Most importantly, thoughthe above-mentioned cardiac therapy might do suggest effective for improving thequality of life in children with symptomatic patients or in reduced LVEF,considering the pathogenesis of DMD, therapies to restore or augment dystrophin,as well as therapies that act downstream of dystrophin, may be more promisingoptions for preserving cardiac function than standard heart failure drugs [32]. This evidence concerns the gene DMD and heart failure.