TY - JOUR
T1 - Effect of Abciximab versus tirofiban on activated clotting time during percutaneous intervention and its relation to clinical outcomes - Observations from the TARGET trial
AU - Casserly, Ivan P.
AU - Topol, Eric J.
AU - Jia, Gang
AU - Lange, Richard A.
AU - Hamm, Christian
AU - Meier, Bernhard
AU - DiBattiste, Peter M.
AU - Lakkis, Nasser
AU - Chew, Derek P.
AU - Stone, Gregg W.
AU - Cohen, David J.
AU - Moliterno, David J.
PY - 2003/7/15
Y1 - 2003/7/15
N2 - Previous evidence suggests that the monoclonal antibody abciximab may have a more potent anticoagulant effect than small-molecule glycoprotein (GP) IIb/IIIa inhibitors. We prospectively reviewed collected heparin dose, activated clotting time (ACT), and corresponding clinical outcome data from The Do Tirofiban and ReoPro Give Similar Efficacy Outcome Trial (TARGET), a direct comparison of tirofiban versus abciximab in patients who underwent percutaneous intervention. Of the 4,809 patients enrolled in the trial, 3,739 patients (78%) had an ACT measured after the administration of GP IIb/IIIa and heparin (peak procedural ACT); this formed the population for the present study. Mean total heparin dose was 75 ± 32 and 76 ± 31 U/kg in the tirofiban and abciximab groups, respectively. The resultant mean peak ACTs were 296 ± 91 and 299 ± 89 seconds (p = 0.09). In a subset of patients with both baseline ACT (before any heparin or GP IIb/IIIa therapy) and peak procedural ACT measurements, the difference in ACT between these time points was 80 ± 97 vs 82 ± 101 seconds (p = 0.44) for the tirofiban and abciximab groups, respectively. After adjusting for patients' weight, weight-adjusted heparin dose, and method of ACT measurement in a multiple linear regression analysis, the type of GP IIb/IIIa inhibitor was not predictive of the peak ACT (p = 0.24). When stratified by ACT quartile, no statistically significant difference in bleeding or ischemic end points between the tirofiban and abciximab cohorts was observed. In this large contemporary percutaneous coronary intervention trial, there was no observed difference in the anticoagulant effect of tirofiban and abciximab, as measured by the ACT, or in the incidence of bleeding or ischemic complications in each ACT quartile.
AB - Previous evidence suggests that the monoclonal antibody abciximab may have a more potent anticoagulant effect than small-molecule glycoprotein (GP) IIb/IIIa inhibitors. We prospectively reviewed collected heparin dose, activated clotting time (ACT), and corresponding clinical outcome data from The Do Tirofiban and ReoPro Give Similar Efficacy Outcome Trial (TARGET), a direct comparison of tirofiban versus abciximab in patients who underwent percutaneous intervention. Of the 4,809 patients enrolled in the trial, 3,739 patients (78%) had an ACT measured after the administration of GP IIb/IIIa and heparin (peak procedural ACT); this formed the population for the present study. Mean total heparin dose was 75 ± 32 and 76 ± 31 U/kg in the tirofiban and abciximab groups, respectively. The resultant mean peak ACTs were 296 ± 91 and 299 ± 89 seconds (p = 0.09). In a subset of patients with both baseline ACT (before any heparin or GP IIb/IIIa therapy) and peak procedural ACT measurements, the difference in ACT between these time points was 80 ± 97 vs 82 ± 101 seconds (p = 0.44) for the tirofiban and abciximab groups, respectively. After adjusting for patients' weight, weight-adjusted heparin dose, and method of ACT measurement in a multiple linear regression analysis, the type of GP IIb/IIIa inhibitor was not predictive of the peak ACT (p = 0.24). When stratified by ACT quartile, no statistically significant difference in bleeding or ischemic end points between the tirofiban and abciximab cohorts was observed. In this large contemporary percutaneous coronary intervention trial, there was no observed difference in the anticoagulant effect of tirofiban and abciximab, as measured by the ACT, or in the incidence of bleeding or ischemic complications in each ACT quartile.
UR - http://www.scopus.com/inward/record.url?scp=0038306398&partnerID=8YFLogxK
U2 - 10.1016/S0002-9149(03)00525-3
DO - 10.1016/S0002-9149(03)00525-3
M3 - Article
C2 - 12860211
AN - SCOPUS:0038306398
SN - 0002-9149
VL - 92
SP - 125
EP - 129
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 2
ER -