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GRAVITAS: Lower platelet reactivity with clopidogrel beneficial after PCI
Price MJ. Circulation. 2011;124:1132-1137.
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On-clopidogrel reactivity less than 208 P2Y12 reaction units at 12 to 24 hours after percutaneous coronary intervention was associated with a lower risk for CV events, according to findings of the GRAVITAS trial.
The trial was held at 83 sites in the United States and Canada and enrolled patients who were treated for stable CAD or acute coronary syndrome with one or more drug-eluting stents. Researchers measured on-treatment platelet reactivity (OTR) at 12 to 24 hours and a mean 30 days after PCI with a P2Y12 test (VerifyNow, Accumetrics). The primary endpoint was a composite of CV death, MI and stent thrombosis.
Researchers evaluated platelet function data for 2,796 patients (99.98%) enrolled in the trial. At 60 days, an OTR less than 208 P2Y12 reaction units (PRU) was associated with a lower risk of CV death, nonfatal MI and stent thrombosis (HR=0.18; 95% CI, 0.04-0.79), which remained similar at 6 months (HR=0.43; 95% CI, 0.23- 0.82).
Furthermore, after adjusting for other predictors of outcome, researchers found an OTR less than 208 PRU was associated with the primary endpoint at 60 days (HR=0.23; 95% CI, 0.05-0.98), and at 6 months there was a trend toward an association (HR=0.54; 95% CI, 0.28-1.04).
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This analysis provides some support for the concept that low residual platelet reactivity during clopidogrel (Plavix, Sanofi-Aventis) therapy after PCI relates to a lower risk of CVD events. However, the absolute difference in events is relatively small, and this study cannot address whether low platelet reactivity as assessed by this new PRU level using the VerifyNow device is causally related to a lower risk of events, or is a marker for other factors related to increased risk. The authors use multivariable analysis to try and reduce the effect of confounders, but a relatively low number of events limits this approach. Low platelet reactivity could be a marker for other low-risk features, particularly as the adjusted HRs were not significant for clinical events at 6 months. In this case, more intensive antiplatelet therapy may be warranted on the basis of these other high-risk characteristics rather than based on platelet reactivity testing. As the authors conclude, further prospective studies will be required to flesh out whether this is truly a causal relationship or one by association, and whether high-platelet reactivity should be defined by a lower PRU level, such as 208 vs. the value used in the main study of 230.
– Scott Kinlay, MBBS, PhD
Cardiology
Today Intervention Editorial Board member
Disclosure: Dr.
Kinlay reports no relevant financial disclosures.