Statin Treatment of Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Trimble, Jason L; Kockler, Denise R

doi:10.1345/aph.1k301

Cited by 17 publications

(10 citation statements)

References 19 publications

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“…Thus, statin treatment in the acute phase of SAH has come to the forefront of prevention of cerebral vasospasm [124], although systematic analysis of acute treatment with statin before 2010 did not lend statistically significant support to the idea that statins have a beneficial effect in preventing DCI or improving the outcomes of SAH patients [125]. …”

Section: The Efficacy Of Other Rho-rock Pathway Inhibitors In the Prementioning

confidence: 99%

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Yanamoto¹,

Kataoka

Nakajo

et al. 2012

Eur Neurol

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Similar to atherosclerosis, platelet-derived growth factor (PDGF)-BB, a major growth factor for vascular smooth muscle cells, is produced in arterial walls to repair arteries after subarachnoid hemorrhage (SAH). On review of a series of research articles that focus on defensive host responses to SAH, PDGF-BB is identified as a spasmogen, based on the following findings: (1) foreign substances injected into the subarachnoid space cause persistent constriction of cerebral arteries with a time course and histological features almost identical to those seen after SAH; (2) persistent constriction induced by SAH or a foreign substance is dependent on the complement system; (3) the complement system, which stimulates platelets, macrophages and endothelial cells to secrete PDGF-BB, is activated in both the cerebrospinal fluid (CSF) and plasma immediately after SAH; (4) PDGF-BB levels in the CSF are significantly elevated in patients with delayed cerebral ischemia; (5) the immunodensity of PDGF-BB in the arterial walls correlates well with the severity of cerebral vasospasm; (6) intracisternal injection of PDGF-BB induces persistent constriction of cerebral arteries in a dose-dependent manner; (7) prolonged contact with blood clots promotes the contractile response of cerebral arteries to PDGF-BB, and (8) administration of an antagonist of PDGF-BB function suppresses the development of cerebral vasospasm.

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Section: The Efficacy Of Other Rho-rock Pathway Inhibitors In the Prementioning

confidence: 99%

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Yanamoto¹,

Kataoka

Nakajo

et al. 2012

Eur Neurol

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“…Vasospasm has been the focus of the majority of experimental and clinical research efforts during the past number of decades. Several types of treatment strategies such as circulatory volume expansion, statins, and magnesium sulfate and calcium antagonists have been studied in clinical trials to prevent or reverse vasospasm (12,34,36,43). Based on the current evidence, only oral nimodipine is recommended as a standard treatment in patients with aneurysmal SAH (34).…”

Section: Introductionmentioning

confidence: 99%

Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Yuksel

Tosun²,

Cahill³

et al. 2012

Turkish Neurosurgery

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Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex clinical disease with high mortality and morbidity. Recent studies suggest that early brain injury (EBI) rather than vasospasm might be responsible for morbidity and mortality within 24-72 hours after SAH. The rise in intracranial pressure following SAH causes a significant drop in cerebral perfusion pressure that leads to global cerebral ischemia and initiates the acute injury cascade. Various molecular mechanisms have been shown to involve in the pathophysiology of EBI including cellular apoptosis. In this review, we summarize apoptotic molecular mechanisms involved in the etiology of EBI and its potential as a target for future therapeutic intervention.KeywoRds: Apoptosis, Early brain injury, p53, Stroke, Subarachnoid hemorrhage ÖZIntrakraniyal anevrizma rüptürüne bağlı gelişen subaraknoid kanama (SAK), yüksek mortalite ve morbidite ile seyreden kompleks bir hastalıktır. Yakın zamanda yapılan çalışmalar SAK sonrası 24-72. saatler içinde gelişen morbidite ve mortaliteden vazospasmdan ziyade, erken beyin hasarının sorunlu olduğunu ileri sürmüştür. SAK sonrasında gelişen intrakraniyal basınç artışı, serebral perfüzyon basıncında ciddi düşüşe neden olup global serebral iskemi ile sonuçlanır ve akut hasar kaskadını başlatır. Hücresel apopitoz dahil pek çok moleküler mekanizmanın erken beyin hasarının (EBH) patofizyolojisinde rol oynadığı gösterilmiştir. Bu derlemede; EBH etiyolojisinde rol alan apopitotik mekanizmalar ve bunların gelecekte potansiyel tedavi hedefi olarak önemleri özetlenmiştir.

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“…However, other known agents, such as tacrolimus, an inhibitor of T-cell maturation similar to Cys-A, have not shown similar results [102]. There are also studies implicating the complement system, the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase pathway, and multiple other systems; however, results even in the experimental stages have been varied [103–106]. …”

Section: Cvs and Inflammationmentioning

confidence: 99%

Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia

Carr

Zuckerman

Mocco

2013

Neurology Research International

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Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets.

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Statin Treatment of Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Abstract: Current data suggest that statins may be a reasonable treatment option for the prevention and management of cerebral vasospasm after aSAH. However, results from large, well-controlled trials have not been published.

Cited by 17 publications

References 19 publications

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia

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