Document Detail

Morphological and quantitative changes of the initial myocardial lymphatics in terminal heart failure.
MedLine Citation:
PMID:  19254175     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Terminal heart failure is associated with chronic myocardial edema, which in part is compensated by increased myocardial lymph flow. However, little is known about the impact of terminal heart failure on lymphangiogenesis. The purpose of the study was to investigate the morphological and quantitative changes of the initial myocardial lymphatics in terminal heart failure.
METHODS: Paraffin-embedded left ventricular endomyocardial biopsies, taken during heart transplantation from 7 heart transplant recipients (failing heart) and 8 heart transplant donors (control), were investigated by immunohistostaining and triple immunofluorescence for lymphatic endothelial markers LYVE-1, PROX-1, and VEGFR-3. The vessel density was calculated and the ratio of open versus collapsed vessels was estimated by analyzing randomly selected marked vessels.
RESULTS: The absolute densities of lymph vessels in failing and control myocardium were not significantly different for all investigated markers. The ratio of open LYVE-1 positive lymph vessels in failing heart was significantly higher than in control (64+/-12.5 vs. 44.3+/-9.3, p<0.008). There was no difference for the ratio of open VEGFR-3 vessels between groups (69.0+/-17.5 vs. 70.7+/-17.2). Triple fluorescent immunohistostaining revealed in failing hearts LYVE-1 and PROX-1 positive open vessels, which were VEGFR-3 negative. VEGFR-3 positive, but LYVE-1 and PROX-1 negative vessels could also be seen.
CONCLUSIONS: Myocardial initial lymphatics in patients with terminal heart failure undergo significant morphological changes in comparison to normal hearts. The ratio of open LYVE-1 vessels was higher in failing hearts by no difference in absolute densities for all markers. These findings suggest that appositional growth of initial lymphatics, rather than "de novo" genesis from pluripotent stem cells or sprouting from preexisting venous vessels, may be the predominant mechanism of lymphangiogenesis in terminal heart failure.
Alexey Dashkevich; Wilhelm Bloch; Albert Antonyan; Jochen U W Fries; Hans Joachim Geissler
Related Documents :
19317655 - A new method for detection and quantification of heartbeat parameters in drosophila, ze...
19254175 - Morphological and quantitative changes of the initial myocardial lymphatics in terminal...
6838395 - Modeling and prospects for study of cardiovascular pathology with the artificial heart.
5723385 - Value and limitations of electrocardiogram in diagnosis of slight and subacute coronary...
18307445 - Proximal coronary hemodynamic changes evaluated by intracardiac echocardiography during...
16675245 - Morbidity and mortality following acute conversion from off-pump to on-pump coronary su...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Lymphatic research and biology     Volume:  7     ISSN:  1539-6851     ISO Abbreviation:  Lymphat Res Biol     Publication Date:  2009  
Date Detail:
Created Date:  2009-03-23     Completed Date:  2009-05-26     Revised Date:  2012-03-02    
Medline Journal Info:
Nlm Unique ID:  101163587     Medline TA:  Lymphat Res Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  21-7     Citation Subset:  IM    
Department of Cardiovascular Surgery, University Medical Center Freiburg, Freiburg, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Biological Markers / metabolism
Fluorescent Antibody Technique
Graft Rejection
Heart Failure / metabolism,  pathology*
Heart Transplantation
Homeodomain Proteins / metabolism
Immunoenzyme Techniques
Lymphatic System / metabolism,  pathology*
Middle Aged
Myocardium / metabolism,  pathology*
Tissue Donors
Tumor Suppressor Proteins / metabolism
Vascular Endothelial Growth Factor Receptor-3 / metabolism
Vesicular Transport Proteins / metabolism
Reg. No./Substance:
0/Biological Markers; 0/Homeodomain Proteins; 0/LYVE1 protein, human; 0/Tumor Suppressor Proteins; 0/Vesicular Transport Proteins; 0/prospero-related homeobox 1 protein; EC Endothelial Growth Factor Receptor-3

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

Previous Document:  Genetic delivery of bevacizumab to suppress vascular endothelial growth factor-induced high-permeabi...
Next Document:  Subpopulations of human embryonic stem cells with distinct tissue-specific fates can be selected fro...