***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 — Oxygen is commonly administered to patients with ST-elevation – myocardial infa rct ion despite previous studies suggesting a possible increase in myocardial injury as a result of coronary vasoconstriction and heightened oxidative stress . Methods and Results — We conducted a multicenter , prospect i ve , r and omized , controlled trial comparing oxygen ( 8 L/min ) with no supplemental oxygen in patients with ST-elevation – myocardial infa rct ion diagnosed on paramedic 12-lead ECG . Of 638 patients r and omized , 441 patients had confirmed ST-elevation – myocardial infa rct ion and underwent primary end-point analysis . The primary end point was myocardial infa rct size as assessed by cardiac enzymes , troponin I , and creatine kinase . Secondary end points included recurrent myocardial infa rct ion , cardiac arrhythmia , and myocardial infa rct size assessed by cardiac magnetic resonance imaging at 6 months . Mean peak troponin was similar in the oxygen and no oxygen groups ( 57.4 versus 48.0 & mgr;g/L ; ratio , 1.20 ; 95 % confidence interval , 0.92–1.56 ; P=0.18 ) . There was a significant increase in mean peak creatine kinase in the oxygen group compared with the no oxygen group ( 1948 versus 1543 U/L ; means ratio , 1.27 ; 95 % confidence interval , 1.04–1.52 ; P=0.01 ) . There was an increase in the rate of recurrent myocardial infa rct ion in the oxygen group compared with the no oxygen group ( 5.5 % versus 0.9 % ; P=0.006 ) and an increase in frequency of cardiac arrhythmia ( 40.4 % versus 31.4 % ; P=0.05 ) . At 6 months , the oxygen group had an increase in myocardial infa rct size on cardiac magnetic resonance ( n=139 ; 20.3 versus 13.1 g ; P=0.04 ) . Conclusion — Supplemental oxygen therapy in patients with ST-elevation – myocardial infa rct ion but without hypoxia may increase early myocardial injury and was associated with larger myocardial infa rct size assessed at 6 months . Clinical Trial Registration — URL : http://www . clinical trials.gov . Unique identifier : NCT01272713 Pathological formation of reactive oxygen species within the coronary circulation has been hypothesized to mediate some clinical manifestations of ischemic heart disease ( IHD ) by interfering with physiological regulation of coronary tone . To determine the degree to which coronary tone responds to acute changes in ambient levels of oxidants and antioxidants in vivo in a clinical setting , we measured the effect of an acute oxidative stress ( breathing 100 % oxygen ) on coronary capacitance artery diameter ( quantitative angiography ) and blood flow velocity through the coronary microcirculation ( intracoronary Doppler ultrasonography ) before and after treatment with the antioxidant vitamin C ( 3-g intravenous infusion ) in 12 IHD patients undergoing a clinical coronary interventional procedure . Relative to room air breathing , 100 % oxygen breathing promptly reduced coronary blood flow velocity by 20 % and increased coronary resistance by 23 % , without significantly changing the diameter of capacitance arteries .  Vitamin C administration promptly restored coronary flow velocity and resistance to a slightly suprabasal level , and it prevented the reinduction of coronary constriction with rechallenge with 100 % oxygen . This suggests that acute oxidative stress produces prompt and substantial changes in coronary resistance and blood flow in a clinical setting in patients with IHD , and it suggests that these changes are mediated by vitamin C-quenchable substances acting on the coronary microcirculation . This observation may have relevance for clinical practice Objective Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infa rct ion ( STEMI ) . In this study , we aim ed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI . Methods Descriptive analysis of data from a multicentre , prospect i ve , r and omised , controlled trial of 441 patients with STEMI r and omised to supplemental oxygen therapy or room air breathing .  The primary endpoint was myocardial infa rct size as assessed by cardiac biomarkers , troponin ( cTnI ) and creatine kinase ( CK ) .  