Aspirin and Clopidogrel Drug Response in Patients Undergoing Percutaneous Coronary Intervention
The Role of Dual Drug Resistance
Eli I. Lev, MD*,
Rajnikant T. Patel, MD*,
Kelly J. Maresh, RN, BSN*,
Sasidhar Guthikonda, MD*,
Juan Granada, MD*,
Timothy DeLao, MLT*,
Paul F. Bray, MD and
Neal S. Kleiman, MD*,*
* Cardiology Section, Methodist DeBakey Heart Center
Thrombosis Research Section, Department of Medicine, Baylor College of Medicine, Houston, Texas
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Figure 1 Distribution of the response to (A) aspirin (assessed by 0.5 mg/ml arachidonic acid [AA]-induced platelet aggregation) and (B) clopidogrel (evaluated by change in 5 µmol/l adenosine diphosphate [ADP]-induced aggregation) from baseline to post-treatment. Both distributions were normal (p = 0.0003 and p = 0.01, respectively).
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Figure 2 Response to clopidogrel among the three tertiles of 0.5 mg/ml arachidonic acid (AA)-induced aggregation (reflecting response to aspirin). Aggregation in response to (A) 5 µmol/l and (B) 20 µmol/l adenosine diphosphate (ADP) (p = 0.006 and p = 0.0001, respectively, for difference between tertiles).
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Figure 3 Incidence of creatinine kinase-myocardial band (CK-MB) elevation above the upper limit of normal in aspirin (ASA)-resistant versus aspirin-sensitive patients, clopidogrel-resistant versus clopidogrel-sensitive patients, and dual drug-resistant versus dual drug-sensitive patients.
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