Cardiac Magnetic Resonance Assessment Of Interstitial Myocardial Fibrosis And Cardiomyocyte Hypertrophy In Hypertensive Mice Treated With Spironolactone.

dc.creatorCoelho-Filho, Otavio R
dc.creatorShah, Ravi V
dc.creatorNeilan, Tomas G
dc.creatorMitchell, Richard
dc.creatorMoreno, Heitor
dc.creatorKwong, Raymond
dc.creatorJerosch-Herold, Michael
dc.date2014-Jun
dc.date2015-11-27T13:42:49Z
dc.date2015-11-27T13:42:49Z
dc.date.accessioned2018-03-29T01:21:12Z
dc.date.available2018-03-29T01:21:12Z
dc.identifierJournal Of The American Heart Association. v. 3, n. 3, p. e000790, 2014-Jun.
dc.identifier2047-9980
dc.identifier10.1161/JAHA.114.000790
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/24965024
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/201515
dc.identifier24965024
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1301748
dc.descriptionNearly 50% of patients with heart failure (HF) have preserved LV ejection fraction, with interstitial fibrosis and cardiomyocyte hypertrophy as early manifestations of pressure overload. However, methods to assess both tissue characteristics dynamically and noninvasively with therapy are lacking. We measured the effects of mineralocorticoid receptor blockade on tissue phenotypes in LV pressure overload using cardiac magnetic resonance (CMR). Mice were randomized to l-nitro-ω-methyl ester (l-NAME, 3 mg/mL in water; n=22), or l-NAME with spironolactone (50 mg/kg/day in subcutaneous pellets; n=21). Myocardial extracellular volume (ECV; marker of diffuse interstitial fibrosis) and the intracellular lifetime of water (τic; marker of cardiomyocyte hypertrophy) were determined by CMR T1 imaging at baseline and after 7 weeks of therapy alongside histological assessments. Administration of l-NAME induced hypertensive heart disease in mice, with increases in mean arterial pressure, LV mass, ECV, and τic compared with placebo-treated controls, while LV ejection fraction was preserved (>50%). In comparison, animals receiving both spironolactone and l-NAME (l-NAME+S) showed less concentric remodeling, and a lower myocardial ECV and τic, indicating decreased interstitial fibrosis and cardiomyocyte hypertrophy (ECV: 0.43 ± 0.09 for l-NAME versus 0.25 ± 0.03 for l-NAME+S, P<0.001; τic: 0.42 ± 0.11 for l-NAME groups versus 0.12 ± 0.05 for l-NAME+S group). Mice treated with a combination of l-NAME and spironolactone were similar to placebo-treated controls at 7 weeks. Spironolactone attenuates interstitial fibrosis and cardiomyocyte hypertrophy in hypertensive heart disease. CMR can phenotype myocardial tissue remodeling in pressure-overload, furthering our understanding of HF progression.
dc.description3
dc.descriptione000790
dc.languageeng
dc.relationJournal Of The American Heart Association
dc.relationJ Am Heart Assoc
dc.rightsfechado
dc.rights© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
dc.sourcePubMed
dc.subjectAnimals
dc.subjectCardiac Imaging Techniques
dc.subjectCardiomegaly
dc.subjectFibrosis
dc.subjectHeart
dc.subjectHypertension
dc.subjectMagnetic Resonance Imaging
dc.subjectMice
dc.subjectMyocardium
dc.subjectMyocytes, Cardiac
dc.subjectNg-nitroarginine Methyl Ester
dc.subjectReceptors, Mineralocorticoid
dc.subjectSpironolactone
dc.subjectStroke Volume
dc.subjectCardiac Magnetic Resonance Imaging
dc.subjectHypertension
dc.subjectHypertrophy/remodeling
dc.titleCardiac Magnetic Resonance Assessment Of Interstitial Myocardial Fibrosis And Cardiomyocyte Hypertrophy In Hypertensive Mice Treated With Spironolactone.
dc.typeArtículos de revistas


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