Toward an optimal "antiplatelet" dose of aspirin: Preliminary observations

It remains unclear which dose of aspirin (ASA) confers the optimal antiplatelet effect. This study focuses on long-term responses to different ASA doses by selected normal subjects. Their baseline platelet aggregabilities exemplified both the average values and the extremes of hyper-and hypoaggregability. Only 41 mg ASA daily stopped all arachidonic acid aggregations and maximally spared endogenous nucleotides. When 2.8 and 9 μM adenosine diphosphate were used as the aggregants, it became evident that higher ASA doses yielded still further grades of change both in aggregation and disaggregation. Disaggregations proved of special interest: distinctive for each subject, they clearly improved more on 325 mg ASA daily than on 41 mg or 81 mg. "Low-dose" ASA, at longer dose intervals of 48 or 72 h, may not be optimal to sustain an adequate antiplatelet effect. More individualized ASA doses, based on selected in vitro measurements of platelet function, might prove useful both in reducing the size and number of cerebral ischemic infarcts and in avoiding hemorrhagic complications in certain patients.