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SIRT1 Activation: A Potential Strategy for Harnessing Endogenous Protection Against Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.

Ananth K. Vellimana,Deepti Diwan,Julian V. Clarke,J. Gidday,G. Zipfel

Published 2018 in Neurosurgery

ABSTRACT

Aneurysmal subarachnoid hemorrhage (SAH) affects nearly 30 000 Americans every year and survivors experience significant morbidity, with nearly a third of them becoming functionally dependent. The 2 principal contributors to poor outcome after SAH are early brain injury (EBI) and delayed cerebral ischemia (DCI). EBI is initiated by the acute increase in intracranial pressure and consequent transient global cerebral ischemia that occurs after aneurysm rupture, and typically manifests in the first 72 h after ictus.1 EBI is characterized by neuroinflammation, blood–brain barrier (BBB) breakdown, cerebral edema, and early neuronal cell death. DCI is multifactorial in etiology with large artery vasospasm being the primary contributor and other pathophysiological events including microvessel autoregulatory dysfunction, microvessel thrombosis, and neuroinflammation being significant contributors.2-5 DCI typically occurs 4 to 14 d after ictus, and is characterized by delayed neurological decline with or without radiographic evidence of cerebral infarction.5 Due to the stereotypical delay between ictus and DCI, a window of opportunity exists to institute a therapeutic intervention that can ameliorate the effects of DCI, or even prevent the occurrence of DCI. Given the multifactorial etiology of DCI, a therapeutic strategy that influences several of

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