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Aspirin "resistance".
Karsten Schrör1, Artur-Aron Weber, Thomas Hohlfeld
1Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Heinrich-Heine-Universität, Universitätsstr. 1, Geb. 22.21, D-40225 Düsseldorf, Germany. kschroer@uni-duesseldorf.de
Blood Cells, Molecules & Diseases
|February 14, 2006
Summary
Aspirin resistance, a reduced response to antiplatelet drugs like aspirin (ASA), can be pharmacologically defined. A novel method identified a specific COX-2 isoform in coronary artery bypass graft patients, potentially explaining their resistance.
Area of Science:
- Pharmacology
- Biochemistry
- Cardiovascular Medicine
Background:
- Variable responsiveness to antiplatelet drugs is a known clinical issue.
- Defining pharmacological aspirin (ASA) resistance and its mechanisms remains challenging.
- Current laboratory methods for assessing ASA sensitivity have limitations.
Purpose of the Study:
- To clarify the existence of "true" pharmacological aspirin resistance.
- To investigate the underlying cellular mechanisms of aspirin resistance.
- To define and subtype aspirin resistance using a novel typological approach.
Main Methods:
- Utilized a typological approach combining in vitro platelet aggregometry and thromboxane measurement.
- Assessed platelet sensitivity to aspirin (ASA) ex vivo.
- Measured inhibition of thromboxane formation.
Main Results:
- Identified a "true" pharmacological aspirin resistance in patients undergoing coronary artery bypass surgery (CABG).
- These patients exhibited reduced antiplatelet response to ASA and diminished thromboxane inhibition.
- Discovered a novel COX-2 isoform (COX-2a) in platelets of CABG patients, potentially linked to resistance.
Conclusions:
- A typological approach aids in defining and subtyping pharmacological aspirin resistance.
- Aspirin resistance in CABG patients may be associated with a newly identified COX-2 isoform.
- Further research is needed to elucidate the role of this COX-2 isoform in aspirin resistance.