C-reactive protein and complement depositions in human infarcted myocardium are more extensive in patients with reinfarction or upon treatment with reperfusion

Eur J Clin Invest. 2004 Dec;34(12):803-10. doi: 10.1111/j.1365-2362.2004.01425.x.

Abstract

Background: Impaired perfusion of the heart induces a local inflammatory response, which involves deposition of C-reactive protein and complement activation products C3d and C5b-9. We investigated whether reperfusion or reinfarction enhances these phenomena in humans.

Materials and methods: Depositions of C-reactive protein and complement were quantified in tissue samples of infarcted myocardium from 76 patients who had died after acute myocardial infarction. The extent of depositions in patients treated with reperfusion or suffering from reinfarction was compared with that in patients who had no reperfusion or reinfarction.

Results: Patients with reinfarction had significantly more extensive depositions of C-reactive protein and complement (C3d and C5b-9) in the infarcted myocardium than patients without reinfarction. Similarly, patients who received reperfusion therapy had more extensive depositions also than those who had not received this therapy.

Conclusions: Both reinfarction and reperfusion therapy significantly increase the extent of C-reactive protein and complement depositions in human myocardial infarcts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • C-Reactive Protein / metabolism*
  • Complement C3d / metabolism
  • Complement Membrane Attack Complex / metabolism
  • Complement System Proteins / metabolism*
  • Female
  • Humans
  • Inflammation Mediators / metabolism
  • Male
  • Middle Aged
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocardial Infarction / therapy
  • Myocardial Reperfusion*
  • Recurrence

Substances

  • Complement Membrane Attack Complex
  • Inflammation Mediators
  • Complement C3d
  • Complement System Proteins
  • C-Reactive Protein