Left ventricular T2 distribution in Duchenne Muscular Dystrophy
نویسندگان
چکیده
منابع مشابه
Left ventricular T2 distribution in Duchenne Muscular Dystrophy
BACKGROUND Although previous studies have helped define the natural history of Duchenne muscular dystrophy (DMD)-associated cardiomyopathy, the myocardial pathobiology associated with functional impairment in DMD is not yet known.The objective of this study was to assess the distribution of transverse relaxation time (T2) in the left ventricle (LV) of DMD patients, and to determine the associat...
متن کاملLeft ventricular noncompaction in Duchenne muscular dystrophy
BACKGROUND Left ventricular noncompaction (LVNC) describes deep trabeculations in the left ventricular (LV) endocardium and a thinned epicardium. LVNC is seen both as a primary cardiomyopathy and as a secondary finding in other syndromes affecting the myocardium such as neuromuscular disorders. The objective of this study is to define the prevalence of LVNC in the Duchenne Muscular Dystrophy (D...
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Duchenne muscular dystrophy (BMD) is an inherited X-link disease. The incidence of this muscle-wasting disease is 1:5000 male live births. Mutation in the gene coding for dystrophin is the main cause of BMD. Most cases of this disease succumb to respiratory and cardiac failure in 3rd to 4th decades. The slow progression of BMD and recent achievement of gene therapies make it as an appropriate c...
متن کاملSerial assessment of myocardial T2 in Duchenne muscular dystrophy
Background Duchenne Muscular Dystrophy (DMD), a lethal X-linked skeletal and cardiac myopathy, affects 1/3500 males[1-2]. MRI studies have shown occult ventricular dysfunction and myocardial fibrosis in DMD patients. Previously we used the Full Width of Half Maximum (FWHM) of T2 distribution in LV to quantify the myocardial structural heterogeneity in DMD patients. In DMD subject groups, we sho...
متن کاملDuchenne muscular dystrophy An overview of Duchenne muscular dystrophy
Duchenne muscular dystrophy (DMD) affects approximately 1 in 3,500 live male births [1]. It is caused by a large variety of mutations in the dystrophin gene. Because of these mutations, the body can no longer make dystrophin which is a protein important for stabilisation of the muscle cell during a contraction. Without dystrophin, muscle cells are damaged and slowly replaced by fat and scar tis...
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ژورنال
عنوان ژورنال: Journal of Cardiovascular Magnetic Resonance
سال: 2009
ISSN: 1532-429X
DOI: 10.1186/1532-429x-11-s1-o51