Role of apoptosis in pressure-overload cardiomyopathy.
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.
Anselmi
Amedeo
A
Division of Cardiac Surgery, Department of Cardiovascular Medicine, Catholic University, Rome, Italy. amedeo.anselmi@aliceposta.it
Gaudino
Mario
M
Baldi
Alfonso
A
Vetrovec
George W
GW
Bussani
Rossana
R
Possati
Gianfederico
G
Abbate
Antonio
A
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D006801:Humans; D032383:Myocytes, Cardiac / Q000473:pathology*; D013318:Stroke Volume / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology*