Open AccessIncreased levels of plasma thrombomodulin in patients with acute myocardial infarction who had thrombolytic therapy and achieved successful reperfusion
Author(s) -
Ileri Mehmet,
Hisar Ismet,
Yetkin Ertan,
KoŞar Feridun,
Cehreli Sengül,
Korkmaz Sule,
Demirkan Deniz
Publication year - 2001
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960240506
Subject(s) - medicine , thrombolysis , thrombomodulin , myocardial infarction , streptokinase , reperfusion therapy , cardiology , reperfusion injury , ischemia , thrombin , platelet
Background: There is a growing body of evidence from animal and in vitro studies for the existence of reperfusion injury after thrombolytic therapy for acute myocardial infarction (AMI), but the patient data are limited. Hypothesis: We aimed to examine the plasma thrombomodulin (TM) levels as a marker of endothelial injury and to investigate the effect of successful reperfusion on these levels. Methods: The study included 32 patients who had a first episode of acute myocardial infarction (AMI) and received intravenous streptokinase therapy. Results: Thrombomodulin levels increased significantly at 60 min after thrombolysis compared with the levels before thrombolytic therapy (0 min) in 21 (66%) patients who had successful reperfusion (49.09 ± 10.51 vs. 25.76 ± 5.55 ng/ml, p < 0.001). There was no difference between the TM levels at 0 and at 60 min of thrombolysis in the remaining 11 (34%) patients who could not achieve reperfusion (27.81 ± 6.32 vs. 28.72 ± 7.28 ng/ml, p = 0.35). Conclusion: There was a significant increase in TM levels at 60 min after thrombolysis in a group of patients with AMI who achieved successful reperfusion; this increase may have been caused by the activation/injury of endothelial cells. Data also suggest that the increment in TM levels may be predictive of the potential success of thrombolytic therapy.