Paradoxic elevation of fibrinopeptide A after streptokinase: evidence for continued thrombosis despite intense fibrinolysis.
Paradoxic elevation of fibrinopeptide A after streptokinase: evidence for continued thrombosis despite intense fibrinolysis.
复制标题
链激酶后纤维蛋白肽 A 反常升高:尽管有强烈的纤维蛋白溶解,但血栓持续形成的证据。
DOI:
10.1016/s0735-1097(87)80194-8
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发表时间:
1987
影响因子:
24
通讯作者:
Jaffe,AS
中科院分区:
文献类型:
--
作者:
Eisenberg,PR;Sherman,LA;Jaffe,AS
Elevated levels of fibrinopeptide A, a marker of thrombin activity associated with acute myocardial infarction, have been found to decrease after administration of streptokinase when reperfusion occurs. In contrast, in patients without reperfusion and those with reocclusion after streptokinase therapy, fibrinopeptide A remains elevated. In the present study early serial measurements of fibrinopeptide A were used to further characterize this paradoxic increase in thrombin activity after streptokinase and to characterize its response to heparin.In 19 patients with acute myocardial infarction fibrinopeptide A was elevated to 82.3 ± 43.5 ng/ml (mean ± SE) before therapy. Thirty minutes after the initiation of streptokinase, fibrinopeptide A increased to 300.1 ± 117.4 ng/ml (p < 0.01), consistent with extensive thrombin activity. Fibrinopeptide A remained elevated until 15 minutes after a heparin bolus injection when levels decreased to 15% of the postStreptokinase value (49.2 ± 13.3 ng/ml) (p < 0.001). These data document a prompt paradoxic increase in thrombin activity after administration of streptokinase that may be responsible for failure of therapy in some patients.