***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 Our study 's aim was to evaluate the prognostic value of early and intensive lipid-lowering treatment on  ventricular premature beat or non-sustained ventricular tachycardia ( NSVT ) after acute coronary syndrome ( STEMI , non-STEMI , and unstable angina pectoris ) . METHODS Some 586 patients with acute coronary syndrome were r and omly divided into two groups : Group A ( with conventional statin therapy , to receive 10 mg/day atorvastatin , n = 289 ) and Group B ( given early and intensive statin therapy , 60 mg immediately and 40 mg/day atorvastatin , n = 297 ) . The frequency of ventricular premature beat and NSVT was recorded via Holter monitoring after hospitalization ( 24 h and 72 h ) . RESULTS Seventy seven ( 11.8 % ) patients had NSVT . When compared to patients with no documented NSVT , patients with NSVT were older and more frequently had myocardial infa rct ion in their history , diabetes mellitus , atrial fibrillation and an ejection fraction < 40 % . Ventricular premature beats decreased significantly in the early and aggressive treatment group ( 24 h , p < 0.01 ; 72 h , p < 0.001 ) . A significant reduction in NSVT was seen in the early and aggressive treatment group ( 24 h , p < 0.01 ; 72 h , p < 0.001 ) . There were no side effects observed in either group . CONCLUSIONS Early and intensive lipid-lowering treatment can clearly decrease ventricular premature beats and NSVT CONTEXT Plasma levels of the inflammatory biomarker C-reactive protein ( CRP ) predict cardiovascular risk , and retrospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ( statins ) may lower CRP in a manner largely independent of low-density lipoprotein cholesterol ( LDL-C ) . However , prospect i ve trial data directly evaluating this anti-inflammatory effect of statins are not available . OBJECTIVE To test the hypothesis that pravastatin has anti-inflammatory effects as evidence d by CRP reduction . DESIGN , SETTING , AND PARTICIPANTS Community-based , prospect i ve , r and omized , double-blind trial including 1702 men and women with no prior history of cardiovascular disease ( primary prevention cohort ) and open-label study including 1182 patients with known cardiovascular disease ( secondary prevention cohort ) who provided at least baseline and 12-week blood sample s. The study was conducted in US office-based practice s from February to December 2000 . INTERVENTIONS Participants in the double-blind primary prevention trial were r and omly assigned to receive 40 mg/d of pravastatin ( n = 865 ) or placebo ( n = 837 ) for 24 weeks . Participants in the secondary prevention cohort received 40 mg/d of open-label pravastatin for 24 weeks . MAIN OUTCOME MEASURE Change in CRP levels from baseline to 24 weeks . RESULTS In the primary prevention trial , compared with placebo , pravastatin reduced median CRP levels by 16.9 % ( P<.001 ) at 24 weeks , reflecting a decrease of 0.02 mg/dL in the pravastatin group while no change in CRP levels was observed in the placebo group . This effect was seen as early as 12 weeks ( median reduction in CRP with pravastatin , 14.7 % ; P<.001 ) and was present among all prespecified subgroups according to sex , age , smoking status , body mass index , baseline lipid levels , presence of diabetes , and use of aspirin or hormone replacement therapy . No significant association was observed between baseline CRP and baseline LDL-C levels , end-of- study CRP and end-of- study LDL-C levels , or change in CRP and change in LDL-C levels over time . In linear regression analyses , the only significant predictors of change in CRP on a log scale were r and omized pravastatin allocation and baseline CRP levels ( P<.001 for both ) . Similar reductions in CRP levels were observed at 12 weeks ( -14.3 % ) and 24 weeks ( -13.1 % ) in the