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Streptokinase, complement activation and hypotension
A Pachaï1, A K Erlendsson, I Brandslund
1Department of Medicine, Vejle County Hospital, Denmark.
Insights
This study investigated if complement activation causes hypotension during streptokinase treatment for myocardial infarction. Results show hypotension occurred in all patients, unrelated to complement activation levels, leaving the mechanism unclear.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Streptokinase is used to treat acute myocardial infarction.
- Transient hypotension is a known side effect of streptokinase infusion.
- The underlying mechanism of this hypotension remains unclear.
Purpose of the Study:
- To determine if complement activation causes transient hypotension during streptokinase infusion in acute myocardial infarction patients.
Main Methods:
- Assessed complement activation using Complement 3d (C3d) levels in venous blood.
- Measured blood pressure in thirteen patients receiving streptokinase for suspected acute myocardial infarction.
- Correlated C3d levels and blood pressure changes.
Main Results:
- All thirteen patients experienced transient hypotension during streptokinase infusion.
- Five patients showed a significant increase (>200%) in C3d levels within 30 minutes.
- Hypotension was not correlated with the presence of myocardial infarction or the degree of complement activation.
Conclusions:
- Complement activation does not appear to be the cause of transient hypotension during streptokinase infusion.
- The mechanism by which streptokinase induces hypotension requires further investigation.
Abstract:
The purpose of this study was to establish whether complement activation is the cause of transient hypotension during streptokinase infusion in patients with acute myocardial infarction. Thirteen patients with suspected acute myocardial infarction and treated with streptokinase were included. Complement 3d (C3d) as an indicator of complement activation was assessed in venous blood and blood pressure was measured. Ten patients had verified myocardial infarction. Three patients did not. Five patients developed an increase in C3d blood levels of more than 200% within 30 min. All patients developed a transient fall in blood pressure during infusion of streptokinase. This was related neither to presence of myocardial infarction nor to degree of complement activation. The mechanism of hypotension observed following the administration of streptokinase is not through complement activation, and thus how streptokinase induces hypotension is still obscure.