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.

Treatment with streptokinase (SK) of patients with acute myocardial infarction (AMI) is known to activate the complement system. In a previous investigation we found a great variation in the degree of complement activation taking place during infusion of SK in patients with AMI (range: 0-293% increase in pretreatment complement split product 3d (C3d) levels). In this in vitro study we added SK to serum with different concentrations of SK-antibodies (SK-Ab) and found that both the relative concentrations and the total concentrations of SK and Ab determined the degree of complement activation elicited by SK. This finding was in accordance with the Kendall-Heidelberger equation of antigen-antibody equivalence. Furthermore, we found parallel rises in C3d and C4d, indicating that complement was activated via the classical pathway. A condition for maximal complement activation is antigen-antibody equivalence.