This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Ramires, F. J. Articles by Mady, C. Search for Related Content PubMed PubMed Citation Articles by Ramires, F. J. Articles by Mady, C. Social Bookmarking                         What's this?

Aldosterone Antagonism in an Inflammatory State: Evidence for Myocardial Protection

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil, carfelix{at}incor.usp.br

Vera MC Salemi

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Barbara M Ianni

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Fábio Fernandes

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Daniel G Martins

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Angelina Billate

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Edécio Cunha, NETO

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Charles Mady

Heart Institute (InCor), University of São Paulo Medical School, São Paulo-SP, Brazil

Introduction. Chagas' disease is one of the most important causes of dilated cardiomyopathy in South and Central America. It is an inflammatory cardiomyopathy. We wanted to investigate whether it could have the same response to aldosterone antagonism as demonstrated before in other dilated cardiomyopathies.

Objective. To evaluate the role of spironolactone in myocardial remodelling in a Chagas' cardiomyopathy model.

Material and Methods. We studied 60 Sirius Hamsters divided into: control (C) infected (Inf) and Inf plus spironolactone (Infsp, 40 mg/kg/day) groups, for 11 months. Echocardiography with colour doppler was performed. Left ventricular end diastolic diameter (LVEDD), fractional shortening (FS) and corrected isovolumic relaxation time (IRT) were evaluated, as well as interstitial collagen volume fraction (ICVF) and myocardial inflammation.

Result. The results demonstrated that survival was improved by use of spironolactone in the chronic phase (p<0.04). Body weight (BW) was C:190 g, Inf:167 g*, Infsp:198 g (*p<0.05, compared to C and Infsp), LVEDD/BW was C:0.31, Inf: 0.35*, Infsp: 0.29 (*p<0.05, compared to C and Infsp), FS was C:38, Inf: 35.5, Infsp: 38 (with no statistical difference) and IRT was C: 23 msec, Inf: 26 msec*, Infsp: 22 msec (p<0.05, compared to C and Infsp). ICVF (%) was attenuated at LV (C: 0.34±0.1, Inf: 1.75±0.7*, Infsp: 0.95±0.2*; *p<0.05, p<0.05).

Conclusion. Spironolactone attenuated the myocardial remodelling in Chagas' cardiomyopathy, reduced mortality during the chronic phase and reduced inflammatory infiltration.

Key Words: Fibrosis • Ventricular function • Cardiomyopathy • Renin-angiotensin system • Animal models

Journal of Renin-Angiotensin-Aldosterone System, Vol. 7, No. 3, 162-167 (2006)
DOI: 10.3317/jraas.2006.026


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?