Myocyte loss in chronic heart failure

This study examined whether or not there is progressive loss of individual myocytes in established heart failure, accounting for the progressive left ventricular dysfunction; whether such loss is by necrosis or apoptosis; and whether such loss is more pronounced in ischaemic heart disease or idiopat...

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Bibliographic Details
Published in:The Journal of pathology 1999-06, Vol.188 (2), p.213-219
Main Authors: Rayment, Neil B., Haven, Aldwyn J., Madden, Brendan, Murday, Andrew, Trickey, Rod, Shipley, Martin, Davies, Michael J., Katz, David R.
Format: Article
Language:English
Subjects:
Adult
Aged
Apoptosis
Biological and medical sciences
Biomarkers - analysis
Cardiology. Vascular system
cardiomyopathy
Cardiomyopathy, Dilated - complications
Cardiomyopathy, Dilated - pathology
Chronic Disease
chronic heart failure
Coronary heart disease
fas Receptor - analysis
Female
Granzymes
Heart
Heart Failure - etiology
Heart Failure - pathology
Humans
Immunohistochemistry
In Situ Nick-End Labeling
ischaemic heart disease
Male
Medical sciences
Membrane Glycoproteins - analysis
Middle Aged
Myocardial Ischemia - complications
Myocardial Ischemia - pathology
Myocardium - pathology
myocyte
Necrosis
Perforin
Pore Forming Cytotoxic Proteins
Serine Endopeptidases - analysis
Tumor Necrosis Factor-alpha - analysis
von Willebrand Factor - analysis
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Summary:This study examined whether or not there is progressive loss of individual myocytes in established heart failure, accounting for the progressive left ventricular dysfunction; whether such loss is by necrosis or apoptosis; and whether such loss is more pronounced in ischaemic heart disease or idiopathic dilated cardiomyopathy. Tissue for patients undergoing cardiac transplantation for clinical end‐stage heart disease was used. The clinical diagnosis was not known to the observer at the time of analysis. Indices of potential myocyte loss were: detection of apoptotic nuclei in situ, using the TUNEL method, immunohistochemistry for CD120a, CD120b, CD95, perforin and granzyme B; binding of C9 complex; and lipofuscin deposition within macrophages. Interstitial macrophages and T cells and their relationship to myocyte loss were also examined. There is indeed low grade myocyte loss in chronic heart failure, but there was no difference between the disease groups; rather, there was marked patient‐to‐patient variation within each category. Thus in chronic heart failure myocyte loss does occur, and both necrosis and apoptosis contribute to this loss, irrespective of the underlying nature of the disease. Any mechanism which accounts for myocyte loss must be common to both conditions, rather than specific for a pre‐operative diagnosis. Copyright © 1999 John Wiley & Sons, Ltd.
ISSN:0022-3417
1096-9896
DOI:10.1002/(SICI)1096-9896(199906)188:2<213::AID-PATH348>3.0.CO;2-5