title: Role of apoptosis in pressure-overload cardiomyopathy.
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.
authors.affiliation: Division of Cardiac Surgery, Department of Cardiovascular Medicine, Catholic University, Rome, Italy. amedeo.anselmi@aliceposta.it
authors.forename: Amedeo
authors.initials: A
authors.lastname: Anselmi
authors.forename: Mario
authors.initials: M
authors.lastname: Gaudino
authors.forename: Alfonso
authors.initials: A
authors.lastname: Baldi
authors.forename: George W
authors.initials: GW
authors.lastname: Vetrovec
authors.forename: Rossana
authors.initials: R
authors.lastname: Bussani
authors.forename: Gianfederico
authors.initials: G
authors.lastname: Possati
authors.forename: Antonio
authors.initials: A
authors.lastname: Abbate
mesh_terms: 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*