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A pilot study of streptokinase-induced endothelial injury and platelet activation following acute myocardial infarction.

作者信息

Lip G Y, Lydakis C, Nuttall S L, Landray M J, Watson R D, Blann A D

机构信息

University Department of Medicine, City Hospital, Birmingham, UK.

出版信息

J Intern Med. 2000 Oct;248(4):316-8. doi: 10.1046/j.1365-2796.2000.00738.x.

Abstract

OBJECTIVE

To relate the changes in serum vitamin E, an essential antioxidant, to changes in fibrinogen, as well as indices of endothelial damage [as indicated by plasma markers, soluble thrombomodulin (sTM) and von Willebrand factor (vWf), and an index of platelet activation (soluble P selectin (sPsel)], in myocardial infarction treated with thrombolytic therapy.

DESIGN AND SETTING

Prospective longitudinal pilot study in a teaching hospital Coronary Care Unit.

SUBJECTS AND INTERVENTION

Seventeen patients (12 men: mean age (62 years +/- SD 11 years) admitted with acute myocardial infarction (AMI), who were given thrombolytic therapy, and 59 healthy controls.

RESULTS

Baseline levels of fibrinogen (Mann-Whitney test, P = 0.0055) and vWf (P < 0.001) were significantly higher than controls, but sPsel, sTM or vitamin E levels were not significantly different. Following thrombolysis, as expected, median concentrations of plasma fibrinogen fell profoundly (Friedman ANOVA P < 0.001) so that after 45 min, levels were undetectable in 13 patients. At 24-h median fibrinogen concentration had recovered to approximately 30% of baseline (P < 0.01) and was still undetectable in three patients. Levels of vWf and sPsel increased steadily, reaching significance after three hours (both P < 0.05). However, levels of sTM rose immediately after thrombolysis, peaking between 1 and 3 h, and remained elevated at 24 h. These increases corresponded to a simultaneous early fall in serum vitamin E concentrations.

CONCLUSION

The present pilot study demonstrates significant endothelial damage and platelet activation in association with increased oxidative stress following streptokinase therapy for AMI.

摘要

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