Systematic assessment and meta-analysis of the efficacy and safety of fasudil in the treatment of cerebral vasospasm in patients with subarachnoid hemorrhage

Liu, Guang Jian; Wang, Zheng Jun; Wang, Yun Fu; Xu, Lijun; Wang, Xiao Ling; Liu, Yong; Luo, Guo Jun; He, Guo Hou; Zeng, Yan

doi:10.1007/s00228-011-1100-x

Cited by 71 publications

(41 citation statements)

References 21 publications

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“…103 Fasudil was studied in eight randomized clinical trials that included 843 patients (386 exposed to the drug). 104 Treatment significantly reduced the incidence of angiographic vasospasm and cerebral infarction, and improved the odds ratio for good recovery compared with placebo or nimodipine and other drugs (OR 1.58, 95% CI 1.12-2.23). Limitations of the studies included outcome assessment very early after SAH, small sample sizes, and concomitant use of other medications such as steroids and ozagrel.…”

Section: Clinical Trialsmentioning

confidence: 94%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

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Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) that is mediated by effects of transient cerebral ischaemia during bleeding plus effects of the subarachnoid blood. Secondary effects of SAH include increased intracranial pressure, destruction of brain tissue by intracerebral haemorrhage, brain shift, and herniation, all of which contribute to pathology. Many patients survive these phenomena, but deteriorate days later from delayed cerebral ischaemia (DCI), which causes poor outcome or death in up to 30% of patients with SAH. DCI is thought to be caused by the combined effects of angiographic vasospasm, arteriolar constriction and thrombosis, cortical spreading ischaemia, and processes triggered by EBI. Treatment for DCI includes prophylactic administration of nimodipine, and current neurointensive care. Prompt recognition of DCI and immediate treatment by means of induced hypertension and balloon or pharmacological angioplasty are considered important by many physicians, although the evidence to support such approaches is limited. This Review summarizes the pathophysiology of DCI after SAH and discusses established treatments for this condition. Novel strategies--including drugs such as statins, sodium nitrite, albumin, dantrolene, cilostazol, and intracranial delivery of nimodipine or magnesium--are also discussed.

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Section: Clinical Trialsmentioning

confidence: 94%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

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“…Fasudil is a potent RhoA/Rho kinase (ROCK) inhibitor, which is also thought to inhibit the action of free intracellular calcium, as well as inhibit protein kinases A, G and C, and myosin light-chain directly. Fasudil has been repeatedly shown to have beneficial effects on development of CVS, delayed cerebral infarcts as well as outcome 181. Furthermore, fasudil has been compared with nimodipine (although intravenous rather than oral) demonstrating improved outcome 182.…”

Section: Treatment Of DCImentioning

confidence: 99%

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

Budohoski

Guilfoyle

Helmy

et al. 2014

J Neurol Neurosurg Psychiatry

226

189

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Cerebral vasospasm has traditionally been regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral infarction and poor neurological outcome. However, data from recent studies argue against a pure focus on vasospasm as the cause of delayed ischaemic complications. Findings that marked reduction in the incidence of vasospasm does not translate to a reduction in DCI, or better outcomes has intensified research into other possible mechanisms which may promote ischaemic complications. Early brain injury and cell death, blood-brain barrier disruption and initiation of an inflammatory cascade, microvascular spasm, microthrombosis, cortical spreading depolarisations and failure of cerebral autoregulation, have all been implicated in the pathophysiology of DCI. This review summarises the current knowledge about the mechanisms underlying the development of DCI. Furthermore, it aims to describe and categorise the known pharmacological treatment options with respect to the presumed mechanism of action and its role in DCI.

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“…Liu Guang Jian et al [29] conducted a systematic assessment and meta-analysis on fasudil, which demonstrated that occurrence of CVS and cerebral infarction was greatly reduced by fasudil in SAH patients, and clinical outcomes of the patients (as assessed by the Glasgow Outcome Scale) were significantly improved. Due to the limited number of samples and trials, the conclusion still requires further verification by large randomized controlled clinical trials.…”

Section: Fasudilmentioning

confidence: 99%

Drug treatment of cerebral vasospasm after subarachnoid hemorrhage following aneurysms

Liu

Qiu

et al. 2016

Chin Neurosurg Jl

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Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS begins most often on the third day after the ictal event and reaches the maximum on the 5th-7th postictal days. Several therapeutic modalities have been employed to prevent or reverse CVS. The aim of this review is to summate all the available drug treatment modalities for vasospasm.

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Systematic assessment and meta-analysis of the efficacy and safety of fasudil in the treatment of cerebral vasospasm in patients with subarachnoid hemorrhage

Cited by 71 publications

References 21 publications

Delayed neurological deterioration after subarachnoid haemorrhage

Delayed neurological deterioration after subarachnoid haemorrhage

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

Drug treatment of cerebral vasospasm after subarachnoid hemorrhage following aneurysms

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