1. ¹Department of Neurological Surgery, Columbia University, New York, New York, USA
2. ²Department of Genetics, Columbia Genome Center, Columbia University, New York, New York, USA
3. ³Department of Genetics, Epidemiology and Public Health, Albert Einstein Medical College, Bronx, New York, USA
4. ⁴Department of Neurology, Columbia University, New York, New York, USA

Correspondence: Dr RJ Komotar, Department of Neurological Surgery, Columbia University, 710 West 168th Street, Room 431, New York, NY 10032, USA. E-mail: rjk2103@columbia.edu

⁵These authors contributed equally to this work.

Received 7 January 2008; Revised 28 January 2008; Accepted 3 February 2008; Published online 5 March 2008.

Abstract

Vasospasm is a major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). Studies have shown a link between single-nucleotide polymorphisms (SNPs) in the endothelial nitric oxide synthase (eNOS) gene and the incidence of coronary spasm and aneurysms. Alterations in the eNOS T-786 SNP may lead to an increased risk of post-aSAH cerebral vasospasm. In this prospective clinical study, 77 aSAH patients provided genetic material and were followed for the occurrence of vasospasm. In multivariate logistic regression analysis, genotype was the only factor predictive of vasospasm. The odds ratio (OR) for symptomatic vasospasm in patients with one T allele was 3.3 (95% confidence interval (CI): 1.1 to 10.0, P=0.034) and 10.9 for TT. Patients with angiographic spasm were 3.6 times more likely to have a T allele (95% CI: 1.3 to 9.6, P=0.013; for TT: OR 12.6). Patients with severe vasospasm requiring endovascular therapy were more likely to have a T allele (OR 3.5, 95% CI: 1.3 to 9.5, P=0.016; for TT: OR 12.0). Patients with the T allele of the eNOS gene are more likely to have severe vasospasm. Presence of this genotype may allow the identification of individuals at high risk for post-aSAH vasospasm and lead to early treatment and improved outcome.