***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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    Input: Background Antiplatelet therapy with aspirin and antithrombotic therapy with heparin both prevent the complications of unstable angina ; however , no definitive data exist on the relative clinical efficacy of the two drugs . Methods and Results Aspirin ( 325 mg bid ) or heparin ( 5000-U intravenous bolus followed by a perfusion titrated to the APTT ) were compared in a double-blind r and omized trial of 484 patients in two cohorts enrolled sequentially . The study was initiated at admission to hospital at a mean of 8.3±7.8 hours after the last episode of pain . End points were assessed 5.7±3.3 days later , when the decision for long-term management was made . Myocardial infa rct ion occurred in 2 ( 0.8 % ) of the 240 patients r and omized to heparin  and in 9 ( 3.7 % ) of the 244 r and omized to aspirin ( P=.035 ) , an odds ratio of 0.22 and a risk difference of 2.9%o ( 95 % confidence limits , 0.3 % to 5.6 % ) with heparin . The only death result ed from a myocardial infa rct ion in an aspirin patient . Survival curves with Cox logistic regression analysis showed that the improvement in survival without myocardial infa rct ion  with heparin ( P=.035 ) was independent of other baseline characteristics . Conclusions This study documents that heparin prevents myocardial infa rct ion better than aspirin during the acute phase of unstable angina BACKGROUND The CAPTURE ( C7E3 fab AntiPlatelet Therapy in Unstable REfactory angina ) trial enrolled patients with refractory unstable angina and documented a therapeutic benefit for abciximab , a platelet glycoprotein IIb/IIIa receptor antagonist , that was particularly evident in patients with elevated troponin T ( TnT ) levels . In the current study , we related the angiographic data to the TnT status of the CAPTURE patients . METHODS AND RESULTS In 853 patients , angiographic data at baseline and 18 to 24 hours after treatment were available and assessed by an Angiographic Committee with respect to TIMI flow , lesion severity , and visibility of thrombus . TnT levels > 0.1 microg/L were found in 30.9 % of the patients . Before r and omization , thrombus was visible in 14.6 % of TnT-positive patients ( TnT levels > 0.1 microg/L ) and 4.2 % of TnT-negative patients ( P=0.004 ) . Complex lesion characteristics B2+/C ( 72.0 % versus 53.9 % ; P<0.001 ) and TIMI flow < 2 ( 15.6 % versus 5 . 1 % ; P<0.001 ) were more frequent in TnT-positive patients . Abciximab was effective with respect to reduction of visible thrombus , increase of TIMI flow , and reduction of cardiac events in TnT-positive patients only . Multivariate analysis identified TnT status , but not angiographic findings , as an independent predictor for both outcome and efficacy of treatment with abciximab . CONCLUSIONS Complex lesion characteristics and visible thrombus formation at baseline were significantly linked to TnT elevation . However , TnT status was a more powerful predictor of increased cardiac risk and efficacy of treatment with abciximab than either . Relative to the angiogram , TnT can thus be considered a more sensitive marker for the underlying pathology , identifying patients with unstable angina who will particularly benefit from antiplatelet treatment CONTEXT Patients with unstable angina/non-ST-segment elevation myocardial infa rct ion ( MI ) ( UA/NSTEMI ) present with a wide spectrum of risk for death and cardiac ischemic events . OBJECTIVE To develop a simple risk score that has broad applicability , is easily calculated at patient presentation , does not require a computer , and identifies patients with different responses to treatments for UA/NSTEMI . DESIGN , SETTING , AND PATIENTS Two phase 3 , international , r and omized , double-blind trials ( the Thrombolysis in Myocardial Infa rct ion [ TIMI ] 11B trial [ August 1996-March 1998 ] and the Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non-Q-Wave MI trial [ ESSENCE ; October 1994-May 1996 ] ) . A total of 1957 patients with UA/NSTEMI were assigned to receive unfractionated heparin ( test cohort )  and 1953 to receive enoxaparin in TIMI 11B ; 1564 and 1607 were assigned respectively in ESSENCE . The 3 validation cohorts were the unfractionated heparin group from ESSENCE and both enoxaparin groups . MAIN OUTCOME MEASURES The TIMI risk score was derived in the test cohort by selection of independent prognostic variables using multivariate logistic regression , assignment of value of 1 when a factor was present and 0 when it was absent , and summing the number of factors present to categorize patients into risk strata . Relative differences in response to therapeutic interventions were determined by comparing the slopes of the rates of events with increasing score in treatment groups and by testing for an interaction between risk score and treatment . Outcomes were TIMI risk score for developing at least 1 component of the primary end point ( all-cause mortality , new or recurrent MI , or severe recurrent ischemia requiring urgent revascularization ) through 14 days after r and omization . RESULTS The 7 TIMI risk score predictor variables were age 65 years or older , at least 3 risk factors for coronary artery disease , prior coronary stenosis of 50 % or more ,  ST-segment deviation on electrocardiogram at presentation  , at least 2 anginal events in prior 24 hours , use of aspirin in prior 7 days , and elevated serum cardiac markers . Event rates increased significantly as the TIMI risk score increased in the test cohort in TIMI 11B : 4.7 % for a score of 0/1 ; 8.3 % for 2 ; 13 . 2 % for 3 ; 19.9 % for 4 ; 26.2 % for 5 ; and 40.9 % for 6/7 ( P<.001 by chi(2 ) for trend ) . The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups ( P<.001 ) . The slope of the increase in event rates with increasing numbers of risk factors was significantly lower in the enoxaparin groups in both TIMI 11B ( P = .01 ) and ESSENCE ( P = .03 ) and there was a significant interaction between TIMI risk score and treatment ( P = . 02 ) . CONCLUSIONS In patients with UA/NSTEMI , the TIMI risk score is a simple prognostication scheme that categorizes a patient 's risk of death and ischemic events and provides a basis for therapeutic decision making . JAMA . 2000;284:835 - We conducted a multicenter , double-blind , placebo-controlled , r and omized trial of nifedipine , metoprolol , and their combination in 338 patients whose hospital admission diagnosis was unstable angina and who were not pretreated with a β-blocker , and of nifedipine in 177 patients who were treated with a β-blocker . The main outcome event was the recurrence of ischemia or progression to myocardial infa rct ion within 48 h. Trial medication effects are expressed as ratios of event rates relative to placebo , e.g. , the ratio for nifedipine is the event rate under nifedipine divided by that under placebo . In addition , 95 % confidence intervals are given . In patients not pretreated with a β-blocker , the event rate ratio for nifedipine was 1.15 ( 0.83 , 1.64 ) , for metoprolol 0.76 ( 0.49 , 1.16 ) , and for the combination 0.80 ( 0.53 , 1.19 ) . In patients already on a β-blocker , the addition of nifedipine was favorable ; i.e. , the rate ratio was 0.68 ( 0.47 , 0.97 ) . Equal numbers of patients developed myocardial infa rct ion and reversible ischemia . Most infa rct ions occurred early , within 6 h of r and omization . In patients not already on a β-blocker , the nifedipine rate ratio for infa rct ion was 1.51 ( 0.87 , 2.74 ) . These results suggest that , in patients not on previous β-blockade , metoprolol has a beneficial short-term effect on unstable angina , a fixed combination with nifedipine provides no further gain , and nifedipine may be ineffective or counterproductive . On the other h and , the addition of nifedipine to existing β-blockade when the patient becomes unstable seems beneficial AIMS We evaluated the TIMI Risk Score for Unstable Angina and Non-ST Elevation Myocardial Infa rct ion for predicting clinical outcomes and the efficacy of tirofiban in non-ST elevation acute coronary syndromes . METHODS AND RESULTS Developed in TIMI 11B , the risk score is calculated as the sum of seven presenting characteristics ( age > or = 65 years , > or =3 cardiac risk factors , documented coronary disease , recent severe angina , ST deviation > or = 0.5 mm , elevated cardiac markers , prior aspirin use ) . The risk score was vali date d in the PRISM-PLUS data base ( n=1915 ) and tested for interaction with the efficacy of tirofiban+heparin vs heparin alone . The risk score revealed an increasing gradient of risk for death , myocardial infa rct ion or recurrent ischaemia at 14 days ranging from 7.7 - 30.5 % ( P<0.001 ) . Dichotomized at the median , patients with a score > or = 4 derived a greater relative risk reduction with tirofiban ( P((Interaction))=0.025 ) . Among patients with normal creatine kinase myocardial b and s , the risk score showed a 3.5-fold gradient of risk ( P<0.001 ) and identified a population that derived significant benefit from tirofiban ( RR 0.73 , P=0.027 ) . CONCLUSION The TIMI Risk Score is a simple clinical tool for risk assessment that may aid in the early identification of patients who should be considered for treatment with potent antiplatelet therapy BACKGROUND Glycoprotein IIb/IIIa blockers reduce procedure-related thrombotic complications of percutaneous coronary intervention , and the risk of death and myocardial infa rct ion in patients with acute coronary syndromes . The effect on risk of death and myocardial infa rct ion is particularly apparent in patients undergoing early percutaneous coronary interventions . We did a r and omised , multicentre trial to study the effect of the glycoprotein IIb/IIIa blocker abciximab on patients with acute coronary syndromes who were not undergoing early revascularisation . METHODS We enrolled 7800 patients who were admitted to hospital with chest pain and either ST-segment depression or raised troponin T or I concentrations . 2598 were r and omly assigned placebo , 2590 an abciximab bolus and 24 h infusion , and 2612 an abciximab bolus and 48 h infusion ; all patients received aspirin and either unfractionated or low-molecular-weight heparin . The primary endpoint was death or myocardial infa rct ion at 30 days after r and omisation . Analysis was by intention to treat . FINDINGS There were no drop-outs . 209 ( 8.0 % ) patients on placebo , 212 ( 8.2 % ) on 24 h abciximab , and 238 ( 9.1 % ) on 48 h abciximab  died or had a myocardial infa rct ion before day 30 ( odds ratio 1.0 [ 95 % CI 0.83 - 1.24 ] , for difference between placebo and 24 h abciximab , and 1.1 [ 0.94 - 1.39 ] for difference between placebo and 48 h abciximab ) . The lack of benefit from treatment with abciximab was consistent in most subgroups investigated ; in particular , no benefit was seen in patients with raised cardiac troponin T or I concentrations at enrolment , although these patients did have a strongly increased risk of subsequent events . Bleeding rates were low , but increased with abciximab , particularly when continued for 48 h. Additionally , thrombocytopenia was more frequent with abciximab than with placebo . INTERPRETATIONS Although the explanations for our findings are unclear , this study indicates that abciximab is not beneficial as first-line medical treatment in patients admitted with acute coronary syndromes One hundred consecutive patients hospitalized in the coronary care unit for unstable angina , excluding patients with Prinzmetal 's variant angina , were r and omized within 24 hours of admission to treatment with diltiazem ( 50 patients ) or propranolol ( 50 patients ) . Also excluded were patients with previous coronary artery bypass surgery and those receiving a beta-receptor blocking agent at the time of hospital admission . Left ventricular function and the extent of coronary artery disease 
    Output:
    
The invasive strategy did not reduce death on longer-term follow up .
AUTHORS ' CONCLUSIONS Compared to a conservative strategy for UA/NSTEMI , an invasive strategy is associated with reduced rates of refractory angina and rehospitalization in the shorter term and myocardial infa rct ion in the longer term .
However , the invasive strategy is associated with a doubled risk of procedure-related heart attack and increased risk of bleeding and procedural biomarker leaks .
Available data suggest that an invasive strategy may be particularly useful in those at high risk for recurrent events