Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2008;52:462-464
Published online before print July 21, 2008, doi: 10.1161/HYPERTENSIONAHA.108.117044
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
52/3/462    most recent
HYPERTENSIONAHA.108.117044v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Díez, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Díez, J.
Related Collections
Right arrow Hypertrophy
Right arrow Clinical Studies
Right arrowRelated Article

(Hypertension. 2008;52:462.)
© 2008 American Heart Association, Inc.


Editorial Commentaries

Effects of Aldosterone on the Heart

Beyond Systemic Hemodynamics?

Javier Díez

From the Division of Cardiovascular Sciences, Centre of Applied Medical Research, and Department of Cardiology and Cardiovascular Surgery, University Clinic, University of Navarra, Pamplona, Spain.

Correspondence to Javier Díez, Área de Ciencias Cardiovasculares, Edificio CIMA, Av Pío XII, 55, 31008 Pamplona, Spain. E-mail jadimar@unav.es


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

As predicted by Laplace’s law, the ability of the left ventricle to compensate for increasing loading conditions requires the thickening of the ventricular wall and the growth of left ventricular mass (LVM), defined as left ventricular hypertrophy (LVH) when it exceeds partition values based on distribution in normal reference populations. The presence of LVH, however, does not discriminate between a compensatory and excessive increase in LVM. Therefore, the term "inappropriate LVM" (iLVM) has been applied to conditions in which the observed level of LVM exceeds the theoretical value predicted by sex, body size, and stroke work.1 iLVM is associated with clustered geometric and functional abnormalities of the left ventricle2 and appears to be a marker of adverse cardiovascular prognosis independent of LVH.3 Recent data suggest that changes in the appropriateness of LVM from baseline to follow-up during treatment may predict a subsequent cardiovascular event in hypertensive patients.4 It has been proposed that the pathophysiological process that yields iLVM is probably linked to the protracted activity over time of humoral mediators of LV growth, such as proto-oncogenes, growth factors, hormones, and cytokines, inducing modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue (eg, remodeling) and, as a consequence, impair LV function.5

The study by Muiesan et al in this issue of Hypertension6 points to aldosterone as one of the candidate hormones that may contribute to iLVM. The authors evaluated the inappropriateness of LVM in 125 patients with a diagnosis of primary aldosteronism (PA) and in 125 . . . [Full Text of this Article]


Related Article:

Inappropriate Left Ventricular Mass in Patients With Primary Aldosteronism
Maria Lorenza Muiesan, Massimo Salvetti, Anna Paini, Claudia Agabiti-Rosei, Cristina Monteduro, Gloria Galbassini, Eugenia Belotti, Carlo Aggiusti, Damiano Rizzoni, Maurizio Castellano, and Enrico Agabiti-Rosei
Hypertension 2008 52: 529-534. [Abstract] [Full Text] [PDF]