Streptokinase-induced, antibody-mediated platelet aggregation: a potential cause of clot propagation in vivo
DE Vaughan,
JM Kirshenbaum,
and
J Loscalzo
Division of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts 02115.
The administration of intracoronary streptokinase to a patient with a prior history of rheumatic fever was associated with the retrograde propagation of thrombus from the left anterior descending coronary artery into the left main coronary artery with near catastrophic consequences. The addition of streptokinase to platelet-rich plasma from the patient initiated platelet aggregation and secretion in vitro. Platelet aggregation was also seen in 1 of 15 control subjects after the addition of streptokinase, and the addition of plasma or immunoglobulin G (IgG) from the index patient supported platelet aggregation in the presence of streptokinase in all of the previously nonreactive control subjects. This in vitro platelet aggregation was specific for streptokinase and not initiated by either urokinase or tissue plasminogen activator. Streptokinase-induced platelet aggregation was not inhibited by aprotinin, but was completely attenuated by the addition of an excess of antihuman IgG Fab. These findings suggest that streptokinase can initiate specific antibody-mediated platelet aggregation in vitro and may be more than coincidentally related to clot propagation or thromboembolism in vivo.
