Literature DB >> 16314145

Severe dilated cardiomyopathy and quadriceps myopathy due to lamin A/C gene mutation: a phenotypic study.

Jean-Christophe Charniot1, Michel Desnos, Khaled Zerhouni, Dominique Bonnefont-Rousselot, Jean-Paul Albertini, Jeffrey Zaketto Salama, Guillaume Bassez, Michel Komajda, Jean-Yves Artigou.   

Abstract

UNLABELLED: This study reports a family affected by a new phenotype associated with dilated cardiomyopathy and quadriceps myopathy.
METHODS: 29 family members underwent a physical and neurological examination, including an electromyogram and biopsy of muscle abnormalities. A cardiac examination was performed in all subjects.
RESULTS: The family pedigree (n=72) demonstrated that transmission was autosomal dominant. Eleven subjects had cardiac involvement, only four had quadriceps muscle involvement. Cardiac impairment preceded neurological involvement. The mean age for neurological involvement was 44+/-0.8 years (range 43-45) and cardiac involvement was 37+/-7.9 years (range: 24-45). Cardiac involvement consisted of: hypokinetic dilated cardiomyopathy (64%); atrial fibrillation (100%); ventricular arrhythmias (64%); impaired conduction with bundle branch or complete atrio ventricular block (73%). Four patients required pacemakers and anti arrhythmic therapies. Four patients died: two of refractory heart failure and two of sudden death; two patients were resuscitated following cardiac arrest. Three patients required a prophylactic implantable cardiac defibrillator (ICD). Muscle morphological abnormalities were characterized by a variable number of fibers with rimmed vacuoles. The quadriceps deteriorated progressively without impairment of other muscles. Genotypic study showed a lamin A/C gene mutation.
CONCLUSIONS: This family was affected by a new phenotype composed of an autosomal dominant severe dilated cardiomyopathy with conduction defects or arrhythmias and quadriceps myopathy. Cardiac abnormalities preceded neuromuscular disorders and defined the prognosis of this disease.

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Year:  2005        PMID: 16314145     DOI: 10.1016/j.ejheart.2005.08.007

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


  6 in total

1.  Quadriceps myopathy caused by skeletal muscle-specific ablation of β(cyto)-actin.

Authors:  Kurt W Prins; Jarrod A Call; Dawn A Lowe; James M Ervasti
Journal:  J Cell Sci       Date:  2011-02-15       Impact factor: 5.285

2.  Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.

Authors:  Sahaana Chandran; Jennifer A Suggs; Bingyan J Wang; Andrew Han; Shruti Bhide; Diane E Cryderman; Steven A Moore; Sanford I Bernstein; Lori L Wallrath; Girish C Melkani
Journal:  Hum Mol Genet       Date:  2019-02-01       Impact factor: 6.150

3.  Dilated cardiomyopathy and skeletal myopathy: presenting features of a laminopathy.

Authors:  Hugh P Sims-Williams; Helen J Nye; Paul R Walker
Journal:  BMJ Case Rep       Date:  2013-01-17

4.  Malignant mutation in the lamin A/C gene causing progressive conduction system disease and early sudden death in a family with mild form of limb-girdle muscular dystrophy.

Authors:  Loizos Antoniades; Christos Eftychiou; Theodoros Kyriakides; Kyproula Christodoulou; Demosthenes G Katritsis
Journal:  J Interv Card Electrophysiol       Date:  2007-06-29       Impact factor: 1.900

5.  Altered chromosomal positioning, compaction, and gene expression with a lamin A/C gene mutation.

Authors:  Stephanie K Mewborn; Megan J Puckelwartz; Fida Abuisneineh; John P Fahrenbach; Yuan Zhang; Heather MacLeod; Lisa Dellefave; Peter Pytel; Sara Selig; Christine M Labno; Karen Reddy; Harinder Singh; Elizabeth McNally
Journal:  PLoS One       Date:  2010-12-14       Impact factor: 3.240

6.  Restrictive cardiomyopathy: an unusual phenotype of a lamin A variant.

Authors:  Mark S Paller; Cindy M Martin; Mary Ella Pierpont
Journal:  ESC Heart Fail       Date:  2018-05-09
  6 in total

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