TREATMENT OF ACUTE MYOCARDIAL-INFARCTION WITH STREPTOKINASE DOES NOT APPEAR TO MODULATE CIRCULATING NEUTROPHIL FUNCTION

The administration of thrombolytic therapy is the most common method o f achieving patency of the occluded coronary artery in patients with a cute myocardial infarction (AMI). However, thrombolytic agents and the byproducts of fibrinolysis have the potential to affect neutrophil ac tivation and thus function, thereby augmenting myocardial damage furth er. This study assessed the effect of streptokinase administration on the function of circulating neutrophils in patients with AMT. For this neutrophil adherence to human umbilical vein endothelial cells, homot ypic neutrophil aggregation, and CD11b and L-selectin expression on th e neutrophil membrane prior to and 1 h and 6 h after thrombolytic ther apy was monitored. The study population included patients with AMI who received aspirin and streptokinase, and healthy laboratory workers wh o received aspirin only; all subjects acted as their own controls. Cir culating fibrin degradation products and white cells were markedly rai sed following administration of streptokinase. No significant differen ces in neutrophil adherence to endothelium, homotypic neutrophil inter actions, and CD11b or L-selectin expression were demonstrated between neutrophils, either pre-or post-thrombolytic therapy in the infarct gr oup, or between neutrophils from the infarct group and from the contro l group. It was concluded that streptokinase produces an abrupt neutro phil leukocytosis together with a marked increase in circulating level s of fibrin degradation products. The assay systems used were unable t o show significant sequential changes in circulating neutrophil adhesi on and L-selectin or CD11b expression in patients with AMT following t hrombolytic therapy or when these patients were compared with controls .