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Neutrophil function in ischemic heart disease.

J Mehta1, J Dinerman, P Mehta

  • 1Department of Medicine, University of Florida, College of Medicine, Gainesville 32610.

Circulation
|March 1, 1989
PubMed
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Neutrophil function is enhanced in ischemic heart disease. Increased neutrophil activity and leukotriene B4 (LTB4) generation may signal stable angina, while intense activation in unstable angina or acute myocardial infarction indicates ongoing cellular events.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Ischemic Heart Disease Research

Background:

  • Neutrophils play a role in myocardial healing and scar formation post-ischemic injury.
  • Emerging evidence suggests neutrophils are involved in the development and progression of myocardial ischemia.

Purpose of the Study:

  • To investigate and characterize neutrophil function in patients with ischemic heart disease.
  • To compare neutrophil chemotaxis, leukotriene B4 (LTB4) generation, and elastase release across different stages of ischemic heart disease.

Main Methods:

  • Measured neutrophil chemotaxis, LTB4 generation, and plasma elastase release.
  • Analyzed plasma levels of peptide B beta, a marker of neutrophil elastase activity.
  • Utilized electron microscopy to assess neutrophil morphology in patients with unstable angina or acute myocardial infarction.

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Main Results:

  • Neutrophils from stable angina patients showed increased chemotactic activity and LTB4 generation compared to controls.
  • Neutrophils from unstable angina/AMI patients exhibited signs of prior in vivo activation, with reduced ex vivo activity.
  • Plasma peptide B beta levels were significantly elevated in unstable angina/AMI patients, indicating substantial in vivo neutrophil activation.

Conclusions:

  • Neutrophil function is demonstrably enhanced in patients with ischemic heart disease.
  • Elevated neutrophil chemotactic activity and LTB4 generation may serve as biomarkers for stable angina pectoris.
  • Intense neutrophil activation in unstable angina or acute myocardial infarction is linked to ongoing in vivo cellular processes.