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The complement system in ischemic heart disease

M Yasuda1, K Takeuchi, M Hiruma

  • 1First Department of Internal Medicine, Osaka City University Medical School, Japan.

Circulation
|January 1, 1990
PubMed

Insights

Complement system activation occurs in acute myocardial infarction (AMI) and is linked to heart damage. Mild activation is seen in unstable angina, but not stable angina, without cardiac dysfunction.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Biochemistry

Background:

  • Tissue injury mechanisms post-acute myocardial infarction (AMI) remain unclear.
  • Experimental models suggest complement system involvement in AMI-related microvascular and macrovascular injury.
  • The role of complement activation in angina pectoris is not well-defined.

Purpose of the Study:

  • To investigate the role of the complement system as a mediator of myocardial inflammation.
  • To quantify complement activation products in patients with AMI, unstable angina, stable angina, and healthy volunteers.
  • To assess the association between complement activation and myocardial damage.

Main Methods:

  • Quantification of complement activation products (C3d, C4d, Bb, SC5b-9) in plasma samples.
  • Study included 31 AMI patients, 17 unstable angina patients, 19 stable angina patients, and 20 normal volunteers.
  • Correlations between SC5b-9 levels and peak creatine phosphokinase, ejection fraction, and heart failure status were analyzed.

Main Results:

  • Plasma C3d levels were elevated in AMI and unstable angina patients (p<0.01).
  • Plasma levels of C4d, Bb, and SC5b-9 were increased exclusively in AMI patients (p<0.01).
  • Plasma SC5b-9 levels correlated with creatine phosphokinase (r=0.71) and inversely with ejection fraction (r=-0.71), and were higher in AMI patients with heart failure.

Conclusions:

  • Complement system activation is evident following AMI and associated with myocardial damage.
  • Mild complement system activation occurs in unstable angina pectoris without cardiac functional impairment.
  • The complement system is not activated in stable angina pectoris.

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