***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: The reported results ( The Post Coronary Artery Bypass Graft Trial Investigators . The effect of aggressive lowering of low-density lipoprotein cholesterol levels  and low-dose anticoagulation on obstructive changes in saphenous-vein coronary-artery bypass grafts . New Engl J Med 1997;336:153 - 162 ) of the Post Coronary Artery Bypass Graft ( Post CABG ) trial have shown that aggressive lowering was more effective than moderate lowering of low density lipoprotein ( LDL ) cholesterol in reducing the progression of atherosclerosis in saphenous-vein grafts ( 27 vs. 39 % ; P < 0.001 ) ; low dose warfarin had no effect on the progression of atherosclerosis . The present report describes the effect of long-term ( an average of 4.3 years ) aggressive treatment with high ( 40 - 80 mg/day ) and moderate treatment with low ( 2.5 - 5 mg/day ) doses of lovastatin on lipids , apolipoproteins ( apo ) and apoA- and apoB-containing lipoprotein families . To achieve the target LDL-cholesterol levels ( 60 - 85 mg/dl for aggressive group and 134 - 140 mg/dl for moderate group ) , cholestyramine ( 8 g/day ) was given to 25 % of subjects on aggressive and 5 % of subjects on moderate treatment . Although with both treatment strategies there were significant decreases ( P<0.001 ) in the levels of total cholesterol , LDL-cholesterol , apoB , LDL-apoB and cholesterol-rich Lp-B family , percent changes in the levels of these variables were greater in the aggressive- than in the moderate-treatment groups . These treatments had only marginal effects in increasing the levels of high density lipoprotein cholesterol , apoA-I and Lp-A-I and Lp-A-I : A-II families . The long-term aggressive treatment exerted no effect on the concentrations of triglycerides , apoC-IlI , apoC-III in VLDL + LDL and triglyceride-rich Lp-Bc families . Neither treatment affected the levels of Lp(a ) . The potentially modifying influence of warfarin and apoE phenotypes on lovastatin-induced changes in lipoprotein variables was found to be of little significance . It is likely that the beneficial effect of lovastatin in reducing the progression of atherosclerosis in grafts is mediated through its specific lowering effect on cholesterol-rich Lp-B particles OBJECTIVES This study examines whether obesity accelerates atherogenic progression or adverse outcomes after coronary artery bypass graft ( CABG ) surgery . BACKGROUND Obesity is a major risk factor for developing coronary heart disease . Whether obesity accelerates disease progression after CABG is unclear . METHODS We examined how body mass index ( BMI ) related to atherosclerotic graft progression and a clinical composite outcome of death , nonfatal myocardial infa rct ion , stroke , CABG surgery , or angioplasty among 1,314 participants in the Post CABG trial . Participants who had undergone CABG surgery were r and omly assigned in a 2 x 2 factorial design to warfarin versus placebo and aggressive low-density lipoprotein cholesterol ( LDL-C ) lowering with lovastatin 40 to 80 mg/day ( to achieve LDL-C of 60 to 85 mg/dl ) versus moderate LDL-C lowering with lovastatin 2.5 to 5 mg/day ( to achieve LDL-C of 130 to 140 mg/dl ) . Angiographic progression was assessed by coronary angiography at 4 to 5 years . RESULTS Higher BMI was associated with a higher likelihood of angiographic progression ( p trend = 0.003 ) after adjustment for demographic factors , treatment assignment , smoking status , and years since CABG surgery , but not with clinical events ( p trend = 0.81 ) . In stratified analyses , higher BMI was associated with angiographic progression in the low-dose lovastatin group ( p trend < 0.001 ) but not in the high-dose group ( p = 0.03 for test for interaction of BMI and statin treatment ) . In the high-dose lovastatin group , higher BMI appeared to be protective against clinical events ( p trend = 0.06 , test of interaction : 0.02 ) . CONCLUSIONS Higher BMI is strongly associated with atherogenic progression after CABG surgery . Aggressive statin therapy may be protective against obesity-related acceleration of coronary heart disease CONTEXT Percutaneous coronary intervention ( PCI ) is associated with excellent short-term improvements in ischemic symptoms , yet only three fifths of PCI patients at 5 years and one third of patients at 10 years remain free of major adverse cardiac events ( MACE ) . OBJECTIVE To determine whether treatment with fluvastatin reduces MACE in patients who have undergone PCI . DESIGN AND SETTING R and omized , double-blind , placebo-controlled trial conducted at 77 referral centers in Europe , Canada , and Brazil . PATIENTS A total of 1677 patients ( aged 18 - 80 years ) recruited between April 1996 and October 1998 with stable or unstable angina or silent ischemia following successful completion of their first PCI who had baseline total cholesterol levels between 135 and 270 mg/dL ( 3.5 - 7.0 mmol/L ) , with fasting triglyceride levels of less than 400 mg/dL ( 4.5 mmol/L ) . INTERVENTIONS Patients were r and omly assigned to receive treatment with fluvastatin , 80 mg/d ( n = 844 ) , or matching placebo ( n = 833 ) at hospital discharge for 3 to 4 years . MAIN OUTCOME