Tirofiban optimizes platelet inhibition for immediate percutaneous coronary intervention in high-risk acute coronary syndromes.
It was the aim of this study to compare the efficacy of early platelet inhibition by 600 mg clopidogrel and acetylsalicylic acid (ASA) to a triple therapy including a glycoprotein IIb-IIIa receptor blocker. Immediate percutaneous coronary intervention (PCI) is recommended for high-risk acute coronary syndromes. In this setting the efficacy of platelet inhibition is unknown. One hundred patients were randomized to receive ASA and 600 mg clopidogrel, or additional open-label tirofiban (bolus of 10 microg/kg body weight followed by continued infusion of 0.15 microg/kg body weight per minute) as soon as non-ST-segment elevation myocardial infarction was diagnosed. The primary endpoint was the reduction of infarct size determined by post-interventional increases of cardiac troponin T (cTnT). Secondary endpoints included platelet function measured by optical and impedance aggregometry using ADP (5 and 20 microM) and collagen (1 microg/ml) as platelet agonists. Tirofiban maximized platelet inhibition (p < 0.0001) immediately and was associated with significantly lower post-interventional cTnT concentrations (p = 0.0352). In the dual platelet inhibition arm, clopidogrel was not effective in 69% of patients at the time of coronary intervention, and still in 47%, if pre-treatment time was >120 minutes. The frequency of cardiovascular (death, myocardial infarction, revascularization) and bleeding events was comparable. Platelet aggregation is not adequately inhibited in cTnT-positive patients in the setting of immediate PCI with very short pre-treatment times. Only tirofiban provided consistent and effective inhibition of platelet aggregation at the time of immediate or very early invasive therapy.
Ivandic
Boris T
BT
Innere Medizin, Abt. III, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. boris.ivandic@med.uni-heidelberg.de
Kurz
Kerstin
K
Keck
Frieder
F
Staritz
Peter
P
Lehrke
Stephanie
S
Katus
Hugo A
HA
Giannitsis
Evangelos
E
D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000706:statistics & numerical data; D001241:Aspirin / Q000008:administration & dosage; D001792:Blood Platelets / Q000187:drug effects*; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000188:drug therapy*; D003328:Coronary Thrombosis / Q000453:epidemiology / Q000473:pathology / Q000517:prevention & control*; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000473:pathology / Q000517:prevention & control; D009336:Necrosis; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D012307:Risk Factors; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D000077466:Tirofiban; D016896:Treatment Outcome; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives*
D010975:Platelet Aggregation Inhibitors; D014443:Tyrosine; D000077144:Clopidogrel; D000077466:Tirofiban; D013988:Ticlopidine; D001241:Aspirin