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European Heart Journal Advance Access originally published online on March 21, 2005
European Heart Journal 2005 26(8):751-754; doi:10.1093/eurheartj/ehi208
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Dilated cardiomyopathy: more genes means more phenotypes

Karl Josef Osterziel* and Andreas Perrot

Charité Universitätsmedizin Berlin, Campus Buch, Franz-Volhard Klinik, Department of Cardiology, Haus 129, Wiltbergstrasse 50, 13125 Berlin, Germany

* Corresponding author. Tel: +49 30 9417 2500; fax: +49 30 9417 2279. E-mail address: osterziel@fvk-berlin.de

This editorial refers to ‘Mutation screening in dilated cardiomyopathy: prominent role of the beta myosin heavy chain gene’{dagger} by E. Villard et al., on page 794

The first 10% of the full text of this article appears below.

Dilated cardiomyopathy (DCM) is the third most common cause of heart failure after coronary artery disease and hypertension. DCM is the most frequent form of primary myocardial disease. Clinically, DCM is characterized by a progressive course of ventricular dilatation and systolic dysfunction. The different stages of DCM are reflected by the presentation of asymptomatic patients with left ventricular dilatation or impaired systolic function, patients with exercise-induced symptoms of heart failure, or overt congestive heart failure. The life expectancy is limited and varies according to the underlying aetiology.1 Myocarditis, immunological abnormalities, toxic myocardial damage, and genetic factors are all assumed to be causes. The familial occurrence of DCM, mostly as an autosomal dominant trait, is more common than generally believed. As a matter of fact, 20–30% of all cases of DCM are caused by genetic mutations.2

In the past decade, major progress has been achieved by investigating families with . . . [Full Text of this Article]

Acknowledgement


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Mutation screening in dilated cardiomyopathy: prominent role of the beta myosin heavy chain gene
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EHJ 2005 26: 794-803. [Abstract] [FREE Full Text]  



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