Efficacy of Cilostazol in Prevention of Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage: A Meta-Analysis

Saber, Hamidreza; Desai, Aaron; Palla, Mohan; Mohamed, Wazim; Seraji‐Bozorgzad, Navid; Ibrahim, Mohammed

doi:10.1016/j.jstrokecerebrovasdis.2018.06.027

Cited by 44 publications

(24 citation statements)

References 20 publications

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“…Hemoglobin and its breakdown products after SAH have been demonstrated to disrupt NO signaling between the endothelium and underlying smooth muscle [13,14]. However, though narrowing of large vessel diameter has a major role in delayed ischemic injury, recent studies proposed alternative mechanisms such as early brain injury (EBI), loss of autoregulation of cerebral microcirculation and microthrombosis [15]. EBI term has been defined as the period from the onset of hemorrhage to the beginning of vasospasm suggesting that EBI also may be one of the precipitating events that eventually lead to vasospasm [16].…”

Section: Discussionmentioning

confidence: 99%

The effect of pentoxifylline on cerebral vasospasm following experimental subarachnoid hemorrhage

Bahadır

Narin

Başar

et al. 2020

International Journal of Neuroscience

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Objects: Cerebral vasospasm is an important event that occurs following subarachnoid hemorage which has significant mortality and morbidity. The goal in this study was to investigate the effect of pentoxifylline on vasospasm in an experimental subarachnoid hemorrhage model. Methods: In this study, 20 male New Zeland White rabbits weighing 3000-3500 g were assigned randomly to four groups. Animals in group 1 served as controls. Animals in group two received only intravenous pentoxifylline injection 3 times in 12 h intervals. In group 3, SAH was induced and no injection was given. Animals in group 4 received intravenous pentoxifylline (6 mg/kg) injections 3 times at 12 th , 24 th and 36 th hours after subarachnoid hemorrhage induction. All animals were sacrificed and basilar arteries were removed at 48th hour. Basilar artery vessel diameters, wall thicknesses and luminal section areas were measured with Spot for Windows version 4.1. Statistical analysis was performed using ANOVA and Kruskall-Wallis tests. Results: Mean basilar artery luminal section areas and luminal diameters in group 4 were significantly higher compared to group 3 (p < 0.05). Basilar artery wall thicknesses and were found to be higher in group 3 than in other groups and this was also statistically significant (p < 0.05). Conclusion: Our study demonstrated that intravenous administration of pentoxifylline significantly decreases vasospasm after subarachnoid hemorrhage.

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Section: Discussionmentioning

confidence: 99%

The effect of pentoxifylline on cerebral vasospasm following experimental subarachnoid hemorrhage

Bahadır

Narin

Başar

et al. 2020

International Journal of Neuroscience

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“…After coiling, combination antiplatelet therapy with aspirin, which is selected to prevent thrombus formation, and cilostazol, which is selected to prevent the development of cerebral vasospasm, is performed. 13,14) These drugs may have inhibited platelet aggregation, reducing the appearance of cerebral-vasospasm-related symptoms or incidence of cerebral infarction. Comparing patients before and after January 2011, when the oral administration of cilostazol was started, the incidence of AV was lower in a group treated with cilostazol after January 2011.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vasospasm and Patient Outcome after Coiling or Clipping for Intracranial Aneurysmal Subarachnoid Hemorrhage

Shimoda

Kamiya

Kano

et al. 2019

JNET

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It is still controversial whether coiling or clipping has a lower incidence of cerebral vasospasm following an aneurysmal subarachnoid hemorrhage (SAH). In this study, we compared angiographic vasospasm (AV), symptomatic vasospasm (SV), and the outcome of both procedures for ruptured cerebral aneurysms. Methods: From 2007 to 2018, 127 patients were coiled and 127 were clipped for ruptured cerebral aneurysms. We retrospectively reviewed AV, SV, and the outcome of both procedures. Results: The incidence of AV was 32 (25%) patients for coiling and 59 (46%) patients for clipping. SV occurred in eight (6%) patients for coiling and 19 (15%) patients for clipping, and was significantly less in the coiling group. A favorable outcome (modified Rankin scale [mRS] 0-2 on discharge) was in 71 (56%) patients for coiling and 77 (61%) patients for clipping, and there was no significant difference between the two groups. Conclusion: The incidence of SV was significantly less in the coiling group for ruptured cerebral aneurysms. Even if SV occurred following aneurysmal SAH, early therapeutic intervention may prevent deterioration of the outcome. Keywords▶ coil embolization, symptomatic vasospasm, aneurysmal subarachnoid hemorrhage This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives International License.

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“…Three additional RCTs have examined the efficacy of cilostazol in the prevention of DCI in SAH patients, 79–81 and a meta-analysis by Saber et al. summarizing all five RCTs has shown positive results for cilostazol against DCI, 82 though no definitive evidence for improve in long-term neurological outcome currently exists. While these RCTs do not specifically show benefit against microvascular thrombi, the mechanism of action of cilostazol suggests this may be one of its therapeutic properties.…”

Section: Therapies Targeting Sah-induced Microvascular Platelet Aggrementioning

confidence: 99%

Microvascular platelet aggregation and thrombosis after subarachnoid hemorrhage: A review and synthesis

Clarke

Suggs

Diwan

et al. 2020

J Cereb Blood Flow Metab

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Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) has been associated with numerous pathophysiological sequelae, including large artery vasospasm and microvascular thrombosis. The focus of this review is to provide an overview of experimental animal model studies and human autopsy studies that explore the temporal-spatial characterization and mechanism of microvascular platelet aggregation and thrombosis following SAH, as well as to critically assess experimental studies and clinical trials highlighting preventative therapeutic options against this highly morbid pathophysiological process. Upon review of the literature, we discovered that microvascular platelet aggregation and thrombosis occur after experimental SAH across multiple species and SAH induction techniques in a similar time frame to other components of DCI, occurring in the cerebral cortex and hippocampus across both hemispheres. We discuss the relationship of these findings to human autopsy studies. In the final section of this review, we highlight the important therapeutic options for targeting microvascular platelet aggregation and thrombosis, and emphasize why therapeutic targeting of this neurovascular pathology may improve patient care. We encourage ongoing research into the pathophysiology of SAH and DCI, especially in regard to microvascular platelet aggregation and thrombosis and the translation to randomized clinical trials.

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Efficacy of Cilostazol in Prevention of Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage: A Meta-Analysis

Cited by 44 publications

References 20 publications

The effect of pentoxifylline on cerebral vasospasm following experimental subarachnoid hemorrhage

The effect of pentoxifylline on cerebral vasospasm following experimental subarachnoid hemorrhage

Cerebral Vasospasm and Patient Outcome after Coiling or Clipping for Intracranial Aneurysmal Subarachnoid Hemorrhage

Microvascular platelet aggregation and thrombosis after subarachnoid hemorrhage: A review and synthesis

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