Document Detail

Molecular basis of regression of cardiac hypertrophy.
MedLine Citation:
PMID:  8166049     Owner:  NLM     Status:  MEDLINE    
Cardiac hypertrophy due to a chronic mechanical overload puts into play a biologic cascade, including a trigger (the mechanical stretch), a transmitter (very likely to be the phosphoinositol pathway), and the final target (which is the DNA). The permanent changes in genetic expression resulting from the activation of this cascade allows the heart to produce normal active tension at a lower cost in terms of energy expenditure. The process is reversible, providing the treatment reduces the real load on the heart--i.e., not only the peripheral resistances but also the aortic impedance--during a period of time that has to be several times the half-life of cardiac proteins, and also that the treatment has an effect on the detrimental consequences of cardiac hypertrophy, namely, the systolic and diastolic dysfunction and the incidence of arrhythmias. In this report semisenescent spontaneously hypertensive rats were treated for 3 months with the converting enzyme inhibitor trandolapril. The treatment had a rather modest effect on blood pressure but resulted in a pronounced reduction in cardiac hypertrophy and in cardiac fibrosis, an improved coronary reserve, and attenuated both the effects of anoxia on the left ventricular diastolic compliance and the incidence of ventricular arrhythmias.
B Chevalier; F Callens-el Amrani; C Heymes; B Swynghedauw
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The American journal of cardiology     Volume:  73     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  1994 Apr 
Date Detail:
Created Date:  1994-05-20     Completed Date:  1994-05-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  10C-17C     Citation Subset:  AIM; IM    
U127-INSERM, Hopital Lariboisière, Paris, France.
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MeSH Terms
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Anoxia / physiopathology
Arrhythmias, Cardiac / etiology,  physiopathology
Hypertrophy, Left Ventricular / drug therapy,  physiopathology*
Indoles / pharmacology
Rats, Inbred SHR
Rats, Inbred WKY
Ventricular Function, Left / drug effects
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Indoles; 87679-37-6/trandolapril

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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