Failing human myocardium, regardless of etiology, exhibited a significantly enhanced ICAM-1/PECAM-1 ratio and increased presence of inflammatory cells compared to normal control tissue.
Observational
Are cell adhesion molecules and inflammatory markers upregulated in failing human hearts compared to normal ventricles?
Chronic low-grade inflammation and upregulation of cell adhesion molecules are present in failing human myocardium, potentially contributing to structural deterioration in heart failure.
BACKGROUND: In the present study, the hypothesis was tested that cell adhesion molecules are expressed in failing human hearts and that a chronic inflammatory process contributes to chronic degeneration known to occur in cardiac incompetence. The cell adhesion molecules: ICAM-1, VCAM-1, PECAM-1, and E-selectin were studied, in addition to cellular markers of inflammation. METHODS AND RESULTS: Tissue was obtained at transplantation from patients with either myocarditis, chronic ischaemic heart disease, or dilated cardiomyopathy. Controls were taken from patients with normal ventricles. Cell adhesion molecules were qualitatively evaluated and counted using specific antibodies and confocal microscopy. Additionally, semiquantitative evaluation of the presence of the CD3 antigen (T-lymphocytes), CD68 (macrophages), CD11a/CD18 (ICAM-1 receptor) and human tumour necrosis factor-a were used as indicators of chronic inflammation. PECAM-1 stained all endothelial cells but ICAM-1 was only present in 80% of all capillaries in control tissue. The ratio ICAM-1/PECAM-1 was significantly enhanced in all groups of diseased hearts. Myocytes in myocarditic hearts expressed ICAM-ICAM. CD3 positive lymphocytes, CD68 positive macrophages and CD11a/CD18 positive cells were more abundantly present than in control. Macrophages expressing tumour necrosis factor-a were found in failing myocardium but not in control tissue. CONCLUSION: Independent of the cause of heart failure, chronic low grade inflammation is present in failing human myocardium. This may significantly contribute to the structural deterioration that is the basis of reduced cardiac function in congestive heart failure.
Devaux et al. (1997) conducted an observational in Chronic heart failure. Failing myocardium vs. Normal ventricles was evaluated on Expression of cell adhesion molecules and cellular markers of inflammation. Failing human myocardium, regardless of etiology, exhibited a significantly enhanced ICAM-1/PECAM-1 ratio and increased presence of inflammatory cells compared to normal control tissue.