The effect of enteric-coated aspirin on the morning increase in platelet activity.

In vitro platelet aggregability to adenosine diphosphate (ADP) and epinephrine increases in the morning, as does the frequency of myocardial infarction. A single-blind, randomized, cross-over study of 15 healthy males was conducted to determine: (1) if other measures of platelet activity show a morning increases and (2) if aspirin eliminates any increases in platelet activity detected. Subjects received 325 mg of enteric-coated aspirin (ECA) or placebo. During placebo therapy,platelet thromboxane A2 production (following collagen stimulation) increased significantly after the subjects got up, as did platelet aggregability to ADP, epinephrine, and collagen. ECA markedly reduced baseline platelet thromboxane A2 production and eliminated the increase after the subjects got up. It also abolished biphasic aggregation in response to epinephrine and ADP (thereby eliminating the morning increase in aggregability to these agents), lengthened collagen lag time, reduced synergistic aggregation to combined agonists, was effective on day 2, and did not alter increases of tissue plasminogen activator that occurred following the subjects' arising. If aspirin prevents myocardial infarction by its antiplatelet action, as seems likely, the preferential reduction of morning infarction observed in the Physicians' Health Study, and the demonstration that aspirin eliminates the morning increase in platelet activity, suggest that the morning increase in myocardial infarction is due in part to a concurrent relatively modest increase in platelet activity.