ArticleJournal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing2007
Cardiac electrophysiological characteristics of the mdx ( 5cv ) mouse model of Duchenne muscular dystrophy.
Article in Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Conduction defects and arrhythmias inFrontiers in physiology · 2025Article
- Electrocardiographic features of children with Duchenne muscular dystrophy.Orphanet journal of rare diseases · 2022Review
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- Cardiac lesions in Duchenne muscular dystrophy model rats with out-of-frameJournal of toxicologic pathology · 2020Article
- Biochemical and Functional Comparisons of mdx and Sgcg(-/-) Muscular Dystrophy Mouse Models.BioMed research international · 2015Article
- NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Inhibition of CaMKII phosphorylation of RyR2 prevents inducible ventricular arrhythmias in mice with Duchenne muscular dystrophy.Heart rhythm · 2013Article
- Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Phenotyping cardiac gene therapy in mice.Methods in molecular biology (Clifton, N.J.) · 2011Article
- Dystrophin is required for the normal function of the cardio-protective K(ATP) channel in cardiomyocytes.PloS one · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is a progressive muscle disease caused by mutations in the dystrophin gene. Cardiomyopathy, conduction abnormalities, and ventricular arrhythmias are significant complications of this disease. The mdx ( 5cv ) mouse carries a dystrophin mutation and demonstrates a more severe phenotype than the classic mdx mouse.
methodsComprehensive electrophysiological phenotyping was performed in adult mdx ( 5cv ) and wildtype mice, including electrocardiography (ECG), implantable Holter monitoring, intracardiac electrophysiological testing, echocardiography, and exercise treadmill testing.
resultsECG performed in mdx ( 5cv ) mice revealed significantly shorter PR intervals and prominent R waves in surface lead V1. During electrophysiological testing, mdx ( 5cv ) mice exhibited longer ventricle effective refractory periods and mildly increased ventricular tachycardia inducibility. There was no evidence for cardiomyopathy or ventricular dysfunction on echocardiography. Histopathology showed no increased myocardial fibrosis. Exercise endurance was lower in mdx ( 5cv ) mice without arrhythmias or other cardiac abnormalities.
conclusionTaken together at the age range examined, mdx ( 5cv ) mice exhibit discrete cardiac electrophysiological dysfunction but display no evidence of structural or contractile abnormalities. Thus, the mdx ( 5cv ) mouse recapitulates some of the electrophysiological, but not hemodynamic cardiac defects present in human DMD. In certain settings, the mdx ( 5cv ) mouse may be an appropriate subject for studying electrical pathophysiology and therapy of the cardiac complications of DMD.
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