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Treatment of acute myocardial infarction with streptokinase does not appear to modulate circulating neutrophil
S A Adams1, S P Froese, B K Green
1Department of Medicine, University of Cape Town, South Africa.
Insights
Streptokinase therapy for acute myocardial infarction (AMI) increases fibrin degradation products and white blood cells. However, it did not significantly alter neutrophil function, adhesion, or expression markers in AMI patients.
Area of Science:
- Cardiology
- Immunology
- Hematology
Background:
- Thrombolytic therapy is standard for acute myocardial infarction (AMI) to restore coronary artery patency.
- Thrombolytic agents and fibrinolysis byproducts may exacerbate myocardial damage by affecting neutrophil function.
- Understanding streptokinase's impact on neutrophil behavior is crucial for managing AMI.
Purpose of the Study:
- To investigate the effect of streptokinase administration on circulating neutrophil function in patients with AMI.
- To assess changes in neutrophil adherence, aggregation, and surface marker expression (CD11b, L-selectin) post-thrombolysis.
- To compare neutrophil function in AMI patients receiving streptokinase with healthy controls.
Main Methods:
- Monitored neutrophil adherence to endothelial cells and homotypic aggregation.
- Measured CD11b and L-selectin expression on neutrophils before and 6 hours after streptokinase therapy.
- Included AMI patients treated with aspirin and streptokinase, and healthy controls on aspirin only.
Main Results:
- Streptokinase administration led to a marked increase in circulating fibrin degradation products and white blood cells (leukocytosis).
- No significant differences were observed in neutrophil adherence, aggregation, CD11b, or L-selectin expression between pre- and post-therapy neutrophils in AMI patients.
- Neutrophil function markers did not differ significantly between AMI patients and healthy controls.
Conclusions:
- Streptokinase induces acute neutrophil leukocytosis and elevates fibrin degradation products in AMI patients.
- The study's assays did not detect significant changes in neutrophil adhesion or activation markers following streptokinase therapy in AMI.
- These findings suggest streptokinase may not significantly impair neutrophil function in the context of AMI, despite observed leukocytosis.
Abstract:
The administration of thrombolytic therapy is the most common method of achieving patency of the occluded coronary artery in patients with acute myocardial infarction (AMI). However, thrombolytic agents and the byproducts of fibrinolysis have the potential to affect neutrophil activation and thus function, thereby augmenting myocardial damage further. This study assessed the effect of streptokinase administration on the function of circulating neutrophils in patients with AMI. For this neutrophil adherence to human umbilical vein endothelial cells, homotypic neutrophil aggregation, and CD11b and L-selectin expression on the neutrophil membrane prior to and 1 h and 6 h after thrombolytic therapy was monitored. The study population included patients with AMI who received aspirin and streptokinase, and healthy laboratory workers who received aspirin only; all subjects acted as their own controls. Circulating fibrin degradation products and white cells were markedly raised following administration of streptokinase. No significant differences in neutrophil adherence to endothelium, homotypic neutrophil interactions, and CD11b or L-selectin expression were demonstrated between neutrophils, either pre- or post-thrombolytic therapy in the infarct group, or between neutrophils from the infarct group and from the control group. It was concluded that streptokinase produces an abrupt neutrophil leukocytosis together with a marked increase in circulating levels of fibrin degradation products. The assay systems used were unable to show significant sequential changes in circulating neutrophil adhesion and L-selectin or CD11b expression in patients with AMI following thrombolytic therapy or when these patients were compared with controls.