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

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.

Overexpression of Human C-Reactive Protein Exacerbates Left Ventricular Remodeling in Diabetic Cardiomyopathy

“…23, 24 In addition, pathological examination of endomyocardial biopsies in patients with dilated cardiomyopathy revealed that CRP is frequently present in the myocardium and co-localizes with complement and macrophages. 25 These findings suggest that CRP itself might play some role in the development of LV dysfunction.…”

Significance of different non-invasive markers in diagnosis of latent myocarditis in comparison with biopsy data

“…Among 20 patients with "idiopathic" arrhythmias (predominantly atrial fibrillation, but also ventricular extrasystoles and left bundle branch block) myocarditis was observed in 75%, viral genome -only in 15.8% what probably can explain relatively favorable course of myocarditis. In separate cases of atrial fibrillation myocarditis was diagnosed in 66%, viral genome has never been studied [8].…”

“…По некоторым данным [15], он не коррелирует с морфо-логическими признаками миокардита (включая опреде-ление самого С-реактивного белка в ткани) у больных с ДКМП. Нами получены данные о достаточно высокой специфичности основных маркеров воспаления, но еще большее значение имело выявление ряда иммунных по-казателей (АТ к ДНК и др.…”

“…It is true for widely used inflammatory markers which are used in patients with arrhythmias and dilated cardiomyopathy; first of all it is C-reactive protein whose level is rarely compared with biopsy data. According to some data its level does not correlate with morphological signs of myocarditis in patients with dilated cardiomyopathy (including detection of C-reactive protein in tissues) [15]. We obtained data about high specificity of main inflammatory markers but revealing several immune indexes was more important (antibodies to DNA, etc.…”

Role of autoimmunity in dilated cardiomyopathy

“…While many causal mechanisms such as abnormal heart valves, inherited cardiomyopathies, severe coronary artery or hypertensive heart disease are easily identified in clinical practice, the precise mechanisms that determine the progression of heart failure and ventricular remodelling are largely unknown. In recent years, there is growing evidence that autoimmunity and inflammatory mechanisms may contribute to disease progression in heart failure [3,5,8,15].…”