© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Apoptotic cell death in heart failure
Department of Medicine, Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, MI 48202, USA
* Tel.: +1-313-876-7360; fax: +1-313-876-3001 HSABBAH1@hfhs.org
Received 2 June 1999; accepted 31 August 1999
KEYWORDS Apoptosis; Heart failure; Myocytes
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1 Introduction |
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Progressive deterioration of left ventricular (LV) function is a characteristic feature of the failing heart. This hemodynamic deterioration, often accompanied by worsening of clinical symptoms, occurs despite the absence of clinically apparent intercurrent adverse events [1,2] and, invariably, culminates in the syndrome of congestive heart failure. The exact mechanisms that drive this process are not known. For years, a so-called ‘vicious circle’ postulate was adopted to explain this phenomenon whereby compensatory mechanisms, elicited to maintain homeostasis, themselves become factors that exacerbate the heart failure state. Such compensatory mechanisms included LV hypertrophy, LV chamber dilation, and enhanced and sustained activity of the sympathetic nervous system and renin–angiotensin system [3–6]. In recent years, we and others have put forward a working hypothesis that progressive LV dysfunction in heart failure may result, in part, from ongoing loss of cardiomyocytes. The notion that progression of heart failure may be due, in part, to
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2 Cardiomyocyte apoptosis and predisposing factors for heart failure |
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2.1 Myocardial infarction
2.2 Ventricular hypertrophy
2.3 Ventricular dilatation
2.4 Autoimmunity
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3 Evidence for cardiomyocyte apoptosis in animal models of heart failure |
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4 Evidence for cardiomyocyte apoptosis in humans with heart failure |
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5 Molecular triggers of apoptosis in heart failure |
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6 Pathophysiological triggers of apoptosis in heart failure |
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7 Importance of cardiomyocyte apoptosis in the progression of heart failure |
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