Renin-Angiotensin Activation and Oxidative Stress in Early Heart Failure with Preserved Ejection FractionReportar como inadecuado




Renin-Angiotensin Activation and Oxidative Stress in Early Heart Failure with Preserved Ejection Fraction - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

BioMed Research International - Volume 2015 2015, Article ID 825027, 7 pages -

Research Article

MedStar Washington Hospital Center, Georgetown University, Washington, DC 20010, USA

Cardiovascular Research Center and Cardiovascular Institute of Lifespan, The Warren Alpert Medical School, Brown University, Providence, RI 02903, USA

University of Illinois at Chicago, Chicago, IL 60612, USA

Division of Cardiology, Emory University School of Medicine, Atlanta, GA 30322, USA

Division of Pulmonary, Allergy and Critical Care Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA

University of Tennessee, Memphis, TN 38163, USA

Received 20 March 2015; Revised 3 June 2015; Accepted 10 June 2015

Academic Editor: Giacomo Frati

Copyright © 2015 Smita I. Negi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Animal models have suggested a role of renin-angiotensin system RAS activation and subsequent cardiac oxidation in heart failure with preserved ejection fraction HFpEF. Nevertheless, RAS blockade has failed to show efficacy in treatment of HFpEF. We evaluated the role of RAS activation and subsequent systemic oxidation in HFpEF. Oxidative stress markers were compared in 50 subjects with and without early HFpEF. Derivatives of reactive oxidative metabolites DROMs, F2-isoprostanes IsoPs, and ratios of oxidized to reduced glutathione GSH and cysteine CyS were measured. Angiotensin converting enzyme ACE levels and activity were measured. On univariate analysis, HFpEF was associated with male sex , higher body mass index BMI , less oxidized CyS , lower DROMs , and lower IsoP . Higher BMI OR: 1.3; 95% CI: 1.1–1.6 and less oxidized CyS OR: 1.2; 95% CI: 1.1–1.4 maintained associations with HFpEF on multivariate analysis. Though ACE levels were higher in early HFpEF OR: 1.09; 95% CI: 1.01–1.05, ACE activity was similar to that in controls. HFpEF is not associated with significant systemic RAS activation or oxidative stress. This may explain the failure of RAS inhibitors to alter outcomes in HFpEF.





Autor: Smita I. Negi, Euy-Myoung Jeong, Irfan Shukrullah, Emir Veleder, Dean P. Jones, Tai-Hwang M. Fan, Sudhahar Varadarajan, Ser

Fuente: https://www.hindawi.com/



DESCARGAR PDF




Documentos relacionados