Myocardial hypertrophy is not a prerequisite for changes in early gene expression in left ventricular volume overload

Currently it is not certain whether hypertrophy or the underlying disease is the primary trigger of the alterations in early gene expression in the progression of cardiac disease to end‐stage heart failure. In this study, we tested the notion that in left ventricular overload disorders, the changes...

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Bibliographic Details
Published in:Fundamental & clinical pharmacology 2004-02, Vol.18 (1), p.39-44
Main Authors: Dzimiri, Nduna, Al-Bahnasi, Kholod, Al-Halees, Zohair
Format: Article
Language:English
Subjects:
Adult
Aortic Valve Insufficiency - genetics
Aortic Valve Insufficiency - metabolism
Biological and medical sciences
c-fos
c-jun
c-myc
Cardiology. Vascular system
Cardiomegaly - genetics
Cardiomegaly - pathology
Cardiomyopathy, Dilated - genetics
Cardiomyopathy, Dilated - metabolism
dilated cardiomyopathy
DNA Primers
Female
Gene Expression - physiology
Genes, fos - genetics
Genes, fos - physiology
Genes, Immediate-Early - genetics
Genes, jun - genetics
Genes, jun - physiology
Genes, myc - genetics
Genes, myc - physiology
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Heart Ventricles - metabolism
human myocardium
Humans
left ventricular volume overload
Male
Medical sciences
Mitral Valve Insufficiency - genetics
Mitral Valve Insufficiency - metabolism
Myocardium - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - biosynthesis
Tropical medicine
Ventricular Dysfunction, Left - genetics
Ventricular Dysfunction, Left - pathology
Ventricular Function, Left - physiology
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Summary:Currently it is not certain whether hypertrophy or the underlying disease is the primary trigger of the alterations in early gene expression in the progression of cardiac disease to end‐stage heart failure. In this study, we tested the notion that in left ventricular overload disorders, the changes in early gene expression in the progression to heart failure is independent of the manifestation of cardiac hypertrophy. We compared the expression of the early genes c‐fos, c‐myc, and c‐jun in six dilated cardiomyopathic hearts (DCM) and 15 patients with left ventricular volume overload (VOL) resulting from mitral/aortic regurgitation and no significant stenosis or hypertrophic manifestations, using eight healthy donor hearts as controls. In VOL, c‐myc was elevated by 88% (P 
ISSN:0767-3981
1472-8206
DOI:10.1046/j.0767-3981.2003.00212.x