***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 — Experimental studies suggest that deferoxamine ( DFO ) limits the generation of reactive oxygen species by chelating redox-active iron and thereby may reduce ischemia-reperfusion injury and myocardial infa rct ( MI ) size . We investigated whether DFO administered before reperfusion by primary percutaneous coronary intervention ( PPCI ) would ameliorate oxidative stress and MI size . Methods and Results — We r and omly assigned 60 patients with ST-elevation – MI to receive an intravenous bolus of DFO ( 500 mg ) immediately before PPCI followed by a 12-hour infusion ( 50 mg/kg of body weight ) ( n=28 ) or normal saline bolus and infusion ( placebo group , n=32 ) . MI size was measured by contrast-enhanced cardiac MRI ( CMRI ; day 3±1 ) , creatine kinase and troponin I area-under-the-curve , and severity of wall motion abnormality on echocardiography . Clinical follow-up including repeat CMRI and echocardiography were performed at 3 months ( 100±17 days ) . Oxidative stress was assessed by plasma F2-isoprostane levels . DFO and placebo groups were well balanced with respect to baseline characteristics , symptom- and door-to-balloon times , pre-PPCI coronary patency , and infa rct -related artery location . Serum iron levels were decreased with DFO treatment after PPCI compared with placebo ( 3.0±2.5 versus 12.6±5.5 & mgr;mol/L , P<0.0001 ) , which persisted until the end of the infusion . In DFO-treated  patients , there was a significant reduction in plasma F2-isoprostane levels immediately after PPCI ( 2878±1461 versus 2213±579 pmol/L , P=0.04 ) . However , there was no difference in CMRI-determined infa rct size  ( DFO , 17.4±10.8 % , versus placebo , 18.6±10.2 % ; P=0.73 ) , myocardial salvage index at 3 days or at 3 months , or the area-under-the-curve for creatine kinase or troponin I. Conclusions — Adjunctive DFO treatment after the onset of ischemia and continued periprocedurally ameliorates oxidative stress without limiting infa rct size . Clinical Trial Registration — URL : http://www.anzctr.org.au/. Unique identifier : ACTRN12608000308392 OBJECTIVES The aim of this r and omized , single-blind , controlled trial was to assess N-acetylcysteine effects on contrast-induced nephropathy and reperfusion injury in ST-segment elevation myocardial infa rct ion patients undergoing primary angioplasty with moderate contrast volumes . BACKGROUND High-dose N-acetylcysteine reduced the incidence of contrast-induced nephropathy in patients with high contrast volumes and reduced reperfusion injury in animal trials . METHODS Patients undergoing primary angioplasty were r and omized to either high-dose N-acetylcysteine ( 2 x 1,200 mg/day for 48 h ; n = 126 ) or placebo plus optimal hydration ( n = 125 ) . The 2 primary end points were : 1 ) the occurrence of > 25 % increase in serum creatinine level < 72 h after r and omization ; and 2 ) a reduction in reperfusion injury measured as myocardial salvage index by magnetic resonance imaging . RESULTS The median volume of an iso-osmolar contrast agent during angiography was 180 ml ( interquartile range [ IQR ] 140 to 230 ml ) in the N-acetylcysteine and 160 ml ( IQR 120 to 220 ml ) in the placebo group ( p = 0.20 ) . The primary end point contrast-induced nephropathy occurred in 14 % of the N-acetylcysteine group and in 20 % of the placebo group ( p = 0.28 ) . The myocardial salvage index was also not different between both treatment groups ( 43.5 ; IQR 25.4 to 71.9 vs. 51.5 ; IQR 29.5 to 75.3 ; p = 0.36 ) . Activated oxygen protein products and oxidized low-density lipoprotein as markers for oxidative stress were reduced by as much as 20 % in the N-acetylcysteine group ( p < 0.05 ) , whereas no change was evident in the placebo group . CONCLUSIONS High-dose intravenous N-acetylcysteine reduces oxidative stress . However , it does not provide an additional clinical benefit to placebo with respect to CIN and myocardial reperfusion injury in nonselected patients undergoing angioplasty with moderate doses of contrast medium and optimal hydration . ( Myocardial Salvage and Contrast Dye Induced Nephropathy Reduction by N-Acetylcysteine [ LIPSIA-N-ACC ] ; NCT00463749 ) Objective To evaluate the oxidative stress status and the modification with glucose-insulin-potassium ( GIK ) therapy in patients with acute myocardial infa rct ion undergoing primary percutaneous transluminal coronary angioplasty . Design Prospect i ve , r and omized , double-blinded , placebo-controlled study . Setting Cardiac intensive care unit at the university hospital . Patients Twenty patients were r and omized to GIK solution ( 30 % glucose in water with insulin 50 IU/L , and KCl 40 mM ) vs. placebo ( normal saline ) at 1.5 mL/kg/hr for 24 hrs . The control group was 15 healthy volunteers with no heart disease . Interventions Eligible patients were r and omized by a blinded pharmacist , patients with acute myocardial infa rct ion were treated by primary percutaneous transluminal coronary angioplasty and r and omized to GIK or placebo ( saline solution ) . Primary angioplasty was successful in nine of ten patients ( 90 % ) and ten of ten patients ( 100 % ) in the GIK and placebo groups , respectively . Nine ( 100 % ) and six ( 60 % ) patients from GIK and placebo groups , respectively , underwent stent implantation . Measurements and Main Results We determined plasma levels of lipid peroxidation estimated by the malondialdehyde assay , superoxide dismutase , glutathione peroxidase , and catalase erythrocyte activities at admission