Oxygen therapy was commenced by paramedics , and continued for up to 12 h postintervention in hospital . Supplemental oxygen exposure was calculated as the area under the dose × time curve for oxygen administration over the first 12 h , and then assessed for its association with cTnI/CK release using multivariable linear regression . Results The median supplemental oxygen exposure was 1746 L ( IQR : 960–2858 ) . After adjustment for potential confounders , every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4 % ( 95 % CI 0.6 % to 2.2 % , p<0.001 ) and 1.2 % ( 95 % CI 0.7 % to 1.8 % , p<0.001 ) increase in the mean peak cTnI and CK , respectively . Excluding patients who developed cardiogenic shock , recurrent myocardial infa rct ion or desaturations ( SpO2<94 % ) during admission , every 100 L increase in oxygen exposure was associated with a 1.2 % ( 95 % CI 0.2 % to 2.1 % , p=0.01 ) and 1.0 % ( 95 % CI 0.3 % to 1.7 % , p=0.003 ) increase in the mean peak cTnI and CK , respectively . The median supplemental oxygen exposure of 1746 L would result in a 21 % ( 95 % CI 3 % to 37 % ) increase in infa rct size according to the cTnI profile . Conclusions Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinical ly significant increase in cTnI and CK release Background —Few data are available on the impact of heart failure ( HF ) across all types of acute coronary syndromes ( ACS ) . Methods and Results —The Global Registry of Acute Coronary Events ( GRACE ) is a prospect i ve study of patients hospitalized with ACS . Data from 16 166 patients were analyzed : 13 707 patients without prior HF or cardiogenic shock at presentation were identified . Of these , 1778 ( 13 % ) had an admission diagnosis of HF ( Killip class II or III ) . HF on admission was associated with a marked increase in mortality rates during hospitalization ( 12.0 % versus 2.9 % [ with versus without HF ] , P < 0.0001 ) and at 6 months after discharge ( 8.5 % versus 2.8 % , P < 0.0001 ) . Of note , HF increased mortality rates in patients with unstable angina ( defined as ACS with normal biochemical markers of necrosis ; mortality rates : 6.7 % with versus 1.6 % without HF at admission , P < 0.0001 ) . By logistic regression analysis , admission HF was an independent predictor of hospital death ( odds ratio , 2.2 ; P < 0.0001 ) . Admission HF was associated with longer hospital stay and higher readmission rates .  Patients with HF had lower rates of catheterization and percutaneous cardiac intervention , and fewer received & bgr;-blockers and statins . Hospital development of HF ( versus HF on presentation ) was associated with an even higher in-hospital mortality rate ( 17.8 % versus 12.0 % , P < 0.0001 ) . In patients with HF , in-hospital revascularization was associated with lower 6-month death rates ( 14.0 % versus 23.7 % , P < 0.0001 ; adjusted hazard ratio , 0.5 ; 95 % CI , 0.37 to 0.68 , P < 0.0001 ) . Conclusions —In this observational registry , heart failure was associated with reduced hospital and 6-month survival across all ACS subsets , including patients with normal markers of necrosis . More aggressive treatment of these patients may be warranted to improve prognosis Two-hundred consecutive patients thought to have suffered a myocardial infa rct ion were admitted to a r and omised , double-blind controlled trial of oxygen or air administered by MC mask throughout the first 24 hours in hospital . Forty-three patients in whom myocardial infa rct ion was not subsequently confirmed were excluded from the analysis . The remaining air and oxygen groups were comparable except for a significantly higher PaO2 and serum aspartate aminotransferase level in the oxygen group . There was no significant difference in mortality , incidence of arrhythmias , use of analgesics , or systolic time intervals between the two groups , although a higher incidence of sinus tachycardia was found in those given oxygen . There appears to be no evidence of benefit from the routine administration of oxygen in uncomplicated myocardial infa rct ion Patients with heart disease are frequently treated with supplemental oxygen . Although oxygen can exhibit vasoactive properties in many vascular beds , its