Evidence map›Paper›PMID 40292421›Full record

ArticleTranslational neuroscience2025

Association of eNOS T786C genetic polymorphism with the risk of aneurysmal subarachnoid haemorrhage.

Josip Ljevak, Kristina Gotovac Jerčić, Antonela Blažeković, David Ozretić, Ivan Perić, Nikola Blažević, Fran Borovečki, Zdravka Poljaković Skurić

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Article in Translational neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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8 authors.

Josip LjevakDepartment of Neurology, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.
Kristina Gotovac JerčićDepartment for Personalized Medicine, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.
Antonela BlažekovićDepartment for Anatomy and Clinical Anatomy, University of Zagreb School of Medicine, 10 000, Zagreb, Croatia.
David OzretićDepartment of Neuroradiology, University Hospital Center Zagreb, University of Zagreb School of Medicine, 10 000, Zagreb, Croatia.
Ivan PerićDepartment of Neurology, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.
Nikola BlaževićDepartment of Neurology, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.
Fran BorovečkiDepartment of Neurology, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.
Zdravka Poljaković SkurićDepartment of Neurology, University Hospital Center Zagreb, 10 000, Zagreb, Croatia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Unruptured intracranial aneurysms (IAs) are increasingly detected due to advancements in neuroimaging. Despite improvements in treatment, aneurysmal subarachnoid haemorrhage (aSAH) is associated with high mortality and morbidity. Treatment decisions for IA are complex and individualized, considering aneurysm and patient-related risk factors. Genetic factors, particularly endothelial nitric oxide synthase (eNOS) polymorphisms, have been implicated in IA formation and rupture risk. Methods: This study investigated the association between three eNOS polymorphisms (27-bp-VNTR, T786C, and G894T) and aSAH in a cohort of 275 patients with unruptured IA or aSAH. Patients were followed for at least 8 years with clinical and imaging assessments. Genotyping of selected polymorphisms was performed, and statistical analyses were conducted to identify interactions between genetic polymorphisms and established risk factors. Results: A significant difference in the frequencies of genotypes and allele carriers of the T786C polymorphism was observed between patients with unruptured IA and those with aSAH, with an increased proportion of CC homozygotes in the aSAH group. The risk of rupture was higher in patients with the CC genotype. Multilobular aneurysms and those located in the posterior circulation had a higher incidence of rupture. Associations between arterial hypertension and certain genotypes were also found. However, no significant interaction was observed between the polymorphisms and established risk factors in relation to aneurysm rupture. Conclusion: Our data showed a significant and independent correlation between eNOS genetic polymorphism T786C and aSAH.

Indexed as

aneurysmeNOSpolymorphismsubarachnoid haemorrhage

Identifiers

PMID40292421
PMCPMC12032989

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