and 0.5 and 24 hrs after angioplasty . Baseline determinations were compared with a control group ( n = 15 ) . Baseline clinical characteristics and time to treatment ( 4.5 ± 3.5 hrs ) were similar between groups . Angioplasty success rate ( Thrombolysis in Myocardial Infa rct ion [ TIMI ] 3 flow with residual stenosis ≤30 % ) was 90 % and 100 % in GIK and placebo groups , respectively . Patients with acute myocardial infa rct ion had an increase of malondialdehyde at baseline ( 2.9 ± 1.7 vs. 1.1 ± 0.3 & mgr;M , p < .01 ) and lower enzymatic activities of superoxide dismutase ( 0.5 ± 0.5 vs. 1.3 ± 0.4 U/mg hemoglobin , p < .01 ) and catalase ( 147 ± 73 vs. 198 ± 31 U/g hemoglobin , p < .01 ) . These measurements did not change significantly after angioplasty and no differences were observed between GIK and placebo groups . Conclusion Patients with acute myocardial infa rct ion had increased levels of oxidative stress associated with a reduction in enzymatic antioxidant reserve . Administration of GIK solution did not improve these abnormalities among patients undergoing primary angioplasty Background —Accurate models to predict mortality are needed for risk stratification in patients with ST-segment elevation myocardial infa rct ion ( STEMI ) undergoing primary percutaneous coronary intervention ( PCI ) .  Methods and Results —We examined 5745 patients with STEMI undergoing primary PCI in the Assessment of Pexelizumab in Acute Myocardial Infa rct ion Trial within 6 hours of symptom onset . A Cox proportional hazards model incorporating regression splines to accommo date nonlinearity in the log hazard ratio ( HR ) scale was used to determine baseline independent predictors of 90-day mortality . At 90 days , 271 ( 4.7 % ) of 5745 patients died . Independent correlates of 90-day mortality were ( in descending order of statistical significance ) age ( HR , 2.03/10-y increments ; 95 % CI , 1.80 to 2.29 ) , systolic blood pressure ( HR , 0.86/10-mm Hg increments ; 95 % CI , 0.82 to 0.90 ) , Killip class ( class 3 or 4 versus 1 or 2 ) ( HR , 4.24 ; 95 % CI , 2.97 to 6.08 ) , heart rate ( > 70 beats per minute ) ( HR , 1.45/10-beat increments ; 95 % CI , 1.31 to 1.59 ) , creatinine ( HR , 1.23/10-&mgr;mol/L increments > 90 & mgr;mol/L ; 95 % CI , 1.13 to 1.34 ) , sum of ST-segment deviations ( HR , 1.25/10-mm increments ; 95 % CI , 1.11 to 1.40 ) , and anterior STEMI location ( HR , 1.47 ; 95 % CI , 1.12 to 1.93 ) ( c-index , 0.82 ) . Internal validation with bootstrapping confirmed minimal overoptimism ( c-index , 0.81 ) . Conclusions —Our study provides a practical method to assess intermediate-term prognosis of patients with STEMI undergoing primary PCI  , using baseline clinical and ECG variables . This model identifies key factors affecting prognosis and enables quantitative risk stratification that may be helpful in guiding clinical care and for risk adjustment for observational analyses Objectives : The aims of this study were to investigate the effects of atorvastatin pretreatment on the oxygen free radicals and its protective role on the myocardial cell during the ischemic reperfusion injury . Methods : One hundred fifty-six patients with ST elevation myocardial infa rct ion undergoing percutaneous coronary interventions , aged from 29 to 85 years , were selected . Eighty patients were r and omly assigned to placebo group and 76 to statin treatment ( 80-mg loading dose given a mean of 1.5 hours before percutaneous coronary intervention ) . The nitrogen monoxidum , malondialdehyde , and superoxide dismutase ( SOD ) were assayed before and after reperfusion . Thrombolysis in myocardial infa rct ion ( TIMI ) grade and corrected TIMI frame count were measured after reperfusion . The creatine kinase-MB and troponin T peak levels after myocardial infa rct ion were recorded . Results : There was no significant difference in the nitrogen monoxidum , malondialdehyde , and SOD levels ( P > 0.05 ) between the 2 groups before intervention . After the reperfusion , significantly lower creatine kinase-MB ( 289.9 ± 180.8 U/L vs. 360.5 ± 206.4 U/L , P = 0.025 ) and troponin T ( 4.60 ± 3.13 ng/mL vs. 6.01 ± 4.98 ng/mL , P = 0.035 ) peak levels can be observed in the statin versus the placebo group , and the SOD level of the statin group is higher than that of the placebo group ( 34.14 ± 15.07 U/mL vs. 29.06 ± 12.76 U/mL , P = 0.024 ) . Conclusions : Atorvastatin can reduce oxygen free radicals developed in reperfusion , imposing protective effect on the myocardial cell during ischemic reperfusion injury This clinical pilot study was a r and omized , controlled , open-label study in 80 patients with acute myocardial infa rct ion and was design ed to examine the effects of a novel free radical scavenger , edaravone . Administration of edaravone before myocardial reperfusion was associated with smaller enzymatic infa rcts and better clinical outcome Background : In acute myocardial infa rct ion ( AMI ) treated with percutaneous coronary intervention ( PCI ) , myocardial injury results from complex processes during both ischemia and reperfusion . Release of reactive oxygen species ( ROS ) may contribute to the accumulated myocardial damage . Aims : To examine by frequent sampling of peripheral blood oxidative stress and early inflammation in patients under 
    Output:
    
Results Administration of edaravone , allopurinol , atorvastatin and nicor and il as a supplement to primary PCI significantly reduced oxidative stress and myocardial damage as well as improved cardiac function and clinical outcomes .