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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.
Abstract:
Whereas C-reactive protein (CRP) is acknowledged as a cardiovascular risk marker, there is ongoing discussion about its role as a risk factor. Previous studies focused on the effects of CRP on ischaemic heart failure and atherosclerosis. In this study we investigated distribution of CRP, the Terminal Complement Complex (C5b-9) and macrophages (CD68) in the myocardium of patients suffering from non-ischaemic heart failure and their implication on clinical parameters. Endomyocardial biopsies were taken from 66 patients suffering from dilated cardiomyopathy (DCM). Biopsies were analysed by immunohistochemical and immunofluorescent staining for CRP, C5b-9 and CD68. Viral DNA/RNA for adenovirus, enterovirus, parvovirus B19 and human herpes virus 6 was detected by PCR and Southern blot analysis. Myocardial biopsy findings were correlated with plasma level of hsCRP and NT-proBNP as well as echocardiography, exercise test and NYHA class. In 18 (27%) patients, a positive staining for CRP and in 57 (86%) patients a positive staining for C5b-9 was detected. All patients showed myocardial infiltration with macrophages with an average of 39 cells/mm(2). CRP, C5b-9 and CD68 co-localised within the myocardium. No correlation was observed for inflammatory proteins and plasma level of hsCRP, NT-proBNP and clinical parameters. CRP is frequently present in the myocardium of patients suffering from DCM and co-localises with C5b-9 and macrophages. CRP may contribute to myocardial damage in DCM via activation of the complement system and chemotaxis of macrophages.
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