Copyright © 2003 by the European Society of Cardiology.
Review article
Molecular determinants of myocardial hypertrophy and failure: alternative pathways for beneficial and maladaptive hypertrophy
a Department of Cardiology, Academic Hospital Maastricht, P. Debyelaan 25, 6202 AZ Maastricht, The Netherlands
b Interuniversity Cardiology Institute, The Netherlands
c Department of Cardiology, Heart Lung Center Utrecht, 3508 GA Utrecht, The Netherlands
* Corresponding author. Tel.: +31-30-3882100; fax: +31-30-25591111
E-mail address: p.doevendans{at}cardio.azm.nl
Received 8 November 2002; accepted 20 November 2002
Abstract
The implementation of molecular biological approaches has led to the discovery of single genetic variations that contribute to the development of cardiac failure. In the present review, the characteristics that are invariably associated with the development of failure in experimental animals and clinical studies are discussed, which may provide attractive biological targets in the treatment of human heart failure. Findings from the Framingham studies have provided evidence that the presence of left ventricular hypertrophy is the main risk factor for subsequent development of heart failure in man. Conventional views identify myocardial hypertrophy as a compensatory response to increased workload, prone to evoke disease. Recent findings in genetic models of myocardial hypertrophy and human studies have provided the molecular basis for a novel concept, which favours the existence of either compensatory or maladaptive forms of hypertrophy, of which only the latter leads the way to cardiac failure. Furthermore, the concept that hypertrophy compensates for augmented wall stress is probably outdated. In this article, we provide the molecular pathways that can distinguish beneficial from maladaptive hypertrophy.
Key Words: Hypertrophy • Heart failure • Gene-expression • Calcium handling • Apoptosis • Fibrosis
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