TY - JOUR
T1 - Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation
AU - Tantry, Udaya S.
AU - Bliden, Kevin P.
AU - Gurbel, Paul A.
N1 - Funding Information:
This study was supported by the Sinai Center for Thrombosis Research, Baltimore, Maryland.
PY - 2005/11/1
Y1 - 2005/11/1
N2 - OBJECTIVES: This study sought to determine the prevalence of platelet aspirin resistance using methods that directly indicate the degree of platelet cyclooxygenase inhibition. BACKGROUND: Aspirin resistance in platelets may be overestimated by nonspecific laboratory measurements that do not isolate cyclooxygenase activity. METHODS: Arachidonic acid (AA)-induced light-transmittance platelet aggregation (LTA) and thrombelastography (TEG) platelet mapping were performed on the blood of healthy subjects (n = 6) before and 24 h after receiving 325 mg aspirin, and on 223 patients reporting compliance with long-term daily aspirin treatment (n = 203 undergoing percutaneous intervention [PCI] and n = 20 with a history of stent thrombosis). Aspirin resistance was defined as >20% aggregation by LTA or >50% aggregation by TEG. RESULTS: In healthy subjects, AA-induced aggregation by LTA was 82 ± 10% before and 2 ± 1% at 24 h after aspirin (p < 0.001), and aggregation by TEG was 86 ± 14% before and 5 ± 7% at 24 h after aspirin (p < 0.001). In compliant patients, AA-induced aggregation by LTA was 3 ± 2% before PCI and 3 ± 2% after PCI (p = NS), and aggregation by TEG was 5 ± 9% before PCI and 6 ± 14% after PCI (p = NS). Seven PCI patients were noncompliant, and all were aspirin sensitive after in-hospital aspirin treatment. Among 223 patients, only one patient (∼0.4%) was resistant to aspirin treatment. CONCLUSIONS: Platelet aspirin resistance assessed by methods that directly indicate inhibition of cyclooxygenase is rare in compliant patients with coronary artery disease.
AB - OBJECTIVES: This study sought to determine the prevalence of platelet aspirin resistance using methods that directly indicate the degree of platelet cyclooxygenase inhibition. BACKGROUND: Aspirin resistance in platelets may be overestimated by nonspecific laboratory measurements that do not isolate cyclooxygenase activity. METHODS: Arachidonic acid (AA)-induced light-transmittance platelet aggregation (LTA) and thrombelastography (TEG) platelet mapping were performed on the blood of healthy subjects (n = 6) before and 24 h after receiving 325 mg aspirin, and on 223 patients reporting compliance with long-term daily aspirin treatment (n = 203 undergoing percutaneous intervention [PCI] and n = 20 with a history of stent thrombosis). Aspirin resistance was defined as >20% aggregation by LTA or >50% aggregation by TEG. RESULTS: In healthy subjects, AA-induced aggregation by LTA was 82 ± 10% before and 2 ± 1% at 24 h after aspirin (p < 0.001), and aggregation by TEG was 86 ± 14% before and 5 ± 7% at 24 h after aspirin (p < 0.001). In compliant patients, AA-induced aggregation by LTA was 3 ± 2% before PCI and 3 ± 2% after PCI (p = NS), and aggregation by TEG was 5 ± 9% before PCI and 6 ± 14% after PCI (p = NS). Seven PCI patients were noncompliant, and all were aspirin sensitive after in-hospital aspirin treatment. Among 223 patients, only one patient (∼0.4%) was resistant to aspirin treatment. CONCLUSIONS: Platelet aspirin resistance assessed by methods that directly indicate inhibition of cyclooxygenase is rare in compliant patients with coronary artery disease.
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U2 - 10.1016/j.jacc.2005.05.090
DO - 10.1016/j.jacc.2005.05.090
M3 - Article
C2 - 16256872
AN - SCOPUS:27444434164
SN - 0735-1097
VL - 46
SP - 1705
EP - 1709
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 9
ER -