***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: In this pilot study , we show that periprocedural administration of tirofiban during stenting of critically stenosed saphenous vein grafts , significantly reduces the occurrence of postprocedural minor myocardial necroses OBJECTIVES The Troponin in Planned PTCA/Stent Implantation With or Without Administration of the Glycoprotein IIb/IIIa Receptor Antagonist Tirofiban ( TOPSTAR ) trial investigated : 1 ) the amount of troponin T ( TnT ) release after nonacute , elective percutaneous coronary intervention ( PCI ) in patients pretreated with aspirin and clopidogrel ; and 2 ) the effect of additional glycoprotein ( GP ) IIb/IIIa receptor inhibiton on postinterventional TnT release . BACKGROUND No data are available yet as to whether additional administration of a GP IIb/IIIa receptor antagonist might be beneficial in patients undergoing elective PCI already pretreated with aspirin and clopidogrel . METHODS After bolus application of the study medication ( tirofiban [ T ] or placebo [ P ] ) , PCI was performed followed by an 18-h continuous infusion of T/P. Primary end point of the study was incidence and amount of TnT release after elective PCI after 24 h. RESULTS A total of 12 h after PCI troponin release was detected in 63 % of the patients receiving P and in 40 % of the patients receiving T ( p < 0.05 ) , after 24 h in 69 % ( P ) and 48 % ( T ) ( p < 0.05 ) and after 48 h in 74 % ( P ) versus 58 % ( T ) ( p < 0.08 ) of the patients . No differences were observed regarding major bleeding , intracranial bleeding or nonhemorrhagic strokes . After nine months a reduction of combined death/myocardial infa rct ion/target vessel revascularization could be observed in the tirofiban group ( [ T ] 2.3 % vs. [ P ] 13.04 % , p < 0.05 ) . CONCLUSIONS Troponin T release occurs after successful intervention in 74 % of the patients undergoing elective PCI after 48 h even after pretreatment with aspirin and clopidogrel . The GP IIb/IIIa receptor antagonist tirofiban is able to decrease the incidence of troponin release significantly in this patient population OBJECTIVES The objectives of this double-blind , placebo-controlled , r and omized dose-ranging study were 1 ) to examine the safety and tolerability of tirofiban ( MK-383 ) , a new nonpeptide platelet IIb/IIIa receptor antagonist , on a background of intravenous heparin and aspirin therapy ; 2 ) to study the pharmacodynamics and pharmacokinetics of tirofiban ; and 3 ) to evaluate the incidence of adverse cardiac outcomes ( urgent repeat revascularization , myocardial infa rct ion and death ) with tirofiban versus placebo in a high risk subset of patients undergoing coronary angioplasty . BACKGROUND Abrupt vessel closure complicates 4 % to 8 % of angioplasty procedures . Recent data have suggested that agents that antagonize the platelet glycoprotein IIb/IIIa receptor may reduce the incidence of adverse ischemic outcomes after coronary angioplasty . METHODS Seventy-three patients received tirofiban in three sequential dose panels and 20 patients received placebo . Patients within each panel were r and omized to receive either tirofiban or placebo in a 3:1 r and omization design . Bolus doses of 5 , 10 and 10 microg/kg and continuous infusion ( 16 to 24 h ) doses of 0.05 , 0.10 and 0.15 microg/kg per min were administered in panels I , II and III , respectively . Patients received concomitant heparin and aspirin for the angioplasty procedure . Data on patients receiving placebo ( heparin and aspirin only ) were pooled across panels for comparisons . The pharmacodynamic effect of tirofiban on ex vivo platelet aggregation to 5 micromol/liter adenosine diphosphate ( ADP ) and bleeding times were measured . Clinical outcomes were assessed in all patients , but the power to detect clinical ly meaningful differences ( a one-third reduction in clinical events ) between groups was limited ( 5 % ) . RESULTS Tirofiban was associated with a dose-dependent inhibition of ex vivo