SummaryDuring urokinase thrombolytic treatment, for acute myocardial infarction and massive pulmonary embolism, the authors observed the apparition or the exaggeration of platelet hyperaggregation. In vitro experiments reproduced this effect with several fibrinolytic enzymes, including streptokinase and urokinase. Hyperaggregation is obtained with normal plasma, without the addition of the usual aggregation inductors. The possible mechanisms of this side effect of thrombolytic treatments are mentioned. Although the eventual role this iatrogenic hyperaggregation may play in the recurrence of pulmonary embolism or in the secondary extension of myocardial infarction is unknown, it is wise to correct it. Dipyridamole at the daily dose of 60 mg intravenously has shown itself to be useful.