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Aspirin resistance testing not ready for "prime time"
  1. Paul Hjemdahl (paul.hjemdahl{at}ki.se)
  1. Karolinska Institutet, Sweden

    Abstract

    Low-dose aspirin (ASA) treatment is a cornerstone in cardiovascular prevention, and is well documented in several patient categories [1-3]. It inhibits platelet-dependent thromboxane (Tx) formation from arachidonic acid (AA) via irreversible inhibition of cyclooxygenase (COX-1) in platelets in the portal circulation with minimal systemic effects due to efficient clearance in the liver when low doses are ingested. The dosage of ASA must be sufficient to block platelet COX-1 by >95% in order to effectively counteract thromboxane-mediated platelet aggregation [4]. However, platelets also interact with other blood cells, and ASA may have non-platelet-dependent antithrombotic effects [5]. Thus, the clinical efficacy of ASA may not depend entirely upon its ability to block the COX-1 mediated formation of Tx from arachidonic acid (AA) in platelets. The optimal balance between protection against athero-thrombotic events and risks for side-effects appears to be obtained with an ASA dosage of 75-150 mg daily [1-3].

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