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[Thrombocyte aggregation and serum thromboxane in patients with acute myocardial infarction].

Treatment with acetylsalicylic acid reduces the mortality following acute myocardial infarction (AMI). The mode of action is unknown but studies of patients with unstable angina pectoris have revealed that acetylsalicylic acid inhibits the platelet aggregating and vessel-constricting metabolite thromboxane B2. In the present investigation, we have examined ten patients with AMI. Platelet aggregation induced by arachidonic acid and serum thromboxane B2 were compared with findings in patients with unstable angina pectoris and healthy control persons. The investigation reveals that the platelet aggregateability is increased significantly already on the first day after AMI and increases in all cases for 14 days (p less than 0.001). Serum thromboxane B2 concentration is normal on the first day and increases gradually in the course of 14 days (p less than 0.05) to values which are not significantly different from those observed in patients with unstable angina pectoris. Patients with AMI have significantly increased platelet aggregation and increasing concentrations in the blood of thromboxane B2. Acetylsalicylic acid inhibits platelet aggregation and lowers thromboxane B2 concentration in the blood which may explain the effect of this preparation in reducing the mortality after AMI.