Platelet activity in the early stage of acute myocardial infarction: Relation to time of presentation, treatment with either tissue plasminogen activator or streptokinase and cyclooxygenase inhibition

Background. Platelet activation after myocardial infarction and thrombolytic treatment has been documented; but its relationship with the onset of symptoms and with thrombolysis, and the influence of aspirin in this setting is not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or rt-PA and evaluated influence of aspirin in this framework. Methods. 41 patients (age 57 ± 6 years) were treated with thrombolytic therapy during myocardial infarction; 21 patients with 1,5 million units of streptokinase (Group 1) and 20 patients with 100 mg of rt-PA (Group 2); 10 randomly selected patients in each group were given 500 mg aspirin i.v. prior to infusion of thrombolytic drug and, subsequently, 325 mg aspirin a day orally. Consecutive samples of beta-thromboglobulin (BTG), a marker of platelet activity, were collected at admission and after thrombolysis for the following 48 hours. Results. At admission, BTG plasma levels averaged 125 ± 31 IU/ml in Group 1 and 134 ± 35 IU/ml in Group 2 (p = 0.81). Thrombolysis was followed by a similar increase of platelet activity with maximal values reached at the 3rd hour in both groups (196 ± 43 IU/ml in Group 1 and 192 ± 39 in Group 2: p < 001 versus baseline and p NS between the groups). Higher levels of BTG were observed in streptokinase-treated group starting from the 24th hour (p < 0.05). Patients treated with aspirin showed lower levels of BTG only from the 48th hour after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms to admission and BTG value on admission (r = -0.86 p < 0.001); in patients admitted within two hours from the beginning of symptoms, with higher levels of BTG, thrombolysis not induced a significant increase of platelet activity; who was observed in patients admitted later. Conclusions. A marked platelet activation is more evident in the first hours of myocardial infarction and is differently influenced by thrombolytic treatment in relation with the delay of patient presentation. Both streptokinase and rt-PA induce a similar increase of platelet activity which is more persistent after streptokinase; cyclooxygenase inhibition seems to influence the platelet activity only from the second day.