MEASURE Survival time free of MACE , defined as cardiac death , nonfatal myocardial infa rct ion , or reintervention procedure , compared between the treatment and placebo groups . RESULTS Median time between PCI and first dose of study medication was 2.0 days , and median follow-up was 3.9 years . MACE-free survival time was significantly longer in the fluvastatin group ( P = .01 ) . One hundred eighty-one ( 21.4 % ) of 844 patients in the fluvastatin group and 222 ( 26.7 % ) of 833 patients in the placebo group had at least 1 MACE ( relative risk [ RR ] , 0.78 ; 95 % confidence interval [ CI ] , 0.64 - 0.95 ; P = .01 ) . This result was independent of baseline total cholesterol levels ( above [ RR , 0.76 ; 95 % CI , 0.56 - 1.04 ] vs below [ RR , 0.77 ; 95 % CI , 0.57 - 1.02 ] the median ) . In subgroup analysis , the risk of MACE was reduced in patients with diabetes ( n = 202 ; RR , 0.53 ; 95 % CI , 0.29 - 0.97 ; P = .04 ) and in those with multivessel disease ( n = 614 ; RR , 0.66 ; 95 % CI , 0.48 - 0.91 ; P = .01 ) who received fluvastatin compared with those who received placebo . There were no instances of creatine phosphokinase elevations 10 or more times the upper limit of normal or rhabdomyolysis in the fluvastatin group . CONCLUSION Fluvastatin treatment in patients with average cholesterol levels undergoing their first successful PCI significantly reduces the risk of major adverse cardiac events 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 BACKGROUND The 3-hydroxy-3-methylglutaryl coenzyme A ( HMG CoA ) reductase inhibitors competitively inhibit bio synthesis of mevalonate , a precursor of non-sterol compounds involved in cell proliferation . Experimental evidence suggests that fluvastatin may , independent of any lipid lowering action , exert a greater direct inhibitory effect on proliferating vascular myocytes than other statins . The FLARE ( Fluvastatin Angioplasty Restenosis ) Trial was conceived to evaluate the ability of fluvastatin 40 mg twice daily to reduce restenosis after successful coronary balloon angioplasty ( PTCA ) . METHODS Patients were r and omized to either placebo or fluvastatin 40 mg twice daily beginning 2 - 4 weeks prior to planned PTCA and continuing after a successful PTCA ( without the use of a stent ) , to follow-up angiography at 26+/-2 weeks . Clinical follow-up was completed at 40 weeks . The primary end-point was angiographic restenosis , measured by quantitative coronary angiography at a core laboratory , as the loss in minimal luminal diameter during follow-up . Clinical end-points were death , myocardial infa rct ion , coronary artery bypass graft surgery or re-intervention , up to 40 weeks after PTCA . RESULTS Of 1054 patients r and omized , 526 were allocated to fluvastatin and 528 to placebo .  Among these , 409 in the fluvastatin group and 427 in the placebo group were included in the intention-to-treat analysis , having undergone a successful PTCA after a minimum of 2 weeks of pre-treatment . At the time of PTCA , fluvastatin had reduced LDL cholesterol by 37 % and this was maintained at 33 % at 26 weeks . There was no difference in the primary end-point between the treatment groups ( fluvastatin 0.23+/-0.49 mm vs placebo 0.23+/-0.52 mm , P=0.95 ) or in the angiographic restenosis rate  ( fluvastatin 28 % , placebo 31 % , chi-square P=0.42 ) , or in the incidence of the composite clinical end-point at 40 weeks ( 22.4 % vs 23.3 % ; logrank P=0.74 ) . However , a significantly lower incidence of total death and myocardial infa rct ion was observed in six patients ( 1.4 % ) in the fluvastatin group and 17 ( 4.0 % ) in the placebo group ( log rank P=0.025 ) . CONCLUSION Treatment with fluvastatin 80 mg daily did not affect the process of restenosis and is therefore not indicated for this purpose . However , the observed reduction in mortality and myocardial infa rct ion 40 weeks after PTCA in the fluvastatin treated group has not been previously reported with statin therapy . Accordingly , a priori investigation of this finding is indicated and a new clinical trial with this intention is already underway Introduction Severe acute kidney injury ( AKI ) can be treated with either continuous renal replacement therapy ( CRRT ) or intermittent renal replacement therapy ( IRRT ) . Limited evidence from existing studies does not support an outcome advantage of one modality versus the other , and most centers around the word use both modalities according to patient needs . However , cost estimates involve multiple factors that may not be generalizable to other sites , and , to date , only single-center cost studies have been performed . The aim of this study was to estimate the cost difference between CRRT and IRRT in the intensive care unit ( ICU ) . Methods We performed a post hoc analysis of a prospect i ve observational study among 53 centers from 23 countries , from September 20 
    Output:
    
Overall , pre-operative statin treatment was not associated with a reduction in postoperative AKI , need for RRT , or mortality .
Analysis of currently available data did not suggest that preoperative statin use is associated with decreased incidence of AKI in adults after surgery who required cardiac bypass .