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Updated: Jul 29, 2026
Isolation and Physiological Analysis of Mouse Cardiomyocytes
Published on: September 7, 2014
Myocyte loss in chronic heart failure
N B Rayment1, A J Haven, B Madden
1Department of Immunology, UCL Medical School, Windeyer Building, 46 Cleveland Street, London W1P 6DB, U.K.
Insights
Progressive myocyte loss occurs in chronic heart failure, driven by both necrosis and apoptosis. This cell loss shows significant patient-to-patient variation but no difference between ischaemic heart disease and dilated cardiomyopathy.
Area of Science:
- Cardiology
- Pathology
- Cell Biology
Background:
- Established heart failure is characterized by progressive left ventricular dysfunction.
- The precise mechanisms and extent of myocyte loss in chronic heart failure remain incompletely understood.
Purpose of the Study:
- To investigate progressive myocyte loss in established heart failure.
- To determine if myocyte loss occurs via necrosis or apoptosis.
- To compare myocyte loss in ischaemic heart disease versus idiopathic dilated cardiomyopathy.
Main Methods:
- Analysis of cardiac tissue from patients undergoing transplantation for end-stage heart disease.
- Utilized TUNEL method for in situ detection of apoptotic nuclei.
- Employed immunohistochemistry for specific cell markers (CD120a, CD120b, CD95, perforin, granzyme B) and C9 complex binding.
- Assessed lipofuscin deposition in macrophages and examined interstitial immune cells.
Main Results:
- Confirmed low-grade myocyte loss in chronic heart failure.
- Observed significant patient-to-patient variability in myocyte loss within disease categories.
- Found no significant difference in myocyte loss between ischaemic heart disease and idiopathic dilated cardiomyopathy.
- Identified both necrosis and apoptosis as contributors to myocyte loss.
Conclusions:
- Myocyte loss is a feature of chronic heart failure, irrespective of the underlying aetiology.
- Mechanisms driving myocyte loss appear common to both major heart failure disease groups.
- The significant patient variation suggests individual factors influence myocyte loss progression.
Abstract:
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.
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