***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 
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    ***EXAMPLES*** 
    Input: The acute administration of atorvastatin has been reported to reduce myocardial infa rct size in animal studies . However , this cardioprotective effect is lost with the chronic administration of atorvastatin , although it can be recaptured by administering an acute high-dose of atorvastatin . We hypothesised that pre-treatment with high-dose atorvastatin , on a background of chronic st and ard ‘ statin ’ therapy , would reduce myocardial injury in patients undergoing elective coronary artery bypass graft ( CABG ) surgery . One hundred and one consenting patients undergoing elective CABG surgery at a single tertiary cardiac centre were recruited into two r and omised controlled , single-blinded clinical studies . Study 1 : 45 patients were r and omised to receive either 160 mg of atorvastatin 2 h preoperatively and 24 h following surgery or their st and ard statin therapy . Study 2 : 56 patients were r and omised to receive either 160 mg of atorvastatin 12 h preoperatively and 24 h following surgery or their st and ard statin therapy .  Blood sample s for troponin T and creatine kinase were taken prior to surgery and then at 6 , 12 , 24 , 48 and 72 h post-surgery . Cardiac enzyme levels at each time point and the total area-under curve ( AUC ) were calculated . The group characteristics and surgical methods were well matched . High-dose atorvastatin was not associated with any significant side effects . There was no significant difference in serum troponin T or creatine kinase in either study at each time point or over 72 h. Study 1 : AUC , troponin T : atorvastatin 29.6 ± 34.8 μg/L versus control 25.0 ± 22.0 μg/L : P > 0.05 . Creatine kinase : atorvastatin 33,544 ± 20,063 IU/L versus control 30,620 ± 10,776 IU/L : P > 0.05 . Study 2 : AUC , troponin T : atorvastatin 21.8 ± 14.3 μg/L versus control 20.9 ± 8.7 μg/L : P > 0.05 . Creatine kinase : atorvastatin 36,262 ± 28,821 IU/L versus control 33,448 ± 14,984:P > 0.05 . There were no differences in postoperative outcomes . We report that the administration of high-dose atorvastatin to low risk patients undergoing elective CABG surgery , who are already on st and ard dose ‘ statin ’ therapy is safe , but does not further reduce perioperative myocardial injury Purpose Statins , 3-hydroxy-3-methylglutaryl coenzyme A ( HMG-CoA ) reductase inhibitors have the potential to reduce acute kidney injury ( AKI ) after cardiac surgery through their pleiotropic properties . Here we studied the preventive effect of atorvastatin on AKI after valvular heart surgery . Methods Two-hundred statin-naïve patients were r and omly allocated to receive either statin or placebo . Atorvastatin was administered orally to the statin group according to a dosage schedule ( 80 mg single dose on the evening prior to surgery ; 40 mg on the morning of surgery ; three further doses of 40 mg on the evenings of postoperative days 0 , 1 , and 2 ) . AKI incidence was assessed during the first 48 postoperative hours on the basis of Acute Kidney Injury Network criteria . Results The incidence of AKI was similar in the statin and control groups ( 21 vs. 26 % , respectively , p = 0.404 ) . Biomarkers of renal injury including plasma neutrophil gelatinase-associated lipocalin and interleukin-18 were also similar between the groups . The statin group required significantly less norepinephrine and vasopressin during surgery , and fewer patients in the statin group required vasopressin . There were no significant differences in postoperative outcomes . Conclusions Acute perioperative statin treatment was not associated with a lower incidence of AKI or improved clinical outcome in patients undergoing valvular heart surgery . ( Clinical Trials.gov NCT01909739 ) BACKGROUND Neutrophils play a central role in systemic inflammatory reaction after cardiopulmonary bypass . Apoptosis is significantly delayed , and this might exacerbate systemic and myocardial damage . We tested the hypothesis of whether