Increased neutrophil elastase release in unstable angina pectoris and acute myocardial infarction

Neutrophils, a source of proteolytic enzymes and oxygen free radicals, have been shown to participate in animal models of myocardial ischemic injury. To characterize neutrophil activation in human ischemic heart disease, a specific neutrophil elastase-derived fibrinopeptide in plasma was measured in 25 patients with stable angina pectoris, 29 patients with unstable angina pectoris, 17 patients with acute myocardial infarction and 22 control subjects. Mean plasma levels (± standard error) of a neutrophil elastase-derived fibrinopeptide (Bβ 30–43) measured by a specific radioimmunoassay were fivefold higher in patients with acute myocardial infarction (877 ± 337 pmol/liter, p < 0.02) and 13-fold higher in patients with unstable angina (2,277 ± 613 pmol/iter, p < 0.006) as compared with control subjects (172 ± 74 pmol/liter). Mean plasma levels of peptide Bβ 30–43 in paients with stable angina (676 ± 334 pmol/liter), although higher than in control subjects, were not significantly increased (p = 0.64). Total leukocyte counts were 11.0 ± 0.6 × 106/ml In those with acute myocardial infarction,9.2± 0.7 × 106/ml in those with unstable angina, 7.1 ±.3 × 106/ml in those with stable angina and 7.7 ± 0.4 × 106/ml in control subjects. Although total leukocyte counts in patients with unstable angina pectoris and acute myocardial infarction were higher (p < 0.01) than in patients with stable angina or in control subjects, elevations in peptide Bβ 30–43 levels were independent of the differences in both leukocyte count and absolute neutrophil count as well as in history of smoking, hypertension, diabetes mellitus or treatment. These results provide evidence for significant neutrophil activation in acute myocardial ischemia in humans that may represent ongoing in vivo neutrophil stimulation.