Effect of cilostazol in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis

Niu, Peng-Peng; Yang, Ge; Xing, Yingqi; Guo, Zhen‐Ni; Yang, Yi

doi:10.1016/j.jns.2013.10.027

Cited by 40 publications

(19 citation statements)

References 21 publications

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“…The second study showed a reduction in the risk of vasospasm and cerebral infarction, without improvements in outcome 186. In a meta-analysis, which additionally included two non-RCT, a benefit on outcome at discharge was demonstrated (also when the non-RCT studies were excluded) 187. Importantly, only one study reported long-term outcomes, which did not differ between groups 186…”

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

225

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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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

225

189

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“…Recent experimental studies showed simvastatin and mutant thrombin-activated urokinase-type plasminogen activator are effective in reducing microthrombi [65, 66]. Recent clinical studies have also indicated that cilostazol, which is a selective inhibitor of phosphodiesterase 3, an antiplatelet agent marketed in Japan, and which is used to treat ischemic symptoms of peripheral vascular disease, can decrease the incidence of symptomatic vasospasm, severe angiographic vasospasm, vasospasm-related new cerebral infarctions, and poor outcome in patients with aneurysmal SAH [83–85]. …”

Section: Microthrombosismentioning

confidence: 99%

The Role of Arterioles and the Microcirculation in the Development of Vasospasm after Aneurysmal SAH

Naraoka

Matsuda

Shimamura

et al. 2014

BioMed Research International

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Cerebral vasospasm of the major cerebral arteries, which is characterized by angiographic narrowing of those vessels, had been recognized as a main contributor to delayed cerebral ischemia (DCI) in subarachnoid hemorrhage (SAH) patients. However, the CONSCIOUS-1 trial revealed that clazosentan could not improve mortality or clinical outcome in spite of successful reduction of relative risk in angiographic vasospasm. This result indicates that the pathophysiology underlying DCI is multifactorial and that other pathophysiological factors, which are independent of angiographic vasospasm, can contribute to the outcome. Recent studies have focused on microcirculatory disturbance, such as microthrombosis and arteriolar constriction, as a factor affecting cerebral ischemia after SAH. Reports detecting microthrombosis and arteriolar constriction will be reviewed, and the role of the microcirculation on cerebral ischemia during vasospasm after SAH will be discussed.

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“…Selective phophodiesterase 3 inhibitors, such as cilostazol and milrinone, offer promise in the prevention of cerebral vasospasm after SAH because of their direct vasodilation and anti-inflammatory effects. Results of a recent meta-analysis demonstrated that cilostazol is effective in decreasing the incidence of symptomatic cerebral vasospasm, severe cerebral vasospasm, and cerebral vasospasm-related new cerebral infarctions after SAH [19 ▪▪ ]. Similarly, continuous infusion of milrinone significantly improved global cerebral oxygenation, and reduced the incidence of cerebral vasospasm during the critical 4 to 11 day postoperative period following cerebral aneurysm clipping surgery [20].…”

Section: Improving Neurological Outcomes After Subarachnoid Hemorrhagementioning

confidence: 99%

Postoperative ICU management of patients after subarachnoid hemorrhage

Gruenbaum

Bilotta²

2014

Current Opinion in Anaesthesiology

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Purpose of review This article reviews recent advances in the postoperative ICU management of patients after subarachnoid hemorrhage (SAH), especially with regards to hemodynamic management, methods of improving neurological outcomes, and management of cardiac and pulmonary complications. Recent findings Several hemodynamic monitors and parameters may be useful for guiding volume therapy, including cardiac output, stroke volume variation monitoring, and global end-diastolic volume index. Early goal-directed hemodynamic therapy after SAH has recently been shown to improve clinical outcomes in patients with a poor clinical grade or coexisting cardiopulmonary complications. Recent laboratory and imaging modalities are being developed to identify patients at risk for developing vasospasm after SAH. Evidence for the use of various prophylactic adjuvant therapies to prevent vasospasm, including magnesium, phosphodiesterase 3 inhibitors, and therapeutic hypothermia, is emerging. Intrathecal administration of vasodilators or fibrinolytics may have offered advantages over systemic drug administration in the treatment of vasospasm. Pulmonary and cardiac complications are common after SAH, and are associated with an increased risk of mortality. Summary The postoperative ICU period after SAH is associated with a significant morbidity and mortality risk, and recent studies have greatly contributed to our understanding of how to optimally manage these patients.

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Effect of cilostazol in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis

Cited by 40 publications

References 21 publications

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

The Role of Arterioles and the Microcirculation in the Development of Vasospasm after Aneurysmal SAH

Postoperative ICU management of patients after subarachnoid hemorrhage

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