***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: BACKGROUND Intensive statin therapy can lower the risk of recurrence of major cardiac events in patients with acute coronary syndromes . This could be related to the ability of statins to increase levels of Endothelial Progenitor Cells ( EPCs ) , which were demonstrated to be favorably associated with a better prognosis and post-infa rct ion left ventricular remodeling in patients with ischemic heart disease . AIM OF THE STUDY First , to evaluate , in a r and omized clinical trial , the effect of an intensive vs a st and ard treatment with statins on EPC mobilization in patients undergoing a successful primary or rescue percutaneous coronary intervention ; secondary , to evaluate whether left ventricular remodeling could be influenced by statin therapy through EPC mobilization . METHODS Forty ST-segment elevation myocardial infa rct ion ( STEMI ) patients undergoing a successful primary or rescue PCI were r and omized to receive atorvastatin 80 mg immediately after the admission ( Intensive Treatment , IT ) or atorvastatin 20 mg from the day of the discharge ( St and ard Treatment , ST ) . CD34+/KDR+ EPC count by flow cytometry and left ventricular function by 2-D Echo were measured on admission , at discharge and at 4 months follow up . RESULTS We found that EPC count was similar in the two groups of patients both on admission and at discharge . At follow up , however , EPC count was higher in patients r and omized to IT compared to patients r and omized to ST ( 7.59+/-7.30 vs 3.04+/-3.93 , p=0.04 ) . However , LV volumes , ejection fraction and wall motion score index were similar in both groups . CONCLUSIONS An intensive statin treatment after primary or rescue PCI is associated with a higher EPC count at follow up as compared to st and ard treatment . This beneficial effect did not translate in an improvement of LV function Drug therapy for hypercholesterolaemia has remained controversial mainly because of insufficient clinical trial evidence for improved survival . The present trial was design ed to evaluate the effect of cholesterol lowering with simvastatin on mortality and morbidity in patients with coronary heart disease ( CHD ) . 4444 patients with angina pectoris or previous myocardial infa rct ion and serum cholesterol 5.5 - 8.0 mmol/L on a lipid-lowering diet were r and omised to double-blind treatment with simvastatin or placebo . Over the 5.4 years median follow-up period , simvastatin produced mean changes in total cholesterol , low-density-lipoprotein cholesterol , and high-density-lipoprotein cholesterol of -25 % , -35 % , and + 8 % , respectively , with few adverse effects . 256 patients ( 12 % ) in the placebo group died , compared with 182 ( 8 % ) in the simvastatin group . The relative risk of death in the simvastatin group was 0.70 ( 95 % CI 0.58 - 0.85 , p = 0.0003 ) . The 6-year probabilities of survival in the placebo and simvastatin groups were 87.6 % and 91.3 % , respectively . There were 189 coronary deaths in the placebo group and 111 in the simvastatin group ( relative risk 0.58 , 95 % CI 0.46 - 0.73 ) , while noncardiovascular causes accounted for 49 and 46 deaths , respectively . 622 patients ( 28 % ) in the placebo group and 431 ( 19 % ) in the simvastatin group had one or more major coronary events . The relative risk was 0.66 ( 95 % CI 0.59 - 0.75 , p < 0.00001 ) , and the respective probabilities of escaping such events were 70.5 % and 79.6 % . This risk was also significantly reduced in subgroups consisting of women and patients of both sexes aged 60 or more . Other benefits of treatment included a 37 % reduction ( p < 0.00001 ) in the risk of undergoing myocardial revascularisation procedures . This study shows that long-term treatment with simvastatin is safe and improves survival in CHD patients CONTEXT Patients experience the highest rate of death and recurrent ischemic events during the early period after an acute coronary syndrome , but it is not known whether early initiation of treatment with a statin can reduce the occurrence of these early events . OBJECTIVE To determine whether treatment with atorvastatin , 80 mg/d , initiated 24 to 96 hours after an acute coronary syndrome , reduces death and nonfatal ischemic events . DESIGN AND SETTING A r and omized , double-blind trial conducted from May 1997 to September 1999 , with follow-up through 16 weeks at 122 clinical centers in Europe , North America , South Africa , and Australasia . PATIENTS A total of 3086 adults aged 18 years or older with unstable angina or non-Q-wave acute myocardial infa rct ion . INTERVENTIONS Patients were stratified by center and r and omly assigned to receive treatment with atorvastatin ( 80 mg/d ) or matching placebo between 24 and 96 hours after hospital admission . MAIN OUTCOME MEASURES Primary end point event defined as death , nonfatal acute myocardial infa rct ion , cardiac arrest with resuscitation , or recurrent symptomatic myocardial ischemia with objective evidence and requiring emergency rehospitalization . RESULTS A primary end point event occurred in 228 patients ( 14.8 % ) in the atorvastatin group and 269 patients ( 17.4 % ) in the placebo group ( relative risk [ RR ] , 0.84 ; 95 % confidence interval [ CI ] , 0.70 - 1.00 ; P = .048 ) . There were no significant differences in risk of death , nonfatal myocardial infa rct ion , or cardiac arrest between the atorvastatin group and the placebo group , although the atorvastatin group had a lower risk of symptomatic ischemia with objective evidence and requiring emergency rehospitalization ( 6.2 % vs 8.4 % ; RR , 0.74 ; 95 % CI , 0.57 - 0.95 ; P = .02 ) . Likewise , there were no significant differences between the