The association of the Glu298Asp polymorphism of endothelial nitric oxide synthase (eNOS) with outcome after subarachnoid hemorrhage
نویسنده
چکیده
Subarachnoid hemorrhage (SAH) accounts for 25% of all cerebrovascular deaths. Mortality rates after SAH have been reported to be as high as 50%; among the remaining survivors, 50% are left severely disabled. Morbidity and mortality are largely due to rebleeding and vasospasm. Currently, prediction of outcome relies on demographic, clinical, and radiological factors. Yet, accurate prediction of outcome after SAH remains imprecise. Prior studies examining prognostic factors have found that the amount of hemorrhage, clinical grade (Hunt & Hess or WFNS), age, preexisting hypertension, aneurysm size and location, and vasospasm all contribute to poor outcome. Delayed ischemic neurological deficit (DIND) due to the reduction in cerebral blood flow from vessel narrowing in cerebral vasospasm is one of the most serious consequences of SAH. The incidence of angiographic vasospasm can be in excess of 50%, with symptomatic vasospasm occurring in 30% of patients. Predicting the neurological decline of a patient with vasospasm can be difficult, as not every patient with vasospasm becomes clinically symptomatic. However, early detection of vasospasm is essential to ensure rapid treatment before ischemic damage occurs whether patients are symptomatic or not. Considerable research effort has been directed toward demonstrating both the mechanisms and potential predictors of delayed cerebral vasospasm following SAH. The mechanism of vasospasm has not been completely elucidated and multiple factors are likely to play a role. Free radical reactions triggered by oxyhemoglobin released from the subarachnoid clot are considered to be important in the development of cerebral vasospasm. Oxyhemoglobin scavenges nitric oxide after SAH creating a deficit of NO and an imbalance between vasodilatory and vasocontrictive factors. Prior studies have helped to demonstrate the important role of NO in vasospasm. Animal studies have shown that NO replacement reverses cerebral vasospasm. 9 Further, an intracellular NO donor, hydroxylamine, attenuated post-SAH neurological deficit in a rat model of SAH.
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