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Effect of Platelet Antigen Polymorphism on Platelet Inhibition by Aspirin, Clopidogrel, or Their Combination

Glen E. Cooke, MD, FACC^_*,_*, Yiwen Liu-Stratton, PhD^_*, Amy K. Ferketich, PhD, Melvin L. Moeschberger, PhD, David J. Frid, MD, FACC^_*, Raymond D. Magorien, MD, FACC^_*, Paul F. Bray, MD, Philip F. Binkley, MD, MPH, FACC^_* and Pascal J. Goldschmidt-Clermont, MD, FACC

^_* Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio
Division of Epidemiology and Biometrics of the School of Public Health, The Ohio State University, Columbus, Ohio
Thrombosis Research Section, Department of Medicine, College of Medicine, Baylor University, Houston, Texas
Department of Medicine, Duke University Medical Center, Durham, North Carolina.

View larger version (16K): [in a new window]   Figure 1 Aggregation (mean percent ± SEM) with adenosine diphosphate (A), collagen (B), or epinephrine (C) in study subjects by treatment strategy. Significant differences under different conditions of blockade were noted. Multiple comparisons (six included in adjustment per plot) at each agonist’s concentrations revealed significant differences (p < 0.05) between treatment strategies as indicated. *Applies for differences between treatment with acetylsalicylic acid (ASA) and with clopidogrel. Applies for differences between treatment with clopidogrel and with ASA plus clopidogrel in combination. Applies for differences between treatment with ASA and with ASA plus clopidogrel in combination.

View larger version (19K): [in a new window]   Figure 2 Fluorescein isothiocyanate (FITC)-fibrinogen binding (mean fluorescence units ± SEM) with adenosine diphosphate (ADP) in study subjects by treatment strategy. Significant differences under different conditions of blockade were noted (p < 0.01). Multiple comparisons (six included in adjustment per plot) at each agonist’s concentrations revealed significant differences (p < 0.05) between treatment strategies as indicated. *Applies for differences between treatment with acetylsalicylic acid (ASA) and with clopidogrel. Applies for differences treatment with acetylsalicylic acid (ASA) and with ASA plus clopidogrel in combination.

View larger version (24K): [in a new window]   Figure 3 Aggregation (mean percent ± SEM) with adenosine diphosphate (ADP) (A) or collagen (B) dichotomized according to the PlA genotype. There is a significant interaction between agonist concentration and indicated PlA genotype for aggregation induced with ADP (A, p < 0.005) and collagen (B, p = 0.005). Multiple comparisons (six included in adjustment per plot) at each agonist’s concentrations revealed significant differences (p < 0.05) between PlA1/A1 and PlA1/A2 as indicated. *Applies for differences between PlA1/A1 and PlA1/A2.

View larger version (15K): [in a new window]   Figure 4 Collagen-stimulated PlA1/A1 platelets were significantly more inhibited by acetylsalicylic acid (aspirin) than PlA1/A2 platelets (p < 0.0001) as assessed by fluorescein isothiocyanate-fibrinogen binding (mean fluorescence units ± SEM). Multiple comparisons (six included in adjustment per plot) at each concentrations of collagen revealed significant differences (p < 0.05) between PlA1/A1 and PlA1/A2 platelets as indicated. *Applies for differences between PlA1/A1 and PlA1/A2.

View larger version (15K): [in a new window]   Figure 5 In collagen-stimulated platelets, -granule release (as measured by CD62P; P-selectin expression) was dependent on PlA genotype, treatment strategy, and agonist concentration (mean fluorescence units ± SEM; p = 0.005).