NEUTROPHIL ELASTASE IS A MARKER OF NEUTROPHIL ACTIVATION IN ACUTE MYOCARDIAL INFARCTION

Elastase is released from human neutrophils as a result of active secretion, phagocytosis or cell lysis. It is a broad-spectrum protease which not only hydrolyses the major components of tissue matrix, but can also affect platelet aggregation, coagulation and fibrinolysis. Neutrophils localise at the site of myocardial infarction and have been implicated in subsequent cell damage. A radioimmunoassay was developed which detects elastase complexed to its inhibitors α₂- antitrypsin and α₂-macroglobulin as wen as the free enzyme. Plasma concentrations of elastase in 31 healthy controls were 21.3 ± 13.8 ng/ml, and did not differ significantly from those in 22 patients with stable angina (23.6 ± 8.6 ng/nl). In 19 patients with myocardial infarction, however, plasma elastase levels rose to a peak within 48 hours of infarct which was significantly higher than normal levels (95.1 < 83.7; P < 0.001), and then declined. Correction of the data for neutrophil count did not affect the significance of the observed differences. Measurement of whole blood elastase reflected the neutrophil count and was not otherwise informative. Thus, neutrophils are activated after myocardial infarction and release sufficient elastase for it to be detected systemically. This may extend tissue damage and affect coagulation and fibrinolysis at the site of infarction.