***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background and Purpose — The long-st and ing concept that delayed cerebral infa rct ion after aneurysmal subarachnoid hemorrhage results exclusively from large artery vasospasm recently has been challenged . We used data from the CONSCIOUS-1 trial to determine the relationship between angiographic vasospasm and cerebral infa rct ion after subarachnoid hemorrhage . Methods — We performed a post hoc exploratory analysis of the CONSCIOUS-1 data . All patients underwent catheter angiography before treatment and 9±2 days after subarachnoid hemorrhage . CT was performed before and after aneurysm treatment , and 6 weeks after subarachnoid hemorrhage . Angiograms and CT scans were assessed by central ized blinded review . Angiographic vasospasm was classified as none/mild ( 0%–33 % decrease in arterial diameter ) , moderate ( 34%–66 % ) , or severe ( ≥67 % ) . Infa rct ions were categorized as secondary to angiographic vasospasm , other , or unknown causes . Logistic regression was conducted to determine factors associated with infa rct ion . Results — Complete data were available for 381 of 413 patients ( 92 % ) . Angiographic vasospasm was none/mild in 209 ( 55 % ) patients , moderate in 118 ( 31 % ) , and severe in 54 ( 14 % ) . Infa rcts developed in 6 ( 3 % ) of 209 with no/mild , 12 ( 10 % ) of 118 patients with moderate , and 25 ( 46 % ) of 54 patients with severe vasospasm . Multivariate analysis found a strong association between angiographic vasospasm and cerebral infa rct ion ( OR , 9.3 ; 95 % CI , 3.7–23.4 ) . The significant association persisted after adjusting for admission neurological grade and aneurysm size . Method of aneurysm treatment was not associated with a significant difference in frequency of infa rct ion . Conclusions — A strong association exists between angiographic vasospasm and cerebral infa rct ion . Efforts directed at further reducing angiographic vasospasm are warranted Background : Several clinical studies have indicated the efficacy of cilostazol , a selective inhibitor of phosphodiesterase 3 , in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage ( SAH ) . They were not double-blinded trial result ing in disunited results on assessment of end points among the studies . The r and omized , double-blind , placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm . Methods : Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study : SAH on CT scan was diffuse thick , diffuse thin , or local thick , Hunt and Hess score was less than 4 , administration of cilostazol or placebo could be started within 48 h of SAH . Patients were r and omly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling , and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment . The primary end point was the occurrence of symptomatic vasospasm ( sVS ) , and secondary end points were angiographic vasospasm ( aVS ) evaluated on digital subtraction angiography , vasospasm-related new cerebral infa rct ion evaluated on CT scan or MRI , and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale , in which poor outcome was defined as severe disability , vegetative state , and death . All end points were evaluated with blinded assessment . Results : One hundred forty eight patients were r and omly allocated to the cilostazol group ( n = 74 ) or the control group ( n = 74 ) . The occurrence of sVS was significantly lower in the cilostazol group than in the control group ( 10.8 vs. 24.3 % , p = 0.031 ) , and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS ( OR 0.293 , 95 % CI 0.099 - 0.568 , p = 0.027 ) . The incidence of aVS and vasospasm-related cerebral infa rct ion were not significantly different between the groups . Poor outcome was significantly lower in the cilostazol group than in the control group ( 5.4 vs. 17.6 % , p = 0.011 ) , and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome ( OR 0.221 , 95 % CI 0.054 - 0.903 , p = 0.035 ) . Severe adverse events due to cilostazol administration did not occur during the study period . Conclusions : Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events . A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol OBJECTIVE Cerebral infa rct ion would be expected to be associated with poor outcome after aneurysmal subarachnoid hemorrhage ( SAH ) , although there are few data on which to base this assumption . The goals of this study were to determine the impact of cerebral infa rct ion on outcome and to examine predictors of infa rct ion in these patients . METHODS Univariate and multivariable statistical methods were used to examine the impact of cerebral infa rct ion on the Glasgow Outcome Scale score 3 months after SAH among 3567 patients entered into four prospect i ve , r and omized , double-blind , placebo-controlled trials of tirilazad conducted in neurosurgical centers around the world between 1991 and 1997 . Patient demographics , clinical variables , radiographic characteristics , and treatment variables associated with cerebral infa rct ion were also determined by the same methods . RESULTS Seven hundred and seven ( 26 % ) out of 2741 patients with complete data had cerebral infa rct ion on computed tomographic scans 6 weeks after SAH . Multivariable logistic regression showed that cerebral infa rct ion increased the odds of unfavorable outcome by a factor of 5.4 ( adjusted odds ratio , 5.4 ; 95 % confidence interval , 4.2–6.8 ; P < 0.0001 ) , which was a higher odds ratio than all other factors associated with outcome . The proportion of explained variance in outcome was also highest for cerebral infa rct ion and accounted for 39 % of the explained variance . Multivariable analysis found that cerebral infa rct ion was significantly associated with increasing patient age , worse neurological grade on admission , history of hypertension or diabetes