atorvastatin group and the placebo group in the incidence of secondary outcomes of coronary revascularization procedures , worsening heart failure , or worsening angina , although there were fewer strokes in the atorvastatin group than in the placebo group ( 12 vs 24 events ; P = .045 ) . In the atorvastatin group , mean low-density lipoprotein cholesterol level declined from 124 mg/dL ( 3.2 mmol/L ) to 72 mg/dL ( 1.9 mmol/L ) . Abnormal liver transaminases ( > 3 times upper limit of normal ) were more common in the atorvastatin group than in the placebo group ( 2.5 % vs 0.6 % ; P<.001 ) . CONCLUSION For patients with acute coronary syndrome , lipid-lowering therapy with atorvastatin , 80 mg/d , reduces recurrent ischemic events in the first 16 weeks , mostly recurrent symptomatic ischemia requiring rehospitalization Objectives We investigated the effects of short-term use of atorvastatin on CD34+/VEGF-R2+/CD133+/CD45- endothelial progenitor cell ( EPC ) count after on-pump coronary artery bypass surgery ( CABG ) . Methods Between Feb-2010 and May-2010 , we r and omly assigned , in a placebo-controlled , double-blind study , 60 consecutive patients who underwent isolated , first-time CABG to receive either 14-day atorvastatin  ( 40 mg/day ) or placebo  preoperatively . Urgent CABG and recent myocardial infa rct ion were excluded . EPCs were quantified ( cells/μl ) by flow cytometric phenotyping obtained from venous blood sample s collected preoperatively ( T1 ) , 6-hours ( T2 ) , and on the 5th day postoperatively ( T3 ) . Levels of markers of inflammation and serum cardiac troponin I were also measured preoperatively and daily until day-5 after surgery . Results There were no differences in baseline risk factors including cholesterol profiles , and EuroSCORES between the groups . The composite primary end-point , favored statin group with higher amount of circulating , early EPC count ( cells/μl ) at all time points compared with placebo ( T1 , 2.30 ± 0.02 versus 1.58 ± 0.03 , p < 0.001 ; T2 , 5.00 ± 0.06 versus 2.19 ± 0.06 , p < 0.001 ; T3 , 3.03 ± 0.08 versus 1.78 ± 0.02 , p < 0.001 ) . Postoperative hsCRP rise were inversely correlated with EPC count , and were significantly lower in the statin group ( T1 , 0.8 ± 0.1 versus 2.2 ± 1.5 , p < 0.001 ; T2 , 72.9 ± 3.2 versus 96.0 ± 3.6 , p < 0.001 ; T3 , 4.3 ± 1.2 versus 11.4 ± 4.1 , p < 0.001 ) . Furthermore , the incidence of postoperative atrial fibrillation was significantly lower in the statin group compared to placebo ( 3.3 % versus 23 % , p = 0.02 ) . Conclusions Short-term atorvastatin use increases circulating early EPCs both pre- and post-operatively and is associated with better preservation of sinus rhythm and reduced hsCRP levels . ( Clinical Trials.gov number , NCT01096875 BACKGROUND Smoking is a major cardiovascular risk factor , leading to endothelial dysfunction . The present study investigated the hypothesis that pitavastatin , an HMG-CoA reductase inhibitor , may improve endothelial function in chronic smokers via its antioxidant properties . METHODS AND RESULTS The 30 male chronic smokers who exhibited mild hypercholesterolemia at the time of physical check-up were enrolled and r and omized to the pitavastatin group ( 2 mg/day , n=15 ) or the untreated control group ( n=15 ) . Before and after the 4-week treatment period , endothelium-dependent flow-mediated dilation ( FMD ) and endothelium-independent dilation by glyceryl trinitrate ( GTD ) were examined , and the FMD/GTD ratio was calculated . The pitavastatin group showed a significant restoration of endothelial function ( percent change in FMD : + 49.6 % vs + 1.4 % ; percent change in FMD/GTD ratio : + 26.6 % vs 4.5 % , P<0.05 respectively ) , and a significant reduction in oxidative stress levels ( malondialdehyde-low-density lipoprotein-cholesterol : 16.6 % vs + 7.5 % ; free radical activity : 1.8 % vs + 9.7 % , P<0.05 respectively ) compared with the control group . Pitavastatin had no effect on the number of circulating CD34(+)CD133(+ ) progenitor cells , endothelial progenitor cells , or the MMP-2 , MMP-9 and VEGF levels . In vitro oxidative stress monitoring assay revealed that pitavastatin protected endothelial cells against oxidative stress . CONCLUSIONS Pitavastatin restores endothelial function , even in chronic smokers , possibly through its antioxidative properties . ( Circ J 2010 ; 74 : 195 - 202 ) Background —Endothelial nitric oxide ( eNO ) bioavailability is severely reduced after myocardial infa rct ion ( MI ) and in heart failure .  Statins enhance eNO availability by both increasing eNO production and reducing NO inactivation . We therefore studied the effect of statin treatment on eNO availability after MI and tested its role for endothelial progenitor cell mobilization , myocardial neovascularization , left ventricular ( LV ) dysfunction , remodeling , and survival after MI . Methods and Results —Wild-type ( WT ) and eNO synthase (eNOS)−/− mice with extensive anterior MI were r and omized to treatment with vehicle ( V ) or atorvastatin ( Ator , 50 mg/kg QD by gavage ) for 4 weeks starting on day 1 after MI . Ator markedly improved endothelium-dependent , NO-mediated vasorelaxation ; mobilization of endothelial progenitor cells ; and myocardial neovascularization of the infa rct border in WT mice after MI while having no effect in eNOS−/− mice . LV dysfunction and interstitial fibrosis were markedly attenuated by Ator in WT mice , whereas no effect was observed in eNOS−/− mice after MI . Importantly , Ator significantly increased the survival rate during 4 weeks after MI in WT mice ( Ator 
    Output:
    
In conclusion , r and omized studies in humans suggest that statin therapy  mobilizes EPCs into the circulation .