ADP-mediated platelet aggregation that was sustained during intravenous infusion and resolved rapidly after drug cessation . Adverse bleeding events , largely related to vascular access site hemorrhage , were slightly increased at the highest dose . Adverse clinical outcomes were infrequent in all patients and were not different among the small number of patients within each group . CONCLUSIONS This study establishes a rational and generally well tolerated dosing regimen for administration of tirofiban as adjunctive therapy in high risk angioplasty patients . The impact of tirofiban on adverse clinical outcomes after angioplasty awaits definition by a larger clinical trial BACKGROUND The use of intravenous glycoprotein IIb/IIIa-receptor antagonists has been shown to improve outcomes in patients undergoing percutaneous transluminal coronary angioplasty ( PTCA ) .  Tirofiban has shown benefit in a wide range of patients presenting with acute coronary syndromes . Although this agent has been used in patients undergoing percutaneous coronary intervention , a literature search identified no prospect i ve data comparing tirofiban with placebo in patients undergoing planned intracoronary stent placement . OBJECTIVE This study examined the tolerability of tirofiban in patients undergoing percutaneous intervention with planned intracoronary stent placement . METHODS This was a multinational , multicenter , prospect i ve , r and omized , double-blind , placebo-controlled trial in patients scheduled to undergo PTCA with planned intracoronary stent placement . Patients were r and omized in a 3:2 ratio to receive tirofiban as an intravenous bolus ( 10 microg/kg over 3 minutes ) and maintenance infusion ( 0.10 microg/kg per minute for 36 hours ) or a bolus and infusion of placebo . All patients received periprocedural aspirin and heparin and an optional postprocedural thienopyridine ( ticlopidine or clopidogrel ) . Laboratory and safety monitoring were performed throughout the 36 hours after the procedure and at hour 40 or hospital discharge . The primary end point was the proportion of patients with bleeding , defined according to Thrombolysis in Myocardial Infa rct ion ( TIMI ) trial criteria . The number of patients with cardiac events ( death , myo- cardial infa rct ion , urgent revascularization ) during the first 30 days after stent placement was also assessed . RESULTS Eight hundred ninety-four patients ( 536 tirofiban , 358 placebo ) were enrolled , all of whom received aspirin and heparin periprocedurally and optional ticlopidine or clopidogrel after the procedure . No significant between-group differences were observed in the incidence of TIMI major bleeding ( 0.2 % tirofiban , 0.6 % placebo ) or any TIMI bleeding ( 3.2 % and 1.7 % , respectively ) . The incidence of TIMI minor bleeding was higher with tirofiban than with placebo ( 2.8 % vs 0.6 % ) . The 30-day incidence of the composite end point of any cardiac event was 3.9 % in both groups . CONCLUSIONS On a background of concomitant aspirin , heparin , and a thienopyridine , tirofiban was generally well tolerated in patients undergoing PTCA with planned intracoronary stent placement . Further investigation is needed to ascertain the optimal dosing of tirofiban and heparin to achieve reductions in ischemic complications of intracoronary stenting with an acceptable incidence of bleeding complications OBJECTIVES The aims of the Safety and Efficacy of Subcutaneous Enoxaparin Versus Intravenous Unfractionated Heparin and Tirofiban Versus Placebo in the Treatment of Acute ST-Segment Elevation Myocardial Infa rct ion Patients Ineligible for Reperfusion ( TETAMI ) study were to demonstrate that enoxaparin was superior to unfractionated heparin ( UFH ) and that tirofiban was better than placebo in patients with acute ST-segment elevation myocardial infa rct ion ( STEMI ) who do not receive timely reperfusion . BACKGROUND An optimal treatment strategy has not been identified for the many STEMI patients ineligible for acute