformations.Frontiers in neurology · 2024Article
Corrections and comments
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Authors and funding
33 authors at 17 institutions in 3 countries.
Funding
Abstract
backgroundThrombolytic recombinant tissue plasminogen activator (r-tPA) treatment is the only pharmacologic intervention available in the ischemic stroke acute phase. This treatment is associated with an increased risk of intracerebral hemorrhages, known as hemorrhagic transformations (HTs), which worsen the patient's prognosis.
objectivesTo investigate the association between genetically determined natural hemostatic factors' levels and increased risk of HT after r-tPA treatment.
methodsUsing data from genome-wide association studies on the risk of HT after r-tPA treatment and data on 7 hemostatic factors (factor [F]VII, FVIII, von Willebrand factor [VWF], FXI, fibrinogen, plasminogen activator inhibitor-1, and tissue plasminogen activator), we performed local and global genetic correlation estimation multitrait analyses and colocalization and 2-sample Mendelian randomization analyses between hemostatic factors and HT.
resultsLocal correlations identified a genomic region on chromosome 16 with shared covariance: fibrinogen-HT, P = 2.45 × 10
conclusionWe identified 4 shared loci between hemostatic factors and HT after r-tPA treatment, suggesting common regulatory mechanisms between fibrinogen and VWF levels and HT. Further research to determine a possible mediating effect of fibrinogen on HT risk is needed.
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