Predictors of Heightened Platelet Reactivity Despite Dual-Antiplatelet Therapy in Patients Undergoing Percutaneous Coronary Intervention Academic Article uri icon

Overview

MeSH Major

  • Blood Platelets
  • Coronary Disease
  • Platelet Aggregation
  • Ticlopidine

abstract

  • Small studies have indicated that drug-drug interactions and such clinical characteristics as diabetes mellitus may increase residual platelet reactivity in patients on clopidogrel therapy. The independent contribution of these variables to high residual platelet reactivity (HRPR) is not well studied. Residual platelet reactivity was assessed using the VerifyNow P2Y12 assay (Accumetrics Inc., San Diego, California) in 377 patients with stable coronary artery disease on maintenance clopidogrel therapy. HRPR was defined using a threshold previously shown to predict adverse clinical outcomes. Residual platelet reactivity was significantly higher in women (220 +/- 82 vs 200 +/- 77 P2Y12 reaction units [PRU]; p = 0.041), non-Caucasians (229 +/- 79 vs 202 +/- 78 PRU; p = 0.047), patients with diabetes mellitus (220 +/- 73 vs 196 +/- 80 PRU; p = 0.005), and those treated with nitrates (233 +/- 70 vs 200 +/- 80 PRU; p = 0.018) or proton-pump inhibitors (218 +/- 79 vs 198 +/- 78 PRU; p = 0.02), whereas residual platelet reactivity was significantly lower in active smokers (168 +/- 82 vs 208 +/- 77 PRU; p = 0.006). Independent predictors of HRPR were female gender (odds ratio [OR] 1.91, 95% confidence interval [CI] 1.14 to 3.19, p = 0.014), non-Caucasian ethnicity (OR 3.05, 95% CI 1.49 to 6.28, p = 0.002), use of proton-pump inhibitors (OR 1.64, 95% CI 1.03 to 2.59, p = 0.035), and active smoking (OR 0.37, 95% CI 0.14 to 0.94, p = 0.037). HRPR was associated with increased 6-month mortality rates (3.0% vs 0%; p = 0.016). In conclusion, our findings support the hypothesis that clopidogrel nonresponsiveness is primarily the result of genetic mechanisms and factors that may influence activity of the cytochrome P-450 system.

publication date

  • May 15, 2009

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.amjcard.2009.01.341

PubMed ID

  • 19427425

Additional Document Info

start page

  • 1339

end page

  • 43

volume

  • 103

number

  • 10