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[A current problem in atherothrombotic diseases--aspirin resistance: definition, mechanisms, determination with
Burak Pamukçu1, Hüseyin Oflaz, Yilmaz Nişanci
1Istanbul Universitesi, Istanbul Tip Fakültesi, Kardiyoloji Anabilim Dali, Istanbul, Türkiye. burakpamukcu@ttnet.net.tr
Insights
Aspirin resistance, where patients do not benefit from aspirin therapy, is a growing concern. Further research is needed to optimize antiplatelet treatments for these individuals.
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Context:
- Aspirin (acetylsalicylic acid) is a cornerstone antiplatelet medication for preventing atherothrombotic events.
- Patient response to aspirin therapy is variable, leading to the identification of aspirin resistance or non-response.
- Aspirin resistance poses a clinical challenge, potentially increasing cardiovascular event risk.
Purpose:
- To review the diagnostic methods for identifying aspirin resistance.
- To discuss the implications of aspirin resistance on cardiovascular outcomes.
- To highlight the need for further research into the mechanisms and management of aspirin resistance.
Summary:
- Aspirin resistance is defined by a lack of antiplatelet effect, detectable through various assays like aggregometry and platelet function analyzers.
- Several methods exist to assess aspirin resistance, including bleeding time, PFA-100, and thromboxane B2 levels.
- The precise mechanisms underlying aspirin resistance remain unclear, but it is linked to an increased risk of cardiovascular events.
Impact:
- Understanding aspirin resistance is crucial for tailoring antiplatelet therapy to individual patient needs.
- Identifying aspirin-resistant patients may allow for the implementation of alternative or additional therapies to mitigate cardiovascular risks.
- Further studies are essential to optimize antiplatelet strategies and reduce the incidence of major cardiovascular events in aspirin-resistant populations.
Abstract:
Aspirin (acetylsalicylic acid) is a powerful antiplatelet agent used in prevention of atherothrombotic vascular events. However, antiplatelet effect of aspirin is not uniform and some patients could not benefit from aspirin. These patients are clinically called as aspirin resistant or aspirin non-responders. Aspirin resistance could be determined by: bleeding time, optical aggregometry, PFA-100 (Platelet Function Analyzer), Ultegra-RPFA (Rapid Platelet Function Assay), activated aggregation time, whole blood aggregometry, platelet aggregate ratio, flow cytometry, measurements of platelet surface proteins and blood or urine thromboxane B2 levels. Mechanisms of aspirin resistance have not been elucidated yet. There is evidence that aspirin resistance increases clinical cardiovascular events. Adequate additional therapies may reduce atherothrombotic risks and major cardiovascular events rate in aspirin resistant subjects. However, we need further studies to decrease major cardiovascular events risk in aspirin resistant subjects and to optimize antiplatelet therapy.
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