In patients with acute myocardial infarction (AMI) treated with streptokinase (SK) or recombinant tissue-type plasminogen activator (rtPA) we found high levels of thrombin-antithrombin (TAT) complexes signalling a significant activation of the coagulation cascade. In the SK-treated group the median pretreatment TAT complexes levels were 5.0 μg/l and in all patients, whatever the pretreatment level, TAT complexes increased following treatment. A statistically significant increase (medians = 20.3 and 12.0 μg/l) was observed 90 and 180 min after starting SK. The mean pretreatment level in the rtPA-treated group was also 5.0 μg/l and in all but one patients TAT complexes increased following treatment. A statistically significant increase (medians = 37.0 and 30.5 μg/l) was observed 90 and 180 min after starting rtPA. There was no statistically significant difference between TAT complexes in the two groups of patients either before or 90 min after treatment, whereas at 180 min the median concentration of TAT complexes was significantly higher for rtPA- than for SK-treated patients. We did not find an association between coronary vessels patency after thrombolysis and concentrations of TAT complexes; however, the rate of occluded vessels was very low (4 out of 30 patients), so that a difference was perhaps lost due to the insufficient size of the sample. In conclusion, we found thrombin activity during thrombolytic therapy in patients with AMI. There is no important difference in this respect between rtPA and SK. Whether or not this phenomenon is responsible for early rethrombosis remains to be explored by larger studies.
- Myocardial infarction
- Thrombin-antithrombin complexes
- Tissue-plasminogen activator
ASJC Scopus subject areas
- Clinical Biochemistry