Document Detail


Heart failure: an update on pathophysiology.
MedLine Citation:
PMID:  7864717     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial hypertrophy is an established risk factor for cardiovascular morbidity and mortality. Beyond quantitative and mechanical aspects hypertrophy is associated with alterations in cardiac gene expression, resulting in a more fetal-like myocyte phenotype with a fragile Ca++ homeostasis. Depressed expression of sarcoplasmatic reticulum ATPase is the hallmark of this overload phenotype. Conversely, the gene expression and the activity of sodium calcium exchanger is up-regulated in endstage heart failure. Both alterations contribute to prolonged cytosolic Ca++ transients, disturbed relaxation and, probably, to electrophysiologic instability. Angiotensin II is a growth promoting agent and several lines of circumferential evidence suggest that the local formation of angiotensin II might contribute to the trophic response and phenotype shift in cardiac overload. The cardiac gene expression of angiotensin converting enzyme and angiotensinogen is increased early after cardiac overload and in patients with severe heart failure. Chronic ACE inhibition suppresses plasma and tissue ACE activity, reduces LV hypertrophy and improves long-term survival. The hallmark of the peripheral adaptation in chronic heart failure is systemic vasoconstriction, associated with neurohumoral activation. Several mechanisms are involved in the impaired peripheral perfusion, including increased sympathetic tone and increased vascular stiffness. Recently, data suggest an important role of the endothelium for perfusion of skeletal muscle in heart failure. Endothelium-dependent dilation of resistance vessels is blunted in patients with severe chronic heart failure. Conceivably, this abnormality may be involved in the impaired reactive hyperemia in patients with chronic heart failure. Moreover, alterations of skeletal muscle emerge in chronic heart failure contributing to reduced exercise performance.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
H Drexler
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Archives des maladies du coeur et des vaisseaux     Volume:  87 Spec No 2     ISSN:  0003-9683     ISO Abbreviation:  Arch Mal Coeur Vaiss     Publication Date:  1994 Jun 
Date Detail:
Created Date:  1995-03-23     Completed Date:  1995-03-23     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0406011     Medline TA:  Arch Mal Coeur Vaiss     Country:  FRANCE    
Other Details:
Languages:  eng     Pagination:  13-6     Citation Subset:  IM    
Affiliation:
Medizinische Klinik III, University of Freiburg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Angiotensin-Converting Enzyme Inhibitors / therapeutic use
Cardiomegaly / drug therapy,  physiopathology*
Endothelium, Vascular / physiopathology
Gene Expression Regulation, Enzymologic
Heart Failure / drug therapy,  physiopathology*
Humans
Myosins / genetics
Peptidyl-Dipeptidase A / genetics
Vasoconstriction
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.6.4.1/Myosins

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


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