Activated clotting times in the setting of eptifibatide use during percutaneous coronary intervention

被引:7
作者
Dauerman, HL
Ball, SA
Goldberg, RJ
Desourdy, MA
Furman, MI
机构
[1] Univ Vermont, Coll Med, Cardiac Unit, Burlington, VT 05401 USA
[2] Univ Massachusetts, Sch Med, Div Cardiovasc, Worcester, MA USA
关键词
activated clotting time; percutaneous coronary intervention; glycoprotein IIb-IIIa inhibition;
D O I
10.1023/A:1020493705138
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Previous studies have demonstrated a prolongation of activated clotting times (ACT) with abciximab administration during percutaneous coronary interventions (PCI). The impact of the short acting glycoprotein (GP) IIb-IIIa inhibitor, eptifibatide, on ACT measurements has not been studied. Methods: Seventy consecutive patients undergoing PCI in the setting of eptifibatide administration were prospectively enrolled in a single center study. Eptifibatide was administered as two 180 mug/kg boluses 10 minutes apart followed by a continuous infusion of 2.0 mug/kg/min. In 15 patients (Group I), the initial eptifibatide and heparin boluses were separated by 5 minutes, and ACT's were assessed after each bolus as well as at 3 subsequent time points. In 55 patients (Group II), an ACT level was drawn 10 minutes after the initial heparin/eptifibatide bolus and 20 minutes following the second eptifibatide bolus. Two different ACT measuring devices-CoaguChek(TM) Pro DM and Hemochron 801-were used to examine the impact of eptifibatide on ACT values. Results: The devices differed in the reproducibility of their measurements, but the overall trends were consistent with both devices. The ACT value was unchanged after the initial eptifibatide bolus (with a delta of 0.6 seconds by CoaguChek Pro DM and 4.2 seconds by Hemochron). While the ACT value rose significantly after the heparin bolus, the second eptifibatide bolus did not result in any further rise in ACT values. Conclusions: Unlike abciximab, eptifibatide does not significantly prolong the ACT in patients undergoing PCI. This may have implications regarding the need for separate heparin dosing algorithms for patients undergoing PCI in the setting of different GPIIb-IIIa inhibitors.
引用
收藏
页码:127 / 132
页数:6
相关论文
共 18 条
[1]   In vivo demonstration of an antithrombin effect of Abciximab [J].
Ambrose, JA ;
Hawkey, M ;
Badimon, JJ ;
Coppola, J ;
Geagea, JP ;
Rentrop, KP ;
Domiguez, A ;
Duvvuri, S ;
Elmquist, T ;
Arias, J ;
Doss, R ;
Dangas, G .
AMERICAN JOURNAL OF CARDIOLOGY, 2000, 86 (02) :150-152
[2]   In vitro effects of the platelet glycoprotein IIb/IIIa receptor antagonist c7E3 Fab on the activated clotting time [J].
Ammar, T ;
Scudder, LE ;
Coller, BS .
CIRCULATION, 1997, 95 (03) :614-617
[3]   COMPARISON OF HEMOCHRON AND HEMOTEC ACTIVATED COAGULATION TIME TARGET VALUES DURING PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY [J].
AVENDANO, A ;
FERGUSON, JJ .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1994, 23 (04) :907-910
[4]   Bleeding complications of glycoprotein IIb-IIIa receptor inhibitors [J].
Blankenship, JC .
AMERICAN HEART JOURNAL, 1999, 138 (04) :S287-S296
[5]   Activation of αVβ3 on vascular cells controls recognition of prothrombin [J].
Byzova, TV ;
Plow, EF .
JOURNAL OF CELL BIOLOGY, 1998, 143 (07) :2081-2092
[6]   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
[7]  
Furman MI, 2000, THROMB HAEMOSTASIS, V84, P492
[8]  
GEMMELL CH, 1993, J BIOL CHEM, V268, P14586
[9]   Treatment with a GPIIb/IIIa antagonist inhibits thrombin generation in platelet rich plasma from patients [J].
Keularts, IMLW ;
Béguin, S ;
de Zwaan, C ;
Hemker, HC .
THROMBOSIS AND HAEMOSTASIS, 1998, 80 (03) :370-371
[10]   Modifiable risk factors for vascular access site complications in the IMPACT II trial of angioplasty with versus without eptifibatide [J].
Mandak, JS ;
Blankenship, JC ;
Gardner, LH ;
Berkowitz, SD ;
Aguirre, FV ;
Sigmon, KN ;
Timmis, GC ;
Gilchrist, IC ;
McIvor, M ;
Resar, J ;
Weiner, BH ;
George, BS ;
Talley, JD ;
Lincoff, AM ;
Tcheng, JE ;
Califf, RM ;
Topol, EJ .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 31 (07) :1518-1524