A Clinical Diagnosis of Laminopathy without Systolic Dysfunction: When Does Nuclei Malformation Start?
Author:
Affiliation:
1. Second Department of Internal Medicine, University of Toyama, Japan
Publisher
Japanese Society of Internal Medicine
Subject
General Medicine,Internal Medicine
Link
https://www.jstage.jst.go.jp/article/internalmedicine/63/3/63_1928-23/_pdf
Reference11 articles.
1. 1. Fatkin D, MacRae C, Sasaki T, et al. Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease. N Engl J Med 341: 1715-1724, 1999.
2. 2. Kumar S, Baldinger SH, Gandjbakhch E, et al. Long-term arrhythmic and nonarrhythmic outcomes of lamin A/C mutation carriers. J Am Coll Cardiol 68: 2229-2307, 2016.
3. 3. Otomo J, Kure S, Shiba T, et al. Electrophysiological and histopathological characteristics of progressive atrioventricular block accompanied by familial dilated cardiomyopathy caused by a novel mutation of lamin A/C gene. J Cardiovasc Electrophysiol 16: 137-145, 2005.
4. 4. Gupta P, Bilinska ZT, Sylvius N, et al. Genetic and ultrastructural studies in dilated cardiomyopathy patients: a large deletion in the lamin A/C gene is associated with cardiomyocyte nuclear envelope disruption. Basic Res Cardiol 105: 365-377, 2010.
5. 5. Saga A, Karibe A, Otomo J, et al. Lamin A/C gene mutations in familial cardiomyopathy with advanced atrioventricular block and arrhythmia. Tohoku J Exp Med 218: 309-316, 2009.
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