CLINICAL STUDIES
Myocardial cell death in fibrillating and dilated human right atria
Christine Aimé-Sempé, PhD*,
Thierry Folliguet, MD ,
Catherine Rücker-Martin, PhD ,
Maryla Krajewska, MD||,
Stanislaw Krajewski, MD||,
Michèle Heimburger, PhD ,
Michel Aubier, MD, PhD*,
Jean-Jacques Mercadier, MD, PhD,
John C. Reed, MD, PhD|| and
Stephane N. Hatem, MD, PhD
* INSERM U408, Faculté de Médecine, Xavier Bichat, Paris, France
INSERM U460, Faculté de Médecine, Xavier Bichat, Paris, France
Université de Paris XI-CNRS ERS 566, Hôpital Marie Lannelongue, Le Plessis Robinson, France
the Department de Chirurgie Cardiaque, Institut Mutualiste Montsouris, Paris, France
|| the Burnham Institute, La Jolla, California, USA
Manuscript received March 12, 1999;
revised manuscript received May 20, 1999,
accepted June 29, 1999.
Reprint requests and correspondence: Dr. S. Hatem, INSERM Unité 460, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75018 Paris, France
hatem{at}bichat.inserm.fr
OBJECTIVES
The aim of the present study was to determine if myocytes can die by apoptosis in fibrillating and dilated human atria.
BACKGROUND
The cellular remodeling that occurs during atrial fibrillation (AF) may reflect a degree of dedifferentiation of the atrial myocardium, a process that may be reversible.
METHODS
We examined human right atrial myocardium specimens (n = 50) for the presence of apoptotic myocytes. We used immunohistochemical and Western blotting analysis to examine the expression of a final effector of programmed cell death, caspase-3 (CASP-3) and of regulatory proteins from the BCL-2 family.
RESULTS
Sections from atria in AF contained a high percentage of large myocytes with a disrupted sarcomeric apparatus replaced by glycogen granules (64.4 ± 6.3% vs. 12.2 ± 5.8%). These abnormal myocytes, which also predominated in atria from hearts with decreased left ventricular ejection fraction (42.3 ± 10.1%), contained large nuclei, most of which were TUNEL positive, indicating a degree of DNA breakage. None of these abnormal myocytes expressed the proliferative antigen Ki-67. A small percentage of the enlarged nuclei (4.2 ± 0.8%) contained condensed chromatin and were strongly TUNEL positive. Both the pro- and activated forms of CASP-3 were detected in diseased myocardial samples, which also showed stronger CASP-3 expression than controls. Expression of the antiapoptotic BCL-2 protein was decreased in diseased atria, whereas that of the proapoptotic BAX protein remained unchanged.
CONCLUSIONS
In fibrillating and dilated atria, apoptotic death of myocytes with myolysis contributes to cellular remodeling, which may not be entirely reversible.
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Abbreviations and Acronyms
| | AF | = atrial fibrillation | | CASP-3 | = caspase 3 | | ICAD/CAD | = caspase-activated deoxyribonuclease inhibitor/caspase-activated deoxyribonuclease | | DAB | = diaminobenzidine | | LLVEF | = low left ventricular ejection fraction | | PBS | = phosphate-buffered saline | | PCD | = programmed cell death |
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541 - 553.
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M. A. Allessie, P. A. Boyden, A. J. Camm, A. G. Kleber, M. J. Lab, M. J. Legato, M. R. Rosen, P. J. Schwartz, P. M. Spooner, D. R. Van Wagoner, et al.
Pathophysiology and Prevention of Atrial Fibrillation
Circulation,
February 6, 2001;
103(5):
769 - 777.
[Full Text]
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C. Boixel, W. Gonzalez, L. Louedec, and S. N. Hatem
Mechanisms of L-Type Ca2+ Current Downregulation in Rat Atrial Myocytes During Heart Failure
Circ. Res.,
September 28, 2001;
89(7):
607 - 613.
[Abstract]
[Full Text]
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