Key result
Dogs with dilated cardiomyopathy had a significantly lower percentage of dystrophin-positive cells in the left atrium compared to healthy controls (19.18% vs 69.57%, p=0.02).
Observational (n=56)
Single-blind
Absolute Event Rate: 19.18% vs 69.57%
p-value: p=0.02
INTRODUCTION: Dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD) are common heart conditions in dogs. They have different etiology and pathogenesis and although other studies focused on changes in the left ventricles of the affected hearts, the aim of our study was to assess the expressions of some intrinsic proteins in the enlarged left atria. MATERIAL AND METHODS: We performed an immunohistochemical analysis of left atrial specimens obtained from 15 dogs with DCM, 35 dogs with MMVD and six control dogs. We assessed the expression of following proteins: SERCA1, SERCA2, sarcomeric actinin, smooth muscle actin, and dystrophin. RESULTS: We noted a higher percentage of SERCA1-positive cells in the MMVD group and lower percentage of dystrophin-positive cells in the DCM group as compared to control group. The expression of other proteins was similar in the hearts of control dogs and dogs with heart diseases. CONCLUSIONS: The observed changes in the expression patterns of some proteins in the atria of dogs with DCM and MMVD suggest that atrial enlargement relies not only on volume overload, but also alterations of the intrinsic proteins can contribute to the pathogenesis of dilated cardiomyopathy.
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Janus et al. (2017) conducted an observational in Dilated cardiomyopathy and myxomatous mitral valve disease (n=56). Dilated cardiomyopathy and myxomatous mitral valve disease vs. Healthy control dogs was evaluated on Percentage of dystrophin (DMD)-immunoreactive cells in left atrial tissue (DCM vs Control) (p=0.02). Dogs with dilated cardiomyopathy had a significantly lower percentage of dystrophin-positive cells in the left atrium compared to healthy controls (19.18% vs 69.57%, p=0.02).
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