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Aldosterone Antagonism in an Inflammatory State: Evidence for Myocardial Protection
Felix JA Ramires
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
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Journal of Renin-Angiotensin-Aldosterone System, Vol. 7, No. 3,
162-167 (2006)
DOI: 10.3317/jraas.2006.026

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