Update on Evidence for a Genetic Predisposition to Cerebral Vasospasm
Update on Evidence for a Genetic Predisposition to Cerebral Vasospasm
Considerable evidence links cerebral vasospasm to the decreased bioavailability of endothelial nitric oxide synthase (eNOS) after aneurysmal subarachnoid hemorrhage (SAH). In recent studies from the cardiology literature, researchers have suggested that a genetic predisposition to coronary vasospasm might develop as the result of a T-786C single nu cleotide polymorphism (SNP) in the eNOS gene. The authors of this study attempted to determine if there may be a si milar genetic predisposition toward cerebral vasospasm.
The authors prospectively identified 28 patients with Fisher Grade 3 SAH from a group of 51 consecutive patients with ruptured intracranial saccular aneurysms. Genomic DNA was isolated from a peripheral blood sample obtained with permission from each patient. Gene microarray technology was used to assay the samples for the presence and dis tribution of certain key eNOS gene polymorphisms. Clinical, radiological, and genomic data were analyzed. The finding of eNOS T-786C SNP could be used to significantly differentiate between the presence and severity of cerebral vasospasm (p = 0.04).
The findings from this preliminary study support similar findings in the coronary vasospasm literature as well as the hy pothesis that a predisposition toward cerebral vasospasm may be related partially to genetic factors, which needs to be confirmed in a larger study. Such gene-based information may be important in rapidly identifying patients at in creased risk of vasospasm after SAH, independent of their Fisher grade. In this article, the authors review key studies in this area.
The only accepted predictor for the occurrence of ce rebral vasospasm after SAH is the amount of subarachnoid blood detected on head CT scans, which is classified as Fisher Grades 1 through 4. Anecdotally, however, the occurrence and neurological effects of vaso spasm have been found to vary markedly, even among patients with the same Fisher grade. Such observations raise the possibility that genes encoding key proteins im pli cated in cerebrovascular regulation may exhibit functionally significant variations that can account for individual differences in vasomotor integrity after aneurysmal rupture. That is, the possibility exists for a genetic susceptibility to cerebral vasospasm. This article is intended as an update on the evolving evidence supporting such a possibility.
Abstract and Introduction
Abstract
Considerable evidence links cerebral vasospasm to the decreased bioavailability of endothelial nitric oxide synthase (eNOS) after aneurysmal subarachnoid hemorrhage (SAH). In recent studies from the cardiology literature, researchers have suggested that a genetic predisposition to coronary vasospasm might develop as the result of a T-786C single nu cleotide polymorphism (SNP) in the eNOS gene. The authors of this study attempted to determine if there may be a si milar genetic predisposition toward cerebral vasospasm.
The authors prospectively identified 28 patients with Fisher Grade 3 SAH from a group of 51 consecutive patients with ruptured intracranial saccular aneurysms. Genomic DNA was isolated from a peripheral blood sample obtained with permission from each patient. Gene microarray technology was used to assay the samples for the presence and dis tribution of certain key eNOS gene polymorphisms. Clinical, radiological, and genomic data were analyzed. The finding of eNOS T-786C SNP could be used to significantly differentiate between the presence and severity of cerebral vasospasm (p = 0.04).
The findings from this preliminary study support similar findings in the coronary vasospasm literature as well as the hy pothesis that a predisposition toward cerebral vasospasm may be related partially to genetic factors, which needs to be confirmed in a larger study. Such gene-based information may be important in rapidly identifying patients at in creased risk of vasospasm after SAH, independent of their Fisher grade. In this article, the authors review key studies in this area.
Introduction
The only accepted predictor for the occurrence of ce rebral vasospasm after SAH is the amount of subarachnoid blood detected on head CT scans, which is classified as Fisher Grades 1 through 4. Anecdotally, however, the occurrence and neurological effects of vaso spasm have been found to vary markedly, even among patients with the same Fisher grade. Such observations raise the possibility that genes encoding key proteins im pli cated in cerebrovascular regulation may exhibit functionally significant variations that can account for individual differences in vasomotor integrity after aneurysmal rupture. That is, the possibility exists for a genetic susceptibility to cerebral vasospasm. This article is intended as an update on the evolving evidence supporting such a possibility.
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