Platelet hyporesponsiveness to acetylsalicylic acid can be transferred by plasma in humans.

In the present study, we investigated prospectively whether an existing platelet hyporesponsiveness to acetylsalicylic acid (ASA) can be transferred to platelets with a previously normal reactivity to ASA. Therefore, 80 patients who had undergone coronary bypass surgery were selected, and the efficacy of their oral aspirin therapy was tested. Platelet aggregation was measured by means of light transmission aggregometry (LTA) after stimulation by 1 mmol/l arachidonic acid (ARA) as well as by 1 mmol/l ARA + in vitro addition of 25 micromol/l ASA. The threshold for a sufficient inhibition of platelet aggregation was set to < or = 30% aggregation after ARA stimulation. A group of healthy volunteers with normal, almost complete inhibition of ARA-induced aggregation after in vitro addition of ASA served as control (group A). On the basis of the LTA measurement, 20 patients exhibited a hyporesponsiveness to oral and in vitro ASA (group B). Despite oral ASA treatment, in these patients ARA stimulation still induced aggregation, which could not be inhibited by in vitro addition of ASA. If group B plasma (from these hyporesponsive patients) was added to group A platelets (with normal reaction to ASA), this resulted in a conversion to hyporesponsive platelets, which then showed full aggregation in response to ARA (81%), and which could no longer be inhibited by in vitro ASA addition. In contrast, the normal ASA-responsive patients (group C) exhibited a nearly complete inhibition of ARA-induced aggregation by ASA. If group C plasma was incubated with group A platelets, ARA-induced aggregation could nearly completely be inhibited by in vitro addition of aspirin (ARA aggregation before ASA: 79%; after ASA addition: 7%). In conclusion, it can be stated that platelet hyporesponsiveness to ASA seems to be mediated by a transferable plasma factor.