Antiplatelet effects of abciximab, tirofiban and eptifibatide in patients undergoing coronary stenting

被引:62
作者
Neumann, FJ
Hochholzer, W
Pogatsa-Murray, G
Schömig, A
Gawaz, M
机构
[1] Tech Univ Munich, Med Klin, D-81674 Munich, Germany
[2] Tech Univ Munich, Deutsch Herzzentrum, D-81674 Munich, Germany
关键词
D O I
10.1016/S0735-1097(01)01165-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES We sought to investigate Whether abciximab, tirofiban and eptifibatide achieve comparable antiplatelet effects with coronary stenting. BACKGROUND The glycoprotein (GP) IIb/IIIa antagonists abciximab, tirofiban and eptifibatide differ in chemical structure, binding site and pharmacokinetics. METHODS Sixty patients undergoing coronary stenting were randomly assigned to abciximab (bolus 0.25 mg/kg body weight, infusion 10 mug per min for 12 h), tirofiban (bolus 10 mug/kg, infusion 0.15 mug/kg per min for 72 h) or eptifibatide (bolus 180 mug/kg, infusion 2 mug/kg per min for 72 h). We took serial blood samples tc, analyze platelet function by using how cytometry, turbidimetric aggregometry and the rapid platelet-function assay (RPFA. RESULTS As assessed by RPFA, platelet aggregation after 2 h of infusion was reduced to 5.9 +/- 7.8% (mean +/- SD) of baseline by abciximab, to 5.0 +/- 5.4% by tirofiban and to 7.8 +/- 7.1% by eptifibatide (p = 0.42). Turbidimetric aggregometry with adenosine diphosphate stimulation yielded similar results, whereas percent inhibition of platelet aggregation after thrombin receptor stimulation was 45.8 +/- 16.8% with abciximab, 51.3 +/- 17.6% with tirofiban and 52.9 +/- 14.8% with eptifibatide (p = 0.37). Tirofiban and eptifibatide maintained their level of platelet inhibition during infusion. Flow cytometry revealed that the reduction in the monocyte-platelet interaction by abciximab, tirofiban and eptifibatide was not significantly different (20.0 +/- 21.9%, 23.8 +/- 18.2% and 21.0 +/- 19.8%, respectively; p = 0.87). CONCLUSIONS Abciximab, tirofiban and eptifibatide, at currently recommended doses, achieved similar levels of inhibition of platelet aggregation and a similar reduction in the platelet-monocyte interaction. (J Am Coil Cardiol 2001;37:1323-8) (C) 2001 by the American College of Cardiology.
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页码:1323 / 1328
页数:6
相关论文
共 34 条
[1]   USE OF A MONOCLONAL-ANTIBODY DIRECTED AGAINST THE PLATELET GLYCOPROTEIN IIB/IIIA RECEPTOR IN HIGH-RISK CORONARY ANGIOPLASTY [J].
CALIFF, RM ;
SHADOFF, N ;
VALETT, N ;
BATES, E ;
GALEANA, A ;
KNOPF, W ;
SHAFTEL, J ;
BENDER, MJ ;
AVERSANO, T ;
RAQUENO, J ;
GURBEL, P ;
COWFER, J ;
COHEN, M ;
CROSS, P ;
BITTL, J ;
EDDINGS, K ;
TAYLOR, M ;
DEROSA, K ;
HATTEL, L ;
COOPER, L ;
ESHELMAN, B ;
FINTEL, D ;
NIEMYSKI, P ;
KLEIN, L ;
KENNEDY, H ;
THORNTON, T ;
KEREIAKES, D ;
MARTIN, L ;
ANDERSON, L ;
HIGBY, N ;
ELLIS, S ;
BREZINA, K ;
GEORGE, B ;
CHAPEKIS, A ;
SMITH, D ;
ANWAR, A ;
GERBER, TL ;
PRITCHARD, GL ;
MYLER, R ;
SHAW, R ;
MURPHY, M ;
WARD, K ;
MADIGAN, NP ;
BLANKENSHIP, J ;
HALBERT, M ;
FLANAGAN, C ;
TANNENBAUM, M ;
POLICH, M ;
STEVENSON, C ;
TCHENG, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (14) :956-961
[2]   A MURINE MONOCLONAL-ANTIBODY THAT COMPLETELY BLOCKS THE BINDING OF FIBRINOGEN TO PLATELETS PRODUCES A THROMBASTHENIC-LIKE STATE IN NORMAL PLATELETS AND BINDS TO GLYCOPROTEINS-IIB AND OR GLYCOPROTEIN-IIIA [J].
COLLER, BS ;
PEERSCHKE, EI ;
SCUDDER, LE ;
SULLIVAN, CA .
JOURNAL OF CLINICAL INVESTIGATION, 1983, 72 (01) :325-338
[3]  
Coller BS, 1998, CIRCULATION, V97, P4
[4]  
DECKELBAUM LI, 1997, NEW THERAPEUTIC AGEN, P355
[5]   ABCIXIMAB (C7E3 FAB) - A REVIEW OF ITS PHARMACOLOGY AND THERAPEUTIC POTENTIAL IN ISCHEMIC-HEART-DISEASE [J].
FAULDS, D ;
SORKIN, EM .
DRUGS, 1994, 48 (04) :583-598
[6]   Cigarette smoking, weight gain, and coronary mortality - Results from the Chicago Western Electric Study [J].
Fulton, JE ;
Shekelle, RB .
CIRCULATION, 1997, 96 (05) :1438-1444
[7]  
Gawaz M, 1999, CIRCULATION, V99, P2
[8]  
Gawaz M, 1998, THROMB HAEMOSTASIS, V80, P994
[9]   Time course, magnitude, and consistency of platelet inhibition by abciximab, tirofiban, or eptifibatide in patients with unstable angina pectoris undergoing percutaneous coronary intervention [J].
Kereiakes, DJ ;
Broderick, TM ;
Roth, EM ;
Whang, D ;
Shimshak, T ;
Runyon, JP ;
Hattemer, C ;
Schneider, J ;
Lacock, P ;
Mueller, M ;
Abbottsmith, CW .
AMERICAN JOURNAL OF CARDIOLOGY, 1999, 84 (04) :391-395
[10]   DIFFERENTIAL INHIBITION OF PLATELET-AGGREGATION INDUCED BY ADENOSINE-DIPHOSPHATE OR A THROMBIN RECEPTOR-ACTIVATING PEPTIDE IN PATIENTS TREATED WITH BOLUS CHIMERIC 7E3 FAB - IMPLICATIONS FOR INHIBITION OF THE INTERNAL POOL OF GPIIB/IIIA RECEPTORS [J].
KLEIMAN, NS ;
RAIZNER, AE ;
JORDAN, R ;
WANG, AL ;
NORTON, D ;
MACE, KF ;
JOSHI, A ;
COLLER, BS ;
WEISMAN, HF .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 26 (07) :1665-1671