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Influence of ACE‐inhibition and mechanical unloading on the regulation of extracellular matrix proteins in the myocardium of heart transplantation candidates bridged by ventricular assist devices
Author(s) -
Milting Hendrik,
Kassner Astrid,
Arusoglu Latif,
Meyer Helmut E.,
Morshuis Michel,
Brendel Ramona,
Klauke Bärbel,
El Banayosy Aly,
Körfer Reiner
Publication year - 2006
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2005.09.008
Subject(s) - extracellular matrix , ventricle , heart failure , medicine , fibronectin , heart transplantation , transplantation , ventricular assist device , hydroxyproline , cardiology , microbiology and biotechnology , biology
Background: Whether adverse structural changes in the myocardium due to remodelling can be reversed by ventricular assist device (VAD) support in patients with end‐stage heart failure is controversial. Aims: To investigate the effect of VAD support on the extra‐cellular matrix. Methods: We analysed the collagen content in terminal failing ventricles of VAD‐patients and donor hearts using 4‐hydroxyproline for total collagen and real time RT‐PCR for fibronectin (FN), collagen I alpha 1 (Col1A1), III alpha 1 (Col3A1) and TGF beta 1 analysis. Results: Compared to donor hearts we found similar increases in Col1A1 and TGF beta1 but not Col3A1 and FN mRNAs, which were similar in the myocardium from patients receiving a VAD or heart transplant. However, patients receiving ACE‐I during VAD‐support had lower Col1A1 mRNA content at transplantation. The total collagen content was not influenced by mechanical unloading or by ACE‐I medication. Conclusion: Mechanical unloading by VAD does not reduce the collagen content of the terminal failing ventricle possibly due to increased TGF beta1 levels. However, Col1A1 production may be reduced by ACE‐I medication during VAD support.