Myocardial inflammation and non-ischaemic heart failure: is there a role for C-reactive protein?

Oliver Zimmermann1, Magdalena Bienek-Ziolkowski, Bettina Wolf

  • 1Department of Internal Medicine II-Cardiology, University of Ulm, Ulm, Germany. oliver.zimmermann@uniklinik-ulm.de

Insights

C-reactive protein (CRP) is often found in the heart muscle of non-ischaemic heart failure patients. It co-localizes with complement system activation and macrophages, suggesting a role in myocardial damage.

Area of Science:

  • Cardiology
  • Immunology
  • Pathology

Background:

  • C-reactive protein (CRP) is a known cardiovascular risk marker.
  • Its specific role as a risk factor, particularly in non-ischaemic heart failure, requires further investigation.
  • Previous research primarily focused on CRP's effects on ischaemic heart failure and atherosclerosis.

Purpose of the Study:

  • To investigate the distribution of CRP, Terminal Complement Complex (C5b-9), and macrophages (CD68) in the myocardium of patients with non-ischaemic heart failure.
  • To explore the association between these myocardial factors and clinical parameters.
  • To understand the potential mechanisms of myocardial damage in dilated cardiomyopathy (DCM).

Main Methods:

  • Endomyocardial biopsies were obtained from 66 patients with dilated cardiomyopathy (DCM).
  • Immunohistochemical and immunofluorescent staining were used to detect CRP, C5b-9, and CD68.
  • Viral DNA/RNA was analyzed using PCR and Southern blot; findings were correlated with plasma biomarkers and clinical assessments.

Main Results:

  • CRP was detected in the myocardium of 27% of DCM patients, and C5b-9 in 86%.
  • All patients exhibited myocardial macrophage infiltration (CD68 positive).
  • CRP, C5b-9, and macrophages (CD68) were found to co-localize within the myocardium, with no correlation to plasma hsCRP, NT-proBNP, or clinical parameters.

Conclusions:

  • CRP is frequently present in the myocardium of DCM patients.
  • CRP co-localizes with complement activation (C5b-9) and macrophages within the heart muscle.
  • CRP may contribute to myocardial damage in DCM through complement system activation and macrophage recruitment.

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