Early manifestation of alteration in cardiac function in dystrophin deficient mdx mouse using 3D CMR tagging
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BioMed Central
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Early manifestation of alteration in cardiac function in dystrophin deficient mdx mouse using 3D CMR tagging Wei Li1,4, Wei Liu5, Jia Zhong1,4 and Xin Yu*1,2,3,4 Address: 1Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio, USA, 2Department of Radiology, Case Western Reserve University, Cleveland, Ohio, USA, 3Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA, 4Case Center for Imaging Research, Case Western Reserve University, Cleveland, Ohio, USA and 5Department of Biomedical Engineering, Washington University, St Louis, Missouri, USA Email: Wei Li - [email protected]; Wei Liu - [email protected]; Jia Zhong - [email protected]; Xin Yu* - [email protected] * Corresponding author
Published: 22 October 2009 Journal of Cardiovascular Magnetic Resonance 2009, 11:40
doi:10.1186/1532-429X-11-40
Received: 14 April 2009 Accepted: 22 October 2009
This article is available from: http://www.jcmr-online.com/content/11/1/40 © 2009 Li et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Duchenne muscular dystrophy (DMD) is caused by the absence of the cytoskeletal protein, dystrophin. In DMD patients, dilated cardiomyopathy leading to heart failure may occur during adolescence. However, early cardiac dysfunction is frequently undetected due to physical inactivity and generalized debilitation. The objective of this study is to determine the time course of cardiac functional alterations in mdx mouse, a mouse model of DMD, by evaluating regional ventricular function with CMR tagging. Methods: In vivo myocardial function was evaluated by 3D CMR tagging in mdx mice at early (2 months), middle (7 months) and late (10 months) stages of disease development. Global cardiac function, regional myocardial wall strains, and ventricular torsion were quantified. Myocardial lesions were assessed with Masson's trichrome staining. Results: Global contractile indexes were similar between mdx and C57BL/6 mice in each age group. Histology analysis showed that young mdx mice were free of myocardial lesions. Interstitial fibrosis was present in 7 month mdx mice, with further development into patches or transmural lesions at 10 months of age. As a result, 10 month mdx mice showed significantly reduced regional strain and torsion. However, young mdx mice showed an unexpected increase in regional strain and torsion, while 7 month mdx mice displayed similar regional ventricular function as the controls. Conclusion: Despite normal global ventricular function, CMR tagging detected a biphasic change in myocardial wall strain and torsion, with an initial increase at young age followed by progressive decrease at older ages. These results suggest that CMR tagging ca
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