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(Circulation Research. 1999;85:867-869.)
© 1999 American Heart Association, Inc.

Editorials

The Role of Cell Death in Heart Failure

Jutta Schaper, Albrecht Elsässer, Sawa Kostin

From the Department of Experimental Cardiology, Max Planck Institute, Bad Nauheim, Germany.

Correspondence to Jutta Schaper, MD, Department of Experimental Cardiology, Max Planck Institute, Benekestr 2, D 61231 Bad Nauheim, Germany. E-mail: jschaper@kerckhoff.mpg.de

Key Words: apoptosis • necrosis • heart failure • cardiomyopathy

	Introduction

 
In this issue of Circulation Research, Guerra and colleagues¹ report that myocyte death in the failing human heart is gender dependent. This work is in continuation of Dr Anversa's numerous reports on the occurrence of apoptosis, necrosis, and proliferation in the failing human heart, as well as under various experimental conditions including, among others, aging and myocardial infarction in rats as well as insulin-like growth factor (IGF) transgenic mice.^{2 3 4 5 6} In their present work, the authors demonstrate levels of necrosis 7-fold greater than that of apoptosis in patients of either sex with cardiac failure. Interestingly, cell death was 2-fold higher in men than in women. Necrosis comprised 1.2% (male heart) and 0.5% (female heart), and apoptosis was either 0.16% (Taq or terminal deoxynucleotidyl transferase [TdT]) or 0.25% (electron microscopy) in men and 0.076% (Taq or TdT) or 0.08% (electron microscopy) in women. With respect to baseline, myocyte necrosis was 13-fold higher in female and 27-fold higher in male hearts. Compared with control, apoptosis was 85-fold higher in males and 35-fold higher in female hearts. The conclusion was drawn that both necrosis and apoptosis "affect the decompensated heart, each contributing to the evolution of heart failure."¹

This publication provokes many questions about the role of cell death in failing hearts. The problems listed below are involved in the interpretation of the data presented:

1. Specificity of techniques
   
2. Interpretation of cell numbers obtained
   
3. What is the mechanism for either necrosis or apoptosis in cardiomyopathy?
   
4. What is the role of cell death . . . [Full Text of this Article]

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