Abstract
In the natural history of pressure overload, the hypertrophy response of the left ventricle initially normalizes wall stress and allows preservation of a normal ejection fraction. Nevertheless, patients progress gradually or suddenly from compensated hypertrophy to ventricular dilation with heart failure. Long-standing hypertrophy entails a maladaptive response, which is due to derangements inherent in the myocardium rather than to a progressive increase in the cause of pressure overload. Despite this condition being linked to major clinical consequences and an unfavourable prognosis, the cellular and molecular mechanisms in pressure-overload cardiomyopathy have not yet been established. This review discusses the available experimental and clinical evidence with respect to the role played by myocardial apoptosis in pressure-overload cardiomyopathy.
Lingua originale | English |
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pagine (da-a) | 227-232 |
Numero di pagine | 6 |
Rivista | Journal of Cardiovascular Medicine |
Volume | 9 |
DOI | |
Stato di pubblicazione | Pubblicato - 2008 |
Keywords
- Animals
- Apoptosis
- Cardiomyopathy, Hypertrophic
- Disease Progression
- Humans
- Myocytes, Cardiac
- Stroke Volume
- Ventricular Pressure