November 15, 2009Open Access
View Full PaperIntravenous Platelet Blockade with Cangrelor during PCI
Key Result
Intravenous cangrelor during PCI was not superior to placebo in reducing death, MI, or ischemia-driven revascularization at 48 hours (7.0% vs 8.0%; OR 0.87; 95% CI 0.71-1.07; P=0.17).
Study Design
Type
RCT (n=5,362)
Blinding
Double-blind
Structured PICO
Does intravenous cangrelor reduce the composite of death, myocardial infarction, or ischemia-driven revascularization in patients undergoing PCI who have not been treated with clopidogrel?
P
Population
5,362 patients undergoing percutaneous coronary intervention (PCI) who had not been treated with clopidogrel
I
Intervention
Intravenous cangrelor at the time of PCI, followed by 600 mg of clopidogrel
C
Comparator
Placebo at the time of PCI, followed by 600 mg of clopidogrel
O
Outcome
Composite of death, myocardial infarction, or ischemia-driven revascularization at 48 hourscomposite
Intravenous cangrelor during PCI was not superior to placebo in reducing the primary composite ischemic endpoint at 48 hours, though it reduced secondary endpoints of stent thrombosis and death at the cost of increased major bleeding.
Main Result
Effect estimate: OR 0.87 (95% CI 0.71-1.07)
Absolute Event Rate: 7% vs 8%
p-value: p=0.17
Abstract
BACKGROUND: Intravenous cangrelor, a rapid-acting, reversible adenosine diphosphate (ADP) receptor antagonist, might reduce ischemic events during percutaneous coronary intervention (PCI). METHODS: In this double-blind, placebo-controlled study, we randomly assigned 5362 patients who had not been treated with clopidogrel to receive either cangrelor or placebo at the time of PCI, followed by 600 mg of clopidogrel. The primary end point was a composite of death, myocardial infarction, or ischemia-driven revascularization at 48 hours. Enrollment was stopped when an interim analysis concluded that the trial would be unlikely to show superiority for the primary end point. RESULTS: The primary end point occurred in 185 of 2654 patients receiving cangrelor (7.0%) and in 210 of 2641 patients receiving placebo (8.0%) (odds ratio in the cangrelor group, 0.87; 95% confidence interval CI, 0.71 to 1.07; P=0.17) (modified intention-to-treat population adjusted for missing data). In the cangrelor group, as compared with the placebo group, two prespecified secondary end points were significantly reduced at 48 hours: the rate of stent thrombosis, from 0.6% to 0.2% (odds ratio, 0.31; 95% CI, 0.11 to 0.85; P=0.02), and the rate of death from any cause, from 0.7% to 0.2% (odds ratio, 0.33; 95% CI, 0.13 to 0.83; P=0.02). There was no significant difference in the rate of blood transfusion (1.0% in the cangrelor group and 0.6% in the placebo group, P=0.13), though major bleeding on one scale was increased in the cangrelor group, from 3.5% to 5.5% (P<0.001), because of more groin hematomas. CONCLUSIONS: The use of periprocedural cangrelor during PCI was not superior to placebo in reducing the primary end point. The prespecified secondary end points of stent thrombosis and death were lower in the cangrelor group, with no significant increase in the rate of transfusion. Further study of intravenous ADP blockade with cangrelor may be warranted. (ClinicalTrials.gov number, NCT00385138.)