Mutations in genes coding for major protein components of the cytoskeleton in heart and skeletal muscle cells clinically lead to a heterogeneous group of muscular dystrophies frequently associated with severe cardiomyopathy [1]. In Duchenne muscular dystrophy (DMD) and limb girdle muscular dystrophy type 2 F (LGMD2F), absence of dystrophin or δ-sarcoglycan (Sgcd) disrupts the dystrophin-glycoprotein-complex (DGC) progressively damaging cardiac and skeletal muscle cells [2]. In almost every patient with DMD or LGMD2F subclinical or clinical cardiomyopathy can be found with strong impact on mortality.

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