Circulation, Vol 79, 549-556, Copyright © 1989 by American Heart Association
J Mehta, J Dinerman, P Mehta, TG Saldeen, D Lawson, WH Donnelly and R Wallin
Neutrophils contribute to the healing of and scar formation in myocardium
after ischemic injury. Many recent studies indicate that neutrophils may be
involved in the genesis and propagation of myocardial ischemia. To
characterize neutrophil function in ischemic heart disease, neutrophil
chemotaxis, leukotriene B4 (LTB4) generation, and elastase release in
plasma were measured in 20 patients with stable angina, 17 patients with
unstable angina or acute myocardial infarction (AMI), and 20 age-matched
control subjects. Neutrophils from patients with stable angina exhibited
markedly increased chemotactic activity and LTB4 generation as compared
with the age-matched control subjects (p less than 0.01). Neutrophils of
nine of 17 patients with unstable angina or AMI clumped spontaneously ex
vivo and exhibited marked pseudopod formation and granule extrusion on
electron microscopy. Subsequent chemotactic activity and LTB4 generation by
neutrophils from these patients was less than in patients with stable
angina, suggesting previous in vivo activation. Plasma levels of peptide B
beta, a product of fibrin degradation by human neutrophil elastase, were
approximately 15-fold higher (p less than 0.001) in patients with unstable
angina or AMI (588 +/- 171 pmol/l, mean +/- SEM) compared with those in
patients with stable angina (37 +/- 25 pmol/l) or control subjects (40 +/-
22 pmol/l), confirming intense in vivo neutrophil activation. Our study
shows enhanced neutrophil function in patients with ischemic heart disease.
The increased neutrophil chemotactic activity and LTB4 generation may be
markers of stable angina pectoris. Intense neutrophil activation in
unstable angina or AMI, as manifested by morphologic changes in neutrophils
and elastase release, may relate to ongoing in vivo cellular activation.
ARTICLES
Neutrophil function in ischemic heart disease
Department of Medicine, University of Florida, College of Medicine, Gainesville 32610.
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