BETA-THROMBOGLOBULIN PLASMA-LEVELS IN THE FIRST WEEK AFTER MYOCARDIAL-INFARCTION - INFLUENCE OF THROMBOLYTIC THERAPY

In vitro and in vivo studies have shown both an inhibition and an acti vation of platelets after thrombolysis in acute myocardial infarction. Plasma beta-thromboglobulin, a marker of platelet activity, was evalu ated daily during the first week after myocardial infarction in 24 pat ients who received intravenous streptokinase (group 1) and 26 who did not (group 2). On admission, levels of beta-thromboglobulin, as compar ed to those in healthy subjects (35 +/- 9 IU/ml), were similarly augme nted in group 1 (105 +/- 27 IU/ml) and in group 2 (115 +/- 30 IU/ml); 3 hours later, values averaged 191 +/- 58 IU/ml in group 1 (p < 0.001 vs baseline) and 95 +/- 28 IU/ml in group 2 (not significant vs baseli ne; p < 0.001 between the two groups). From the second to the seventh day, beta-thromboglobulin augmented in those patients in both groups w ith postinfarction angina. From day 5 to day 7, patients of group 1 wi thout angina had lower beta-thromboglobulin levels than patients of gr oup 2 who had no symptoms. The lowest levels of platelet activity were observed in group 1 reperfused patients. These data indicate that in myocardial infarction an early platelet activation takes place that is enhanced by thrombolytic treatment; recurrence of angina is associate d with persistent activation; in the absence of recurrent angina, thro mbolysis can limit late platelet activation.