Language:

Left ventricular non-compaction cardiomyopathy

The Lancet (British edition), 2015-08, Vol.386 (9995), p.813-825 [Peer Reviewed Journal]

Elsevier Ltd ;2015 Elsevier Ltd ;Copyright © 2015 Elsevier Ltd. All rights reserved. ;Copyright Elsevier Limited Aug 22, 2015 ;ISSN: 0140-6736 ;EISSN: 1474-547X ;DOI: 10.1016/S0140-6736(14)61282-4 ;PMID: 25865865

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
Left ventricular non-compaction cardiomyopathy
Author: Towbin, Jeffrey A, Dr ; Lorts, Angela, MD ; Jefferies, John Lynn, MD
Subjects: Abnormalities ; Adults ; Age ; Animals ; Anticoagulants - therapeutic use ; Arrhythmias, Cardiac - etiology ; Benign ; Biochemistry ; Blood circulation ; Calcineurin ; Cardiac arrhythmia ; Cardiac muscle ; Cardiology ; Cardiomyopathy ; Cardiomyopathy, Dilated - classification ; Cardiomyopathy, Dilated - diagnosis ; Cardiomyopathy, Dilated - therapy ; Cardiovascular diseases ; Catheters ; Children ; Chin ; Compaction ; Death ; Defects ; Defibrillators, Implantable ; Diagnosis ; Differentiation ; Disease Models, Animal ; Echocardiography ; Elastic scattering ; Electrocardiography ; Embryo cells ; Endothelium ; Female ; Fetuses ; Health risks ; Heart ; Heart diseases ; Heart failure ; Humans ; Incidence ; Infants ; Internal Medicine ; Isolated Noncompaction of the Ventricular Myocardium - classification ; Isolated Noncompaction of the Ventricular Myocardium - diagnosis ; Isolated Noncompaction of the Ventricular Myocardium - therapy ; Jaw ; Magnetic Resonance Angiography ; Magnetic resonance imaging ; Male ; Mice ; Morphogenesis ; Morphology ; Mutation - genetics ; Myocardium ; Notch protein ; Proteins ; Recesses ; Regulators ; Ribonucleic acid ; Risk ; RNA ; Septum ; Signal transduction ; Signal Transduction - genetics ; Solidification ; Stem cells ; Stroke ; Transplantation ; Treatment Outcome ; Ultrasound ; Valves ; Ventricle
Is Part Of: The Lancet (British edition), 2015-08, Vol.386 (9995), p.813-825
Description: Summary Left ventricular non-compaction, the most recently classified form of cardiomyopathy, is characterised by abnormal trabeculations in the left ventricle, most frequently at the apex. It can be associated with left ventricular dilation or hypertrophy, systolic or diastolic dysfunction, or both, or various forms of congenital heart disease. Affected individuals are at risk of left or right ventricular failure, or both. Heart failure symptoms can be induced by exercise or be persistent at rest, but many patients are asymptomatic. Patients on chronic treatment for compensated heart failure sometimes present acutely with decompensated heart failure. Other life-threatening risks of left ventricular non-compaction are ventricular arrhythmias or complete atrioventricular block, presenting clinically as syncope, and sudden death. Genetic inheritance arises in at least 30–50% of patients, and several genes that cause left ventricular non-compaction have been identified. These genes seem generally to encode sarcomeric (contractile apparatus) or cytoskeletal proteins, although, in the case of left ventricular non-compaction with congenital heart disease, disturbance of the NOTCH signalling pathway seems part of a final common pathway for this form of the disease. Disrupted mitochondrial function and metabolic abnormalities have a causal role too. Treatments focus on improvement of cardiac efficiency and reduction of mechanical stress in patients with systolic dysfunction. Further, treatment of arrhythmia and implantation of an automatic implantable cardioverter-defibrillator for prevention of sudden death are mainstays of therapy when deemed necessary and appropriate. Patients with left ventricular non-compaction and congenital heart disease often need surgical or catheter-based interventions. Despite progress in diagnosis and treatment in the past 10 years, understanding of the disorder and outcomes need to be improved.
Publisher: England: Elsevier Ltd
Language: English
Identifier: ISSN: 0140-6736
EISSN: 1474-547X
DOI: 10.1016/S0140-6736(14)61282-4
PMID: 25865865
Source: ProQuest One Psychology
MEDLINE
ProQuest Central

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

Left ventricular non-compaction cardiomyopathy

Elsevier Ltd ;2015 Elsevier Ltd ;Copyright © 2015 Elsevier Ltd. All rights reserved. ;Copyright Elsevier Limited Aug 22, 2015 ;ISSN: 0140-6736 ;EISSN: 1474-547X ;DOI: 10.1016/S0140-6736(14)61282-4 ;PMID: 25865865

Searching Remote Databases, Please Wait