effects on the coronary circulation have not been fully characterized . To examine whether supplemental oxygen administration affects coronary blood flow ( CBF ) in a clinical setting , we measured in 18 patients with stable coronary heart disease the effects of breathing 100 % oxygen by face mask for 15 min on CBF ( via coronary Doppler flow wire ) , conduit coronary diameter , CBF response to intracoronary infusion of the endothelium-dependent dilator ACh and to the endothelium-independent dilator adenosine , as well as arterial and coronary venous concentrations of the nitric oxide ( NO ) metabolites nitrotyrosine , NO(2)(- ) , and NO(3)(- ) . Relative to breathing room air , breathing of 100 % oxygen increased coronary resistance by approximately 40 % , decreased CBF by approximately 30 % , increased the appearance of nitrotyrosine in coronary venous plasma , and significantly blunted the CBF response to ACh . Oxygen breathing elicited these changes without affecting the diameter of large-conduit coronary arteries , coronary venous concentrations of NO(2)(- ) and NO(3)(- ) , or the coronary vasodilator response to adenosine . Administering supplemental oxygen to patients undergoing cardiac catheterization substantially increases coronary vascular resistance by a mechanism that may involve oxidative quenching of NO within the coronary microcirculation OBJECTIVES This study sought to determine whether hyperoxemic reperfusion with aqueous oxygen ( AO ) improves recovery of ventricular function after percutaneous coronary intervention ( PCI ) for acute myocardial infa rct ion ( AMI ) . BACKGROUND Hyperbaric oxygen reduces myocardial injury and improves ventricular function when administered during ischemia-reperfusion . METHODS In a prospect i ve , multicenter study , 269 patients with acute anterior or large inferior AMI undergoing primary or rescue PCI ( < 24 h from symptom onset ) were r and omly assigned after successful PCI to receive hyperoxemic reperfusion ( treatment group ) or normoxemic blood autoreperfusion ( control group ) . Hyperoxemic reperfusion was performed for 90 min using intracoronary AO . The primary end points were final infa rct size at 14 days , ST-segment resolution , and delta regional wall motion score index of the infa rct zone at 3 months . RESULTS At 30 days , the incidence of major adverse cardiac events was similar between the control and AO groups ( 5.2 % vs. 6.7 % , p = 0.62 ) . There was no significant difference in the incidence of the primary end points between the study groups . In post-hoc analysis , anterior AMI patients reperfused < 6 h who were treated with AO had a greater improvement in regional wall motion ( delta wall motion score index = 0.54 in control group vs. 0.75 in AO group , p = 0.03 ) , smaller infa rct size ( 23 % of left ventricle in control group vs. 9 % of left ventricle in AO group , p = 0.04 ) , and improved ST-segment resolution compared with normoxemic controls . CONCLUSIONS Intracoronary hyperoxemic reperfusion was safe and well tolerated after PCI for AMI , but did not improve regional wall motion , ST-segment resolution , or final infa rct size . A possible treatment effect was observed in anterior AMI patients reperfused < 6 h of symptom onset BACKGROUND The use of supplemental oxygen in the setting of suspected acute myocardial infa rct ion ( AMI ) is recommended in international treatment guidelines and established in prehospital and hospital clinical routine throughout the world . However , to date there is no conclusive evidence from adequately design ed and powered trials supporting this practice . Existing data are conflicting and fail to clarify the role of supplemental oxygen in AMI . METHODS A total of 6,600 normoxemic ( oxygen saturation [ SpO2 ] ≥90 % ) patients with suspected AMI will be r and omly assigned to either supplemental oxygen 
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There is no clear effect for oxygen on infa rct size ( the evidence is inconsistent and low quality ) .
There is no evidence from r and omised controlled trials to support the routine use of inhaled oxygen in people with AMI , and we can not rule out a harmful effect .