mellitus , larger aneurysm , use of prophylactically or therapeutically induced hypertension , temperature more than 38 ° C 8 days after SAH , and symptomatic vasospasm . CONCLUSION Cerebral infa rct ion was strongly associated with poor outcome after aneurysmal SAH . The most important potentially treatable factor associated with infa rct ion was symptomatic vasospasm OBJECTIVE In order to prevent cerebral vasospasm ( VS ) following aneurysmal subarachnoid hemorrhage ( SAH ) , we introduced combined enteral nutrition ( EN ) and parenteral nutrition ( PN ) with oral cilostazol administration to the postoperative patient after SAH and investigated the effect on VS . METHODS After aneurysmal SAH , 130 postoperative patients were enrolled in this study between April 2008 and March 2012 . The patients enrolled before April 2010 were treated by conventional therapy ( control group ) . The patients enrolled after April 2010 were administrated cilostazol 200 mg/day and received EN and PN simultaneously ( combined group ) . RESULTS The combined group consisted of 62 patients and the control group of 68 patients .  Angiographic VS occurred in 33.9 % ( n = 21 ) of the combined group and in 51.5 % ( n = 35 ) of the control group ( p = 0.051 , Fisher exact test ) . The incidence of symptomatic VS was significantly lower in the combined group ( p = 0.001 ) . The incidence of new cerebral infa rct ions was also significantly lower in the combined group ( p = 0.0006 ) . Clinical outcome at discharge was also significantly better in the combined group than in control group ( p = 0.031 ) . CONCLUSIONS Cilostazol administration with combination EN and PN is remarkably effective in preventing cerebral VS after aneurysmal SAH Background : Cerebral vasospasm ( VS ) is the most common cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage ( SAH ) . Reversal of VS by intra-arterial infusion of cyclic adenosine monophosphate (cAMP)-elevating agents has been reported ; however , the preventive role in the development of VS is not fully understood . This study is design ed to evaluate the possible efficacy of using cilostazol , a selective inhibitor of phosphodiesterase type 3 and a cAMP-elevating agent , in patients with SAH . Methods : In this prospect i ve r and omized study , we enrolled 100 SAH patients who met the following criteria : neck clipping within 72 h after onset , Hunt and Hess ( HH ) score ≤4 , modified Rankin scale ( mRS ) score ≤2 prior to ictus , and no serious cardiovascular complications . Patients were divided into control and cilostazol groups ; we focused on the effects of cilostazol on the decrease in the incidence of symptomatic VS , cerebral infa rct ion , and the mRS score at discharge . Result : Patients ’ age , male/female ratio , mRS score prior to ictus , HH grade , Fisher group , site of the aneurysm , drugs prescribed during the observation period , and length of hospital stay were not different between the groups . Cilostazol did not significantly decrease the incidence of symptomatic VS ( 37.3 % in the control vs. 22.4 % in the cilostazol group , p = 0.183 ) and cerebral infa rct ion ( 27.5 % in control vs. 10.2 % in the cilostazol , p = 0.091 ) . However , mRS score was significantly improved at discharge ( 2.6 in controls vs. 1.5 in the cilostazol group , p = 0.041 ) . Patients ’ age being ≤65 years ( OR = 8.47 , 95 % CI = 2.45–29.32 , p = 0.0007 ) , Fisher group ≤3 ( OR = 4.64 , 95 % CI = 1.00–21.45 , p = 0.049 ) , HH grade ≤2 ( OR = 4.31 , 95 % CI = 1.27–14.59 , p = 0.019 ) , no hydrocephalus ( OR = 8.55 , 95 % CI = 1.72–19.23 , p = 0.0046 ) , and cilostazol use ( OR = 5.52 , 95 % CI = 1.61–18.90 , p = 0.0065 ) were independent predictors of good outcomes ( mRS score ≤2 ) . Conclusion : Cilostazol may improve outcomes after SAH , but further double-blind , placebo-controlled studies are required for a definitive conclusion BACKGROUND Most patients who have had a stroke are given aspirin ; however , aspirin-related cerebral haemorrhage is a complication that is currently of concern , particularly in China where there is a high incidence of cerebral haemorrhage in secondary prevention programmes and within the community . Cilostazol , a phosphodiesterase 3 ( PDE3 ) inhibitor , is an alternative to aspirin that works through a different mechanism . This trial aim ed to compare the efficacy and safety of cilostazol with that of aspirin for the long-term prevention of the recurrence of ischaemic stroke . METHODS 720 patients ( mean age 60.2 years , SD 9.86 ) who had had an ischaemic stroke within the previous 1 - 6 months were enrolled consecutively in a prospect i ve , multicentre , double-blind , r and omised trial . 360 patients were r and omly assigned to receive cilostazol and 360 patients to receive aspirin .  Analysis was by intention to treat . Patients in both groups took the medication for 12 - 18 months . The primary endpoint was any recurrence of stroke ( ischaemic stroke , haemorrhagic stroke , or subarachnoid haemorrhage ) during the trial period . All patients had MRI with T1 MRI , T2 MRI , diffusion-weighted imaging ( DWI ) , T2 fluid-attenuated inversion recovery ( FLAIR ) , and T2 gradient echo imaging ( T2 * ) at the beginning and the end of the study . This trial is registered with Clinical Trials.gov , number NCT00202020 . FINDINGS The average duration of treatment was 740 person-years , and 719 patients were analysed ( 360 in the cilostazol group and 359 in the aspirin group ) . The primary endpoint was reported in 12 patients in the cilost 
    Output:
    
Under the prescribed dosage , complication was few and non-lethal .
Conclusions Cilostazol was effective and safe to reduce incidences of severe angiographic vasospasm , symptomatic vasospasm , new cerebral infa rct ion and poor outcome in patients after aneurysmal subarachnoid hemorrhage .