Neuromuscular implications in left ventricular hypertrabeculation/noncompaction

被引：77

作者：

Finsterer, Josef ^{[1
]}

Stoellberger, Claudia ^{[1
]}

Blazek, Gerhard ^{[1
]}

机构：

[1] Hanusch Hosp, Dept Med, Vienna, Austria

来源：

INTERNATIONAL JOURNAL OF CARDIOLOGY | 2006年 / 110卷 / 03期

关键词：

metabolic myopathy; polyneuropathy; cardiac involvement; cardiomyopathy; muscular dystrophy; heart failure; rhythm abnormalities;

D O I：

10.1016/j.ijcard.2005.10.028

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

This review focuses on recent advances in the association between left ventricular hypertrabeculation/noncompaction (LVHT), a form of unclassified cardiomyopathy, and neuromuscular disorders (NMD). So far, LVHT has been found in single patients with dystrophinopathy, dystrobrevinopathy, laminopathy, zaspopathy, myotonic dystrophy, infantile glycogenosis type II (Pompe's disease), myoadenylate-deaminase deficiency, mitochondriopathy, Barth syndrome, Friedreich ataxia, and Charcot-Marie-Tooth disease. Most frequently LVHT is found in patients with Barth syndrome and mitochondrial disorders. The prevalence of LVHT in NMD patients is not known. On the contrary, NMD can be detected in up to four fifths of the patients with LVHT. Because LVHT is associated with an increased risk of rhythm abnormalities and heart failure, it is essential to detect LVHT as soon as possible. Because of adequate therapeutic options, all patients with NMD should undergo a comprehensive cardiological examination as soon as their neurological diagnosis is established. In reverse, all patients with LVHT should undergo a comprehensive neurological investigation following the detection of LVHT. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

引用

页码：288 / 300

页数：13

共 150 条

[1] Myoadenylate deaminase deficiency with progressive muscle weakness and atrophy caused by new missense mutations in AMPD1 gene: case report in a Japanese patient [J].