secondary prevention cohort treated with pravastatin ( P<.005 for both ) . CONCLUSIONS In this prospect i ve trial , pravastatin reduced CRP levels at both 12 and 24 weeks in a largely LDL-C-independent manner . These data provide evidence that statins may have anti-inflammatory effects in addition to lipid-lowering effects OBJECTIVES We investigated whether plasma amino-terminal pro-brain natriuretic peptide ( NT-proBNP ) , a marker of cardiac dysfunction and prognosis measured in CORONA ( Controlled Rosuvastatin Multinational Trial in Heart Failure ) , could be used to identify the severity of heart failure at which statins become ineffective . BACKGROUND Statins reduce cardiovascular morbidity and mortality in many patients with ischemic heart disease but not , overall , those with heart failure . There must be a transition point at which treatment with a statin becomes futile . METHODS In CORONA , patients with heart failure , reduced left ventricular ejection fraction , and ischemic heart disease were r and omly assigned to 10 mg/day rosuvastatin or placebo . The primary composite outcome was cardiovascular death , nonfatal myocardial infa rct ion , or stroke . RESULTS Of 5,011 patients enrolled , NT-proBNP was measured in 3,664 ( 73 % ) . The midtertile included values between 103 pmol/l ( 868 pg/ml ) and 277 pmol/l ( 2,348 pg/ml ) . Log NT-proBNP was the strongest predictor ( per log unit ) of every outcome assessed but was strongest for death from worsening heart failure ( hazard ratio [ HR ] : 1.99 ; 95 % confidence interval [ CI ] : 1.71 to 2.30 ) , was weaker for sudden death ( HR : 1.69 ; 95 % CI : 1.52 to 1.88 ) , and was weakest for atherothrombotic events ( HR : 1.24 ; 95 % CI : 1.10 to 1.40 ) . Patients in the lowest tertile of NT-proBNP had the best prognosis and , if assigned to rosuvastatin rather than placebo , had a greater reduction in the primary end point ( HR : 0.65 ; 95 % CI : 0.47 to 0.88 ) than patients in the other tertiles ( heterogeneity test , p = 0.0192 ) . This reflected fewer atherothrombotic events and sudden deaths with rosuvastatin . CONCLUSIONS Patients with heart failure due to ischemic heart disease who have NT-proBNP values < 103 pmol/l ( 868 pg/ml ) may benefit from rosuvastatin BACKGROUND The effectiveness of statins remains to be examined in patients with heart failure ( HF ) with preserved ejection fraction ( EF ) . METHODS AND RESULTS : Among 4,544 consecutive HF patients registered in the Chronic Heart Failure Registry and Analysis in the Tohoku district-2 ( CHART-2 ) between 2006 and 2010 , 3,124 had EF ≥50 % ( HFpEF ; mean age 69 years ; male 65 % ) and 1,420 had EF < 50 % ( HF with reduced EF ( HFrEF ) ; mean age 67 years ; male 75 % ) . The median follow-up was 3.4 years . The 3-year mortality in HFpEF patients was lower in patients receiving statins [ 8.7 % vs. 14.5 % , adjusted hazard ratio ( HR ) 0.74 ; 95 % confidence interval ( CI ) , 0.58 - 0.94 ; P<0.001 ] , which was confirmed in the propensity score-matched cohort ( HR , 0.72 ; 95 % CI , 0.49 - 0.99 ; P=0.044 ) . The inverse probability of treatment weighted further confirmed that statin use was associated with reduced incidence of all-cause death ( HR , 0.71 ; 95 % CI , 0.62 - 0.82 , P<0.001 ) and noncardiovascular death ( HR , 0.53 ; 95 % CI , 0.43 - 0.66 , P<0.001 ) , specifically reduction of sudden death ( HR , 0.59 ; 95 % CI , 0.36 - 0.98 , P=0.041 ) and infection death ( HR , 0.53 ; 95 % CI , 0.35 - 0.77 , P=0.001 ) in HFpEF . In the HFrEF cohort , statin use was not associated with mortality ( HR , 0.87 ; 95 % CI , 0.73 - 1.04 , P=0.12 ) , suggesting a lack of statin benefit in HFrEF patients . CONCLUSIONS These results suggest that statin use is associated with improved mortality rates in HFpEF patients , mainly attributable to reductions in sudden death and noncardiovascular