Literature DB >> 34050592

Prevalence and clinical outcomes of dystrophin-associated dilated cardiomyopathy without severe skeletal myopathy.

Maria A Restrepo-Cordoba1,2,3, Karim Wahbi4, Anca R Florian5, Juan Jiménez-Jáimez6, Luisa Politano7, Michael Arad8, Vicente Climent-Paya9, Ana Garcia-Alvarez2,10, Rasmus B Hansen11, José M Larrañaga-Moreira12, Milos Kubanek13, Luis R Lopes3,14,15, Andrea Ros16, Ruxandra Jurcut3,17, Torsten B Rasmussen18, Luis Ruiz-Guerrero19, Regina Pribe-Wolferts20, Julian Palomino-Doza2,21, Zofia Bilinska22, José F Rodríguez-Palomares2,23, Rosa L E Van Loon24, María Teresa Basurte Elorz25, Giovanni Quarta26, Maria Robledo Iñarritu27, Job A J Verdonschot28, Tanya Stojkovic29, Zornitsa Shomanova5, Francisco Bermudez-Jimenez6, Alberto Palladino7, Dov Freimark8, Maria I García-Álvarez9, Paloma Jorda10, Fernando Dominguez1,2,3, Juan Pablo Ochoa1,30, Francesca Girolami31, Ramon Brugada2,32,33, Benjamin Meder20,34, Roberto Barriales-Villa2,12, Jens Mogensen11, Pascal Laforêt35, Ali Yilmaz5, Perry Elliott3,14,15, Pablo Garcia-Pavia1,2,3,36,37.   

Abstract

AIMS: Dilated cardiomyopathy (DCM) associated with dystrophin gene (DMD) mutations in individuals with mild or absent skeletal myopathy is often indistinguishable from other DCM forms. We sought to describe the phenotype and prognosis of DMD associated DCM in DMD mutation carriers without severe skeletal myopathy. METHODS AND
RESULTS: At 26 European centres, we retrospectively collected clinical characteristics and outcomes of 223 DMD mutation carriers (83% male, 33 ± 15 years). A total of 112 individuals (52%) had DCM at first evaluation [n = 85; left ventricular ejection fraction (LVEF) 34 ± 11.2%] or developed DCM (n = 27; LVEF 41.3 ± 7.5%) after a median follow-up of 96 months (interquartile range 5-311 months). DCM penetrance was 45% in carriers older than 40 years. DCM appeared earlier in males and was independent of the type of mutation, presence of skeletal myopathy, or elevated serum creatine kinase levels. Major adverse cardiac events (MACE) occurred in 22% individuals with DCM, 18% developed end-stage heart failure and 9% sudden cardiac death or equivalent. Skeletal myopathy was not associated with survival free of MACE in patients with DCM. Decreased LVEF and increased left ventricular end-diastolic diameter at baseline were associated with MACE. Individuals without DCM had favourable prognosis without MACE or death during follow-up.
CONCLUSIONS: DMD-associated DCM without severe skeletal myopathy is characterized by incomplete penetrance but high risk of MACE, including progression to end-stage heart failure and ventricular arrhythmias. DCM onset is the major determinant of prognosis with similar survival regardless of the presence of skeletal myopathy.
© 2021 European Society of Cardiology.

Entities:  

Keywords:  DMD; Dilated cardiomyopathy; Dystrophin; Heart failure; Myopathy

Mesh:

Substances:

Year:  2021        PMID: 34050592     DOI: 10.1002/ejhf.2250

Source DB:  PubMed          Journal:  Eur J Heart Fail        ISSN: 1388-9842            Impact factor:   15.534


  4 in total

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2.  Bioinformatics prediction of potential mechanisms and biomarkers underlying dilated cardiomyopathy.

Authors:  Zhou Liu; Ying-Nan Song; Kai-Yuan Chen; Wei-Long Gao; Hong-Jin Chen; Gui-You Liang
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4.  Combination of late gadolinium enhancement and genotype improves prediction of prognosis in non-ischaemic dilated cardiomyopathy.

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Journal:  Eur J Heart Fail       Date:  2022-05-22       Impact factor: 17.349

  4 in total

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