(Circulation. 2001;103:2572.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Point-of-Care Measured Platelet Inhibition Correlates With a Reduced Risk of an Adverse Cardiac Event After Percutaneous Coronary Intervention
Results of the GOLD (AU-Assessing Ultegra) Multicenter Study
From the Department of Cardiology, Wilford Hall Medical Center, San Antonio, Tex (S.R.S.); University of Arkansas, Little Rock (J.D.T., J.F.S.); the Carl and Edyth Lindner Research Center for Clinical Cardiovascular Research, Cincinnati, Ohio (D.J.K.); Wake Forest University School of Medicine, Winston-Salem, NC (G.A.B., D.C.S.); Duke Clinical Research Institute, Durham, NC (J.E.T.); Scripps Clinic, La Jolla, Calif (P.J.C., P.S.T.); Department of Cardiology (D.J.M., A.M.L.) and Department of Biostatistics and Epidemiology (G.J.), Cleveland Clinic Foundation, Cleveland, Ohio; Mother Francis Hospital, Tyler, Tex (F.I.N.); Mayo Clinic and Foundation, Rochester, Minn (P.B.B., D.R.H.); Brigham and Women’s Hospital, Boston, Mass (J.J.P.); Cardiovascular Research Foundation, Washington, DC (G.D.); and Montreal Heart Institute, Montreal, Canada (R.G., P.T.).
Correspondence to Steven R. Steinhubl, MD, Wilford Hall Medical Center, Department of Cardiology, 2200 Bergquist Dr, Lackland AFB, TX 78236. E-mail steven.steinhubl{at}59mdw.whmc.af.mil
Background—The optimal level of platelet inhibition with a glycoprotein (GP) IIb/IIIa antagonist necessary to minimize thrombotic complications in patients undergoing a percutaneous coronary intervention (PCI) is currently unknown.
Methods and
Results—Five hundred patients undergoing a PCI
with the planned use of a GP IIb/IIIa inhibitor had
platelet inhibition measured at 10 minutes, 1 hour, 8 hours, and 24
hours after the initiation of therapy with the Ultegra Rapid
Platelet Function Assay (Accumetrics). Major adverse cardiac events
(MACEs: composite of death, myocardial infarction, and urgent target
vessel revascularization) were prospectively
monitored, and the incidence correlated with the measured level of
platelet function inhibition at all time points. One quarter of all
patients did not achieve 
95% inhibition 10 minutes after the bolus
and experienced a significantly higher incidence of MACEs (14.4%
versus 6.4%, P=0.006).
Patients whose platelet function was <70% inhibited at 8 hours
after the start of therapy had a MACE rate of 25% versus 8.1% for
those 70% inhibited
(P=0.009). By
multivariate analysis, platelet function
inhibition 95% at 10 minutes after the start of therapy was
associated with a significant decrease in the incidence of a MACE (odds
ratio 0.46, 95% CI 0.22 to 0.96,
P=0.04).
Conclusions—Substantial variability in the level of platelet function inhibition is achieved with GP IIb/IIIa antagonist therapy among patients undergoing PCI. The level of platelet function inhibition as measured by a point-of-care assay is an independent predictor for the risk of MACEs after PCI.
Key Words: angioplasty • platelets • complications
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