death BACKGROUND Clinical data on the mortality and morbidity of unselected Japanese patients with heart failure ( HF ) are limited . In this study , we aim ed to determine the clinical characteristics , long-term outcomes , and prognostic factors of Japanese HF patients with preserved or reduced left ventricular ejection fraction ( LVEF ) . METHODS AND RESULTS We used a single hospital-based cohort from the Shinken Data base 2004 - 2011 that comprised all new patients ( n=17,517 ) visiting the Cardiovascular Institute Hospital . A total of 1,525 patients diagnosed with symptomatic HF at the initial visit were included in the analysis . Of these , 1121 patients ( 74 % ) exhibited a preserved LVEF ( > 50 % ) and 404 patients ( 26 % ) had a reduced LVEF ( ≤ 50 % ) . HF patients with preserved LVEF ( HFpEF ) were older and more often female than patients with reduced LVEF ( HFrEF ) . Kaplan-Meier curves and log-rank test results showed that HFpEF patients had a better prognosis than HFrEF patients . However , there were no significant differences in clinical outcomes between HFpEF and HFrEF patients when the analysis was limited to in patients . Cox regression analysis showed that HFpEF patients had a significantly lower risk of all-cause death ( p=0.027 ; hazard ratio , 0.547 , 95 % confidence interval , 0.321 - 0.933 ) . Multivariate analyses performed separately showed that the independent predictors of all-cause death in HFrEF were advanced age , lower body mass index , diabetes mellitus , and the absence of statin treatment , whereas those for HFpEF were advanced age , absence of dyslipidemia , anemia , and left ventricular hypertrophy . CONCLUSIONS This prospect i ve cohort study identified the clinical characteristics , long-term outcomes , and prognostic factors of Japanese HF patients with reduced and preserved ejection fractions in a real-world clinical setting We prospect ively followed 202 patients with ischemic heart failure who underwent percutaneous coronary intervention ( PCI ) for acute myocardial infa rct ion ( left ventricular [ LV ] ejection fraction < 40 % ) . Patients were divided into 2 groups : groups I  ( simvastatin group , n = 106 , aged 60.8 + /- 10.3 years , men 71.7 % ) and II ( non-simvastatin group , n = 96 , aged 60.9 + /- 10.4 years , men 78.1 % ) . During 1-year clinical follow-up , simvastatin therapy was associated with a significant reduction in mortality ( 1.9 % vs 7.5 % , p = 0.048 ) , restenosis rate ( 25.7 % vs 43.1 % , p = 0.033 ) , and repeat PCI rate ( 25.7 % vs 43.1 % , p = 0.033 ) , and with significant improvement in LV ejection fraction ( 31 % to 42 % vs 32 % to 39 % , p = 0.042 ) . The event-free survival rate was higher in group I than in group II ( 79.8 % vs 57.0 % , p = 0.001 ) . In conclusion , simvastatin therapy improves LV systolic function and decreases mortality , restenosis , and repeat PCI rate in patients with ischemic heart failure who underwent PCI for acute myocardial infa rct ion BACKGROUND The effects of statins in patients with heart failure with preserved ejection fraction ( HFpEF ) remain unclear . This study aim ed to assess whether statin therapy is associated with a decreased risk of mortality in patients with HFpEF . METHODS We used data from the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist ( TOPCAT ) trial . The primary outcome was all-cause mortality . We analyzed hazard ratios ( HRs 
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Significant effects on all clinical outcomes were also found in cohort studies ’ analyses ; the effect was also larger and significant for lipophilic than hydrophilic statins .
Conclusions In conclusion , statins may have a beneficial effect on CV outcomes irrespective of HF etiology and LVEF level .
Lipophilic statins seem to be much more favorable for patients with heart failure