Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin
| Autor: | Erick Schampaert, Chantal Pharand, Marie Lordkipanidzé, Jean G. Diodati, Jacques Turgeon, Donald A. Palisaitis |
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| Rok vydání: | 2010 |
| Předmět: |
Blood Platelets
Male medicine.medical_specialty Isoprostane Platelet Aggregation Urinary system Drug Resistance Coronary Artery Disease Drug resistance Platelet inhibition Dinoprost medicine.disease_cause Gastroenterology Coronary artery disease chemistry.chemical_compound Risk Factors Thromboembolism Internal medicine medicine Humans Platelet Treatment Failure Aged Aspirin Platelet Count business.industry Middle Aged medicine.disease Oxidative Stress Endocrinology chemistry Female Cardiology and Cardiovascular Medicine business Platelet Aggregation Inhibitors Oxidative stress medicine.drug |
| Zdroj: | International Journal of Cardiology. 143:43-50 |
| ISSN: | 0167-5273 |
| DOI: | 10.1016/j.ijcard.2009.01.037 |
| Popis: | Background: Several patient characteristics have been shown to increase the risk of inadequate platelet inhibition by aspirin, yet underlying mechanisms remain mostly unknown. We explored whether oxidative stress, via isoprostane formation, was associated with inadequate platelet response to aspirin. Additionally, we sought to investigate whether individual pre-selected demographic, hematological or biochemical parameters further increased the risk of inadequate platelet response to aspirin. Methods: Two hundred consecutive subjects suffering from stable coronary artery disease and under daily aspirin therapy were enrolled in our study. Inadequate platelet response to aspirin was defined as residual platelet aggregation ≥20% per arachidonic acid-induced light transmission aggregometry. Morning urinary samples were used to determine levels of isoprostanes (8-iso-PGF2α) using an enzyme immunoassay. Results: Eight subjects were deemed to present inadequate platelet response to aspirin. Wide intersubject variability was observed in urinary 8-iso-PGF2α levels. However, levels were similar between aspirin responders and non-responders. Patients with inadequate platelet response to aspirin had higher platelet counts and received the lowest daily aspirin dose when compared to responders, suggesting subtherapeutic aspirin therapy due to increased platelet production. Only platelet count remained independently predictive of inadequate platelet response to aspirin in a multiple logistic regression model. Conclusions: Urinary 8-iso-PGF2α levels, a reflection of systemic oxidative stress, did not appear to contribute to impaired platelet responsiveness to aspirin, while increased platelet production may partly explain this phenomenon. © 2009 Elsevier Ireland Ltd. All rights reserved. |
| Databáze: | OpenAIRE |
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