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European Heart Journal Advance Access originally published online on June 27, 2007
European Heart Journal 2007 28(15):1795-1796; doi:10.1093/eurheartj/ehm259
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Towards medical therapy of calcific aortic stenosis—lessons from molecular biology

Jens J. Kaden*

I Medizinische Klinik, Universitätsklinikum Mannheim, Theodor-Kutzer-Ufer 1–3, D-68167 Mannheim, Germany

* Corresponding author. Tel: +49 621 383 3821; fax: +49 621 383 2204. E-mail address: jens.kaden@med.ma.uni-heidelberg.de

This editorial refers to ‘Increased expression of profibrotic neutral endopeptidase and bradykinin type 1 receptors in stenotic aortic valves’ by S. Helske et al., on page 1894

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

Calcific aortic stenosis, with a prevalence of 3–9%, is the most frequent heart valve disease and the main reason for valve replacement in patients over 60 years of age.1 Histopathologically, sclerosis of the aortic valve is defined as fibrous thickening and calcification of the valve cusps.2 For many years, these changes were thought to be caused by passive calcium precipitation within the valve. However, there is increasing evidence that the development and progression of calcific aortic stenosis may be triggered by underlying genetic and acquired risk factors.3 Early . . . [Full Text of this Article]


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Related articles in EHJ:

Increased expression of profibrotic neutral endopeptidase and bradykinin type 1 receptors in stenotic aortic valves
Satu Helske, Mika Laine, Markku Kupari, Jyri Lommi, Heikki Turto, Laura Nurmi, Ilkka Tikkanen, Kalervo Werkkala, Ken A. Lindstedt, and Petri T. Kovanen
EHJ 2007 28: 1894-1903. [Abstract] [Full Text]