Endothelial nitric oxide synthase polymorphism is associated with delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage.

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Endothelial nitric oxide synthase polymorphism is associated with delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage.

World Neurosurg. 2017 Feb 22;:

Authors: Hendrix P, Foreman PM, Harrigan MR, Fisher WS, Vyas NA, Lipsky RH, Lin M, Walters BC, Tubbs RS, Shoja MM, Pittet JF, Mathru M, Griessenauer CJ

Abstract
BACKGROUND: and Purpose: Nitric oxide (NO) is critical in the regulation of cerebral blood flow and smooth muscle proliferation. It is synthesized by three nitric oxide synthase (NOS) isoforms: neuronal (nNOS), inducible (iNOS), and endothelial NOS (eNOS). Aneurysmal subarachnoid hemorrhage (aSAH) causes endothelial dysfunction which, in turn, contributes to pathophysiological processes surrounding aSAH. Previous studies reported an association of an eNOS single nucleotide polymorphism (SNP) with the clinical sequelae of aSAH. Here, we further elucidate the impact of this eNOS SNP on the clinical course after aSAH.
METHODS: The CARAS (Cerebral Aneurysm Renin Angiotensin System) study prospectively enrolled aSAH patients at two academic institutions in the United States from 2012 to 2015. Blood samples from all patients enrolled in the CARAS study were used for genetic evaluation using 5'exonuclease (Taqman) genotyping assays. Associations between the eNOS SNP rs2070744 (786 T->C) and the clinical course after aSAH were analyzed.
RESULTS: Samples from 149 aSAH patients were available for analysis. The C allele of the eNOS SNP independently predicted an increased risk for DCI (OR = 2.936, 95% CI 1.048 - 8.226, p = 0.040). The eNOS SNP rs2070744 was not associated with functional outcome or size of aneurysm at the time of rupture.
CONCLUSIONS: The present study is the first to demonstrate that the C allele of the eNOS SNP 786 T->C rs2070744 is independently associated with an increased risk for DCI following aSAH.

PMID: 28254540 [PubMed - as supplied by publisher]

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