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Is there such a thing as aspirin resistance?

A Aspirin resistance is a poorly defined term. Recurrent vascular events despite use of aspirin should be termed treatment failure instead of aspirin resistance.

It can imply a clinical inability of aspirin to protect individuals from arterial thrombotic events; or laboratory indications of the failure of aspirin to inhibit platelet activity; or a close-to-normal urinary concentration of thromboxane metabolites.

Possible mechanisms of aspirin resistance include:

bio-availability, platelet function, polymorphisms, platelet interactions with other blood cells and cell products, platelet aggregation stimulated by smoking, ASA resistant platelet aggregability by increased norepinephrine from excessive exercise or mental stress, and increased platelet sensitivity to collagen.

However, some patients on aspirin have a second event, which suggests resistance or that aspirin is not enough to stop the thrombotic activity.

Even if a patient is resistant by platelet aggregation measures, I would not stop the aspirin because other effects – for example, anti-inflammatory activity – may be protective. But if patients have recurrent events on aspirin, it would be prudent to increase doses or add another anti-platelet agent.

Aspirin resistance might depend on circumstances unrelated to aspirin and could more aptly be termed aspirin failure. This is also supported by the fact that increasing doses to 150mg in patients with no contraindications can inhibit platelet aggregation in patients who are unresponsive or only partially responsive.

Dr Ferrucio De Lorenzo is a consultant physician in cardiovascular medicine at the Thrombosis Research Institute, London, and senior clinician at Chelsea and Westminster Hospital

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