EDITORIALS
Should we monitor platelet function during antiplatelet therapy?
Correspondence to:
Professor P Hjemdahl, Karolinska Institutet, Department of Medicine, Clinical Pharmacology Unit, Karolinska University Hospital (Solna), SE-171 76 Stockholm, Sweden; Paul.Hjemdahl@ki.se
| The first 150 words of the full text of this article appear below. |
Antiplatelet drug treatment is a cornerstone in cardiovascular prevention. Low-dose aspirin (ASA) inhibits platelet-dependent, cyclo-oxygenase-1 (COX-1)-mediated thromboxane formation from arachidonic acid (AA), and is usually the preferred drug.1 Clopidogrel inhibits platelet ADP (P2Y12) receptors, and is an alternative for patients who cannot take ASA or for co-treatment when dual antiplatelet therapy is needed.2 Benefits of treatment do not outweigh the increased risk of bleeding in primary prevention in low-risk patients. For high-risk coronary patients the benefits may be so large that dual (or even triple) antiplatelet drug therapy is indicated during limited periods of time with very high risk.
Aspirin and clopidogrel "resistance" are much discussed and there are several reviews on the subject (eg, Patrono and Rocca,3 Gurbel and Tantry,4 Cattaneo5). There is, however, still some confusion about how to diagnose and handle antiplatelet drug "resistance", and what high "residual platelet activity" in a treated patient actually means.
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This article has been cited by other articles:
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Hjemdahl, P.
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