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Cardiovascular Research 2000 46(1):17-19; doi:10.1016/S0008-6363(00)00015-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Hypertrophy and dilation: a TOTally new story?

Stéphane Baudet*

Intervet Pharma R&D, Internal Medicine 2, Rue Olivier de Serres, BP 67131, F-49071 Beaucouzé Cedex, France

* Corresponding author. Tel.: +33-241-22-8269; fax: +33-241-22-8251 stephane.baudet@intervet.akzonobel.nl

Received 14 January 2000; accepted 14 January 2000

The first 150 words of the full text of this article appear below.

See article by Sussman et al. [15] (pages 90–101) in this issue.

Myocardial hypertrophy is either a primary disease of the heart as found for genetic cardiomyopathies (hypertrophic or dilated), or an adaptative response secondary to, for instance, hemodynamic disturbances (pressure or volume overload) or endocrine dysfunction (hyperthyroidism, diabetes mellitus) [1,2]. Reactive concentric hypertrophy is fundamentally a compensatory response as the enlargement of the ventricular wall maintains normal hemodynamics and therefore allows physiological tissue perfusion. However, hypertrophy does not proceed indefinitely: the maintenance of the initial stress that induced the compensatory response overwhelms, after a variable delay, the hypertrophic capacity of the heart. From a functional standpoint, systolic dysfunction, metabolic exhaustion and insufficient tissue perfusion, i.e. major signs of heart failure, occur and in absence of adequate treatment, lead to premature death. Cardiac hypertrophy is clearly a double-edged sword: on one hand, it is beneficial as it preserves tissue . . . [Full Text of this Article]


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