Document Detail


Reversal of metallothionein expression is different throughout the human myocardium after prolonged left-ventricular mechanical support.
MedLine Citation:
PMID:  10930816     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We examined the distribution of metallothionein (MT), a stress-inducible protein, and the cardiomyocyte diameter in human hearts after left-ventricular assist device (LVAD) support. BACKGROUND: Remodeling in end-stage heart failure is characterized by myocyte hypertrophy and alterations of several inducible proteins. LVADs used as a bridge to cardiac transplantation unload the left ventricle and may lead to a reversal of the remodeling, but little is known about the pathophysiology of this process. METHODS: The immunoreactivity for MT and the cardiomyocyte diameter was analyzed in left-ventricular tissue specimens of 17 patients with end-stage heart failure before and after LVAD support. RESULTS: MT positive cells were mainly located sub-endocardially in vacuolized cardiomyocytes and in small vessels throughout the myocardium. During LVAD support, MT-positive myocytes decreased in the sub-endocardial (p < 0.008) and sub-epicardial region (p < 0.003), MT-positive vessels decreased similarly (p < 0.003). Cardiomyocyte diameter decreased significantly only in the sub-endocardium (p < 0.03). Hearts of patients supported longer than 88 days (= median) showed substantially lower MT reactivity at the time of LVAD explantation as compared to patients supported less than 88 days. CONCLUSION: Our results suggest that unloading of the left ventricle during prolonged LVAD support leads to regression of cellular hypertrophy and a decrease of MT expression. The preferential reduction of MT-positive vacuolized cardiomyocytes in the sub-endocardium is comparable with the concept of greatest reduction of wall stress in this area of the myocardium and may be due to the improvement of myocardial blood flow and the energy balance.
Authors:
H A Baba; F Grabellus; C August; G Plenz; A Takeda; T D Tjan; C Schmid; M C Deng
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation     Volume:  19     ISSN:  1053-2498     ISO Abbreviation:  J. Heart Lung Transplant.     Publication Date:  2000 Jul 
Date Detail:
Created Date:  2000-10-03     Completed Date:  2000-10-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9102703     Medline TA:  J Heart Lung Transplant     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  668-74     Citation Subset:  IM    
Affiliation:
Gerhard-Domagk-Institute of Pathology, University of Muenster, Münster, Germany. baba@uni-muenster.de
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MeSH Terms
Descriptor/Qualifier:
Adult
Antibodies, Monoclonal / diagnostic use,  immunology
Biological Markers
Cell Size
Foreign-Body Reaction / etiology,  metabolism,  pathology
Heart Failure / metabolism,  pathology,  therapy*
Heart-Assist Devices* / adverse effects
Humans
Metallothionein / immunology,  metabolism*
Middle Aged
Myocardium / metabolism*,  pathology
Severity of Illness Index
Ventricular Remodeling / physiology*
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Biological Markers; 9038-94-2/Metallothionein

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


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