reperfusion . METHODS A total of 1224 patients were enrolled in 91 centers in 14 countries between July 1999 and July 2002 . Patients with STEMI ineligible for reperfusion were r and omized to enoxaparin , enoxaparin plus tirofiban , UFH , or UFH plus tirofiban . All patients received oral aspirin . The primary efficacy end point was the 30-day combined incidence of death , reinfa rct ion , or recurrent angina ; the primary analysis was the comparison of the pooled enoxaparin and UFH groups . RESULTS The incidence of the primary efficacy end point was 15.7 % enoxaparin versus 17.3 % for UFH ( odds ratio 0.89 [ 95 % confidence interval CI = 0.66 to 1.21 ] ) and 16.6 % for tirofiban versus 16.4 % for placebo ( odds ratio 1.02 [ 95 % CI 0.75 to 1.38 ] ) . The Thrombolysis In Myocardial Infa rct ion ( TIMI ) major hemorrhage rate was 1.5 % for enoxaparin versus 1.3 % for UFH ( odds ratio 1.16 [ 95 % CI 0.44 to 3.02 ] ) and 1.8 % versus 1 % for tirofiban versus placebo ( odds ratio 1.82 [ 95 % CI 0.67 to 4.95 ] ) . CONCLUSIONS This study did not show that enoxaparin significantly reduced the 30-day incidence of death , reinfa rct ion , and recurrent angina compared with UFH in non-reperfused STEMI patients . However , enoxaparin appears to have a similar safety and efficacy profile to UFH and may be an alternative treatment . Additional therapy with tirofiban did not appear beneficial Glycoprotein IIb/IIIa receptor inhibition prevents the major cardiac events and improves the prognosis of patients with acute coronary syndromes . The purpose of the study was to evaluate the effects of tirofiban on clinical stabilization parameters in patients with unstable angina ( UA ) and non-Q-wave myocardial infa rct ion ( MI ) . Eighty-three patients presenting with prolonged ongoing chest pain and ST segment depression were included in the study . Forty-two patients were r and omized to aspirin and heparin therapy , and 41 patients to tirofiban therapy in addition to the aspirin and heparin therapy .  The interval between the initiation of the treatment and the disappearance of angina , recovery time of ST segment depression , creatine kinase-MB ( CK-MB ) levels , onset of decrease and normalization of CK-MB , and frequency of in-hospital major cardiac events were compared . The interval between initiation of the treatment and the disappearance of angina was significantly shorter in the tirofiban group ( 3.5 ± 4.2 vs 9.1 ± 8.6 h , P ≪ 0.001 ) . Recovery time of ST depression was also significantly shorter in the tirofiban group ( 5.1 ± 7.3 vs 12.3 ± 11.5 h , P ≪ 0.05 ) . The peak CK-MB values were significantly lower in the non-Q-wave MI and UA subgroups of tirofiban than in the heparin group ( P = 0.04 for both ) . The onset of the CK-MB decrease was significantly earlier in the tirofiban group ( 15 ± 14 vs 24 ± 15 h , P = 0.02 ) . The normalization time of the CK-MB was relatively shorter in the tirofiban group but without statistical significance ( 50 ± 22 vs 60 ± 25 h ) . The tirofiban group had a lower frequency of total major cardiac events ( 26 % vs 54 % , P = 0.01 ) , acute MI ( 2.4 % vs 19 % , P = 0.03 ) , and recurrent angina ( 26 % vs 50 % , P = 0.04 ) . The frequency of death and urgent revascularization did not differ between the groups . Tirofiban , in addition to heparin , provides earlier clinical stability and prevents major in-hospital cardiac events in patients with UA and non-Q-wave MI as compared to heparin therapy alone Background —Thrombocytopenia is a possible complication of treatment with glycoprotein ( GP ) IIb/IIIa antagonists during percutaneous coronary interventions , but it is not clear whether different GP IIb/IIIa inhibitors carry a different risk of 
    Output:
    
Tirofiban administration reduces mortality , the composite of death or MI and increases minor bleedings when compared with placebo .
An early ischaemic hazard disfavouring tirofiban was noted when compared with abciximab in studies based on 10 but not 25 microg/kg tirofiban bolus regimen