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. The paper by Geisler et al in this issue of Heart reports on high residual platelet activity during treatment with ASA and clopidogrel (see article on page 743).6 The data are interesting, but what do they mean for further research or for the care of patients?

CARDIOVASCULAR PREVENTION: A “NUMBERS GAME”

In cardiovascular prevention many patients must be treated so that relatively few can benefit. Patients at risk are selected (based on history, clinical findings and risk factors) and we treat those who have a reasonable chance of benefiting. The risks and benefits of treatment are determined in randomised, prospective clinical trials which give an estimate of the risk reduction one treatment may yield compared with another in a specific patient population. Whether we really achieve these results in the healthcare setting depends on how closely we reproduce the conditions of the trial (patient selection, check-ups and compliance, other …