In vitro and in vivo studies have shown both an inhibition and an activation of platelets after thrombolysis in acute myocardial infarction. Plasma β-thromboglobulin, a marker of platelet activity, was evaluated daily during the first week after myocardial infarction in 24 patients who received intravenous streptokinase (group 1) and 26 who did not (group 2). On admission, levels of β-thromboglobulin, as compared to those in healthy subjects (35 ± 9 IU/ml), were similarly augmented 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 baseline; p <0.001 between the two groups). From the second to the seventh day, β-thromboglobulin augmented in those patients in both groups with postinfarction angina. From day 5 to day 7, patients of group 1 without angina had lower β-thromboglobulin levels than patients of group 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 associated with persistent activation; in the absence of recurrent angina, thrombolysis can limit late platelet activation.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine