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Volume 16, Issue 2, Pages 157-163 (February 2010)


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Plasma ACE2 Activity is an Independent Prognostic Marker in Chagas' Disease and Equally Potent as BNP

Yong Wang, PhD1, Maria da Consolação V. Moreira, MD, PhD2, Silvia Heringer-Walther, MD, PhD3, Linda Ebermann, MSc4, Heinz-Peter Schultheiss, MD4, Niels Wessel, PhD5, Wolf-Eberhard Siems, PhD6, Thomas Walther, PhD17Corresponding Author Informationemail address

Received 6 July 2009; received in revised form 15 September 2009; accepted 23 September 2009. published online 05 November 2009.

Abstract 

Background

Angiotensin-converting enzyme (ACE) 2 is a novel homologue of ACE. It metabolizes angiotensin (Ang)II to Ang-(1-7). This study aims to investigate the diagnostic and prognostic potency of circulating ACE2 activity in patients with heart failure (HF) from Chagas' disease (CD).

Methods and Results

Blood samples were obtained from 111 CD patients and 40 age- and gender-matched healthy subjects. The CD patients were further subdivided according to their New York Heart Association classification. ACE2 activity was significantly increased in CD patients with HF, but not in patients without systolic dysfunction. Moreover, plasma ACE2 activity was significantly correlated with their clinical severity and echocardiographic parameters. Importantly, the potency of circulating ACE2 activity in CD patients was equally potent as that of B-type natriuretic peptide to predict cardiac death and heart transplant. Most importantly, patients with both parameters elevated were on a 5-fold higher risk to reach an endpoint than patients with increase in only 1 of the 2 parameters.

Conclusions

Determination of ACE2 activity may provide a new and important diagnostic and prognostic marker for patients with CD. ACE2 activity and BNP concentration have additive predictive value and may be used in combination to offer a new dimension of prediction in HF.

1 Centre for Biomedical Research, Hull York Medical School, University of Hull, Hull, UK

2 Department of Internal Medicine, UFMG, Belo Horizonte, Brazil

3 Department of Obstetrics, University of Leipzig, Leipzig, Germany

4 Department of Cardiology, Charité, Campus Benjamin Franklin, Berlin, Germany

5 Department of Physics, Humboldt Universität zu Berlin, Berlin, Germany

6 Leibniz-Institute of Molecular Pharmacology, Berlin, Germany

7 Excellence Cluster Cardio-Pulmonary System, Justus-Liebig-Universität Giessen, Germany

Corresponding Author InformationReprint requests: Prof. Thomas Walther, Centre for Biomedical Research, Hull York Medical School, University of Hull, Hull, HU6 7RX, UK. Tel: (+44) 1482-46 5513; Fax: (+44) 1482-46 5008.

 Supported by a DAAD and CAPES grant (415-br-probral/po-D/08/11632).

 Conflict of interests: None.

 Both authors contributed equally to this work.

PII: S1071-9164(09)01089-6

doi:10.1016/j.cardfail.2009.09.005


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