pretreatment with simvastatin increases the apoptotic rate of neutrophils and hence reduces the entity of inflammatory reaction . METHODS Thirty patients undergoing coronary surgery with cardiopulmonary bypass were r and omized to treatment with either simvastatin ( 40 mg/day ) or placebo for 3 weeks before surgery . A group of 15 patients undergoing off-pump coronary surgery served as controls . Blood sample s for detection of serum cytokine levels were obtained before anesthesia , at the end of surgery , and at 4 , 24 , 48 , and 72 hours postoperatively . Apoptosis and indices of activation were assessed in cultured neutrophils . RESULTS Simvastatin significantly reduced the postoperative peak values of interleukin (IL)-6 and IL-8 . The neutrophil apoptotic rate was significantly higher among neutrophils obtained from patients pretreated with simvastatin ( p < 0.05 at both 8 and 24 hours ) compared with placebo . Neutrophils from the statin group had depressed functional activity , as underscored by significantly lower values of CD11b ( p < 0.01 at 24 hours ) and a significantly less percentage of cells positive for nitro-blue tetrazolium ( p < 0.01 at 12 and 24 hours ) compared with placebo . CONCLUSIONS This r and omized , double-blind study indicates that statin therapy before cardiopulmonary bypass is associated with reduction of circulating markers of inflammation and increased neutrophil apoptosis . These data support a routine inclusion of statins as an adjuvant pharmacologic therapy before cardiopulmonary bypass surgery IMPORTANCE Statins affect several mechanisms underlying acute kidney injury ( AKI ) . OBJECTIVE To test the hypothesis that short-term high-dose perioperative atorvastatin would reduce AKI following cardiac surgery . DESIGN , SETTING , AND PARTICIPANTS Double-blinded , placebo-controlled , r and omized clinical trial of adult cardiac surgery patients conducted from November 2009 to October 2014 at V and erbilt University Medical Center . INTERVENTIONS Patients naive to statin treatment ( n = 199 ) were r and omly assigned 80 mg of atorvastatin the day before surgery , 40 mg of atorvastatin the morning of surgery , and 40 mg of atorvastatin daily following surgery ( n = 102 ) or matching placebo ( n = 97 ) . Patients already taking a statin prior to study enrollment ( n = 416 ) continued taking the preenrollment statin until the day of surgery , were r and omly assigned 80 mg of atorvastatin the morning of surgery and 40 mg of atorvastatin the morning after ( n = 206 ) or matching placebo ( n = 210 ) , and resumed taking the previously prescribed statin on postoperative day 2 . MAIN OUTCOMES AND MEASURES Acute kidney injury defined as an increase of 0.3 mg/dL in serum creatinine concentration within 48 hours of surgery ( Acute Kidney Injury Network criteria ) . RESULTS The data and safety monitoring board recommended stopping the group naive to statin treatment due to increased AKI among these participants with chronic kidney disease ( estimated glomerular filtration rate < 60 mL/min/1.73 m2 ) receiving atorvastatin . The board later recommended stopping for futility after 615 participants ( median age , 67 years ; 188 [ 30.6 % ] were women ; 202 [ 32.8 % ] had diabetes ) completed the study . Among all participants ( n = 615 ) , AKI occurred in 64 of 308 ( 20.8 % ) in the atorvastatin group vs 60 of 307 ( 19.5 % ) in the placebo group ( relative risk [ RR ] , 1.06 [ 95 % CI , 0.78 to 1.46 ] ; P = .75 ) . Among patients naive to statin treatment ( n = 199 ) , AKI occurred in 22 of 102 ( 21.6 % ) in the atorvastatin group vs 13 of 97 ( 13.4 % ) in the placebo group ( RR , 1.61 [ 0.86 to 3.01 ] ; P = .15 ) and serum creatinine concentration increased by a median of 0.11 mg/dL ( 10th-90th percentile , -0.11 to 0.56 mg/dL ) in the atorvastatin group vs by a median of 0.05 mg/dL ( 10th-90th percentile , -0.12 to 0.33 mg/dL ) in the placebo group ( mean difference , 0.08 mg/dL [ 95 % CI , 0.01 to 0.15 mg/dL ] ; P = .007 ) . Among patients already taking a statin ( n = 416 ) , AKI occurred in 42 of 206 ( 20.4 % ) in the atorvastatin