Poor Responsiveness to Clopidogrel: Drug-Specific or Class-Effect Mechanism?Evidence From a Clopidogrel-to-Ticlopidine Crossover Study
Gianluca Campo, MD*,
Marco Valgimigli, MD, PhD*, ,*,
Donato Gemmati, MS ,
Gianfranco Percoco, MD*,
Linda Catozzi, MS,
Alice Frangione, MD*,
Federica Federici, MS,
Fabrizio Ferrari, MD*,
Matteo Tebaldi, MD*,
Serena Luccarelli, MD*,
Giovanni Parrinello, PhD and
Roberto Ferrari, MD, PhD*,
* Cardiovascular Institute, Azienda Ospedaliera Universitaria S. Anna, Ferrara, Italy
Cardiovascular Research Centre, Salvatore Maugeri Foundation, IRCCS, Gussago, Italy
Center Study Haemostasis and Thrombosis, University of Ferrara, Ferrara, Italy
Medical Statistics Unit, University of Brescia, Brescia, Italy.
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Figure 1 Study Design
CABG = coronary artery bypass graft; CAD = coronary artery disease; GP = glycoprotein; NSTEACS = non–ST-segment elevation acute coronary syndrome; pts = patients; SA = stable angina; STEMI = ST-segment elevation myocardial infarction; T0 = baseline; T1 = clopidogrel steady state; T2 = ticlopidine steady state.
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Figure 2 Platelet Inhibition After Thienopyridine Treatment
Distribution of the percent inhibition of platelet aggregation from baseline to after-treatment (clopidogrel steady state = solid bars; ticlopidine steady state = open bars).
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Figure 3 Percentage of Nonresponders
Bars to the left of the dashed line = definition 1, absolute difference between baseline and post-treatment Aggmax  10%. Bars to the right of the dashed line = definition 2, %IPA <20%. IPA = inhibition of platelet aggregation.
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