Clinical Research
Aspirin Resistance
Overestimation of Platelet Aspirin Resistance Detection by Thrombelastograph Platelet Mapping and Validation by Conventional Aggregometry Using Arachidonic Acid Stimulation

https://doi.org/10.1016/j.jacc.2005.05.090Get rights and content
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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.

Abbreviations and Acronyms

AA
arachidonic acid
ADP
adenosine diphosphate
COX-1
cyclooxygenase-1
GP
glycoprotein
LTA
light-transmittance aggregometry
MAAA
arachidonic acid-induced clot strength (measurement of aspirin effect)
MAfibrin
activator-induced clot strength (measurement of fibrin contribution)
MAthrombin
thrombin-induced clot strength (maximum clot strength)
PCI
percutaneous coronary intervention
PPP
platelet-poor plasma
PRP
platelet-rich plasma
SAT
stent thrombosis
TEG
thrombelastography

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This study was supported by the Sinai Center for Thrombosis Research, Baltimore, Maryland.