group vs 47 of 210 ( 22.4 % ) in the placebo group ( RR , 0.91 [ 0.63 to 1.32 ] ; P = .63 ) . CONCLUSIONS AND RELEVANCE Among patients undergoing cardiac surgery , high-dose perioperative atorvastatin treatment compared with placebo did not reduce the risk of AKI overall , among patients naive to treatment with statins , or in patients already taking a statin . These results do not support the initiation of statin therapy to prevent AKI following cardiac surgery . TRIAL REGISTRATION clinical trials.gov Identifier : NCT00791648 BACKGROUND Acute kidney injury ( AKI ) is a serious complication of cardiac operations for which there remains no specific therapy . Animal data and several observational studies suggest that statins prevent AKI , but the results are not conclusive , and many studies are retrospective in nature . METHODS We conducted a multicenter prospect i ve cohort study of 625 adult patients undergoing elective cardiac operations . All patients were taking statins  and were grouped according to whether statins were continued or held in the 24 hours before operation . The primary outcome was AKI as defined by a doubling of serum creatinine or dialysis . The secondary outcome was the peak level of several kidney injury biomarkers . The results were adjusted for demographic and clinical factors . RESULTS Continuing ( vs holding ) a statin before operation was not associated with a lower risk of AKI , as defined by a doubling of serum creatinine or dialysis ( adjusted relative risk [ RR ] 1.09 ; 95 % confidence interval [ CI ] 0.44 , 2.70 ) . However , continuing a statin was associated with a lower risk of elevation of the following AKI biomarkers : urine interleukin-18 , urine neutrophil gelatinase-associated lipocalin , urine kidney injury molecule-1 , and plasma neutrophil gelatinase-associated lipocalin ( adjusted RR 0.34 ; 95 % CI 0.18 , 0.62 ) , ( adjusted RR 0.41 ; 95 % CI 0.22 , 0.76 ) , ( adjusted RR 0.37 ; 95 % CI 0.20 , 0.76 ) , ( adjusted RR 0.62 ; 95 % CI 0.39 , 0.98 ) , respectively . CONCLUSIONS Statins may prevent kidney injury after cardiac operations , as evidence d by lower levels of kidney injury biomarkers OBJECTIVE Endothelial dysfunction represents a critical early component of organ injury following cardiopulmonary bypass . Recent studies demonstrate that the treatment with atorvastatin is associated with a significant improvement of endothelial function independently of its efficacy on cholesterol levels . Therefore , we investigated the effects of preoperative atorvastatin treatment on endothelium function after coronary surgery . METHODS Forty patients undergoing coronary surgery were r and omized to treatment with atorvastatin ( 20 mg/die ; N=20 ) or placebo ( N=20 ) 3 weeks before surgery . Twenty normal patients served as control group . The flow-mediated dilations ( FMD ) of the brachial artery after both reactive hyperemia ( endothelium dependent ) and nitroglycerin administration ( endothelium independent ) were evaluated at baseline , at 48 h , and 5 days postoperatively . RESULTS At baseline , the endothelium-dependent FMD was significantly attenuated in coronary versus normal patients ( normal 10.3+/-1.8 % vs coronary 4.1+/-1.6 % , p<0.01 ) . At 48 h postoperatively 
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No difference in postoperative atrial fibrillation , myocardial infa rct ion , stroke , infections , or mortality was present .
On sensitivity analysis , statin therapy was associated with a slight increase in hospital mortality .
Meta- analysis including also trials with high or unclear risk of bias showed no beneficial effects of statin therapy on any postoperative outcomes .
Conclusions There is no evidence that statin therapy in the days prior to cardiac surgery is beneficial for patients ’ outcomes .
Particularly , statins are not protective against postoperative atrial fibrillation , myocardial infa rct ion , stroke , or infections .
Statins are associated with a possible increased risk of acute kidney injury and a detrimental effect on hospital survival could not be excluded .