Intensifying platelet inhibition with tirofiban in poor responders to aspirin or clopidogrel reduced the incidence of troponin elevation compared with placebo (20.4% vs 35.1%; RR 0.58; P=0.009).
RCT (n=263)
Double-blind
randomly assigned
Yes
Does tirofiban reduce troponin elevation in poor responders to aspirin and/or clopidogrel undergoing elective coronary intervention?
In patients with poor response to oral antiplatelets undergoing elective PCI, adding tirofiban significantly reduces periprocedural myocardial infarction and 30-day MACE without increasing bleeding.
Effect estimate: RR 0.58 (95% CI 0.39 to 0.88)
Absolute Event Rate: 20.4% vs 35.1%
p-value: p=0.009
BACKGROUND: Inhibition of platelet aggregation after aspirin or clopidogrel intake varies greatly among patients, and previous studies have suggested that poor response to oral antiplatelet agents may increase the risk of thrombotic events, especially after coronary angioplasty. Whether this reflects suboptimal platelet inhibition per se, which might benefit from more potent antiplatelet agents such as tirofiban, is unknown. METHODS AND RESULTS: We screened 1277 patients to enroll 93 aspirin, 147 clopidogrel, and 23 dual poor responders, based on a point-of-care assay, who underwent elective coronary angioplasty at 10 European sites for stable or low-risk unstable coronary artery disease. Patients were randomly assigned in a double-blind manner to receive either tirofiban (n=132) or placebo (n=131) on top of standard aspirin and clopidogrel therapy. The primary end point, consisting of troponin I/T elevation at least 3 times the upper limit of normal, was attained in 20.4% (n=27) in the tirofiban group compared with 35.1% (n=46) in the placebo group (relative risk, 0.58; 95% confidence interval, 0.39 to 0.88; P=0.009). The rate of major adverse cardiovascular events within 30 days in the tirofiban group also was reduced (3.8% versus 10.7%; P=0.031). The overall incidence of bleeding was low, likely explained by a substantial use of the transradial approach, and did not differ between the 2 groups. CONCLUSIONS: In low-risk patients according to clinical presentation who had poor responsiveness to standard oral platelet inhibitors via a point-of-care assay, intensified platelet inhibition with tirofiban lowers the incidence of myocardial infarction after elective coronary intervention.
Valgimigli et al. (2009) conducted an RCT in Stable or low-risk unstable coronary artery disease (n=263). Tirofiban vs. Placebo was evaluated on Troponin I/T elevation at least 3 times the upper limit of normal (RR 0.58, 95% CI 0.39 to 0.88, p=0.009). Intensifying platelet inhibition with tirofiban in poor responders to aspirin or clopidogrel reduced the incidence of troponin elevation compared with placebo (20.4% vs 35.1%; RR 0.58; P=0.009).