Professor Carlo Patrono, Rome, Italy enlightened us on the pharmacology of aspirin and the platelet ADP receptors blocker, clopidogrel. The anti-platelet effect of these drugs might vary within individuals. This is probably in some cases due to poor patient compliance, but other factors are also involved. NSAID and COX-2 inhibitors interfere with the effect of aspirin. Diclofenac is recommended, if patients on low dose aspirin need NSAID therapy, because this drug interferes very little with aspirin. The antiplatelet response to clopidogrel varies more among individuals than the response to aspirin. Measurement of se-thromboxane B2 or urinary 11-dehydro-thromboxane B2 is recommended for evaluating anti-platelet response to aspirin and VASP evaluated by flow cytometry for anti-platelet effect of clopidogrel.
In the next session Professor A Sturk, Amsterdam, the Netherlands discussed the pros and cons of the laboratory tests available to assess platelet function. Platelet aggregation in platelet-rich plasma or in whole blood, flow cytometry or the newer point-of-care tests PFA-100 and the Rapid Platelet Function Analyzer (Verify Now) and measurement of thromboxane metabolites, are the major possibilities. None of these tests are perfect and so far no definition of either aspirin or clopidogrel is generally accepted. Poor biochemical response to aspirin or clopidogrel has so far not been convincing linked to clinical outcome and more research is needed in this area.
Professor Helmut Schuehlen, Berlin, Germany showed that some of the so called poor reponders to clopidogrel benefit from a higher maintenance dose, and that a 600 mg loading dose of clopidogrel provides a faster response than the conventional loading dose of 300 mg. Schuehlen and the next speaker, Professor David Moliterno, Lexington, USA gave an extensive review of the new ADP receptor blockers (e.g. prasugrel), an intravenous ADP-receptor blocker (cangrelor) and a new platelet thrombin receptor blocker.