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.
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 humantumour 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.
Authors: A A Willette; B B Bendlin; D G McLaren; E Canu; E K Kastman; K J Kosmatka; G Xu; A S Field; A L Alexander; R J Colman; R H Weindruch; C L Coe; S C Johnson Journal: Neuroimage Date: 2010-03-15 Impact factor: 6.556
Authors: Ana Savic-Radojevic; Slavica Radovanovic; Tatjana Pekmezovic; Marija Pljesa-Ercegovac; Dragan Simic; Tatjana Djukic; Marija Matic; Tatjana Simic Journal: J Clin Lab Anal Date: 2013-01-24 Impact factor: 2.352
Authors: Reiner Füth; Wilfried Dinh; Werner Nickl; Lars Bansemir; Michael Coll Barroso; Alexander Bufe; Armin Sause; Thomas Scheffold; Thomas Krahn; Peter Ellinghaus; Mark Lankisch Journal: Exp Clin Cardiol Date: 2009