Skip Navigation


European Journal of Echocardiography Advance Access originally published online on December 23, 2008
European Journal of Echocardiography 2009 10(2):213-215; doi:10.1093/ejechocard/jen311
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
10/2/213    most recent
jen311v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by De Backer, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by De Backer, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

The expanding cardiovascular phenotype of Marfan syndrome

Julie De Backer1,2

1 Department of Medical Genetics, Ghent University Hospital, De Pintelaan 185, Gent 9000, Belgium
2 Department of Cardiovascular Medicine, Ghent University Hospital, De Pintelaan 185, Gent 9000, Belgium

Corresponding author. Tel: +32 9 332 3476; fax: +32 9 332 3462. E-mail address: julie.debacker@UGent.be

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

In this issue of the journal, Kiotsekoglou et al. report on right ventricular systolic dysfunction in patients with Marfan syndrome (MFS). Over the past years, several studies have demonstrated mild, though significant, left ventricular systolic and diastolic dysfunction in patients with MFS.1–5 This is the first study indicating impaired right ventricular function.

Marfan syndrome is an autosomal dominant connective-tissue disorder caused by mutations in the fibrillin-1 gene (FBN1). Cardiovascular manifestations are mainly characterized by progressive dilatation of the aortic root, leading to aneurysm formation which may—when left untreated—lead to aortic dissection or rupture. Other established cardiovascular manifestations include mitral valve prolapse, dilatation of . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?