UNLOAD FAILING HEART

Impact of continuous flow mechanical unloading on the failing human heart

 Coordinatore NATIONAL AND KAPODISTRIAN UNIVERSITY OF ATHENS 

 Organization address address: CHRISTOU LADA 6
city: ATHENS
postcode: 10561

contact info
Titolo: Ms.
Nome: Efi
Cognome: Kafentzi
Email: send email
Telefono: 302104000000
Fax: 302104000000

 Nazionalità Coordinatore Greece [EL]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2010-RG
 Funding Scheme MC-IRG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-12-01   -   2015-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    NATIONAL AND KAPODISTRIAN UNIVERSITY OF ATHENS

 Organization address address: CHRISTOU LADA 6
city: ATHENS
postcode: 10561

contact info
Titolo: Ms.
Nome: Efi
Cognome: Kafentzi
Email: send email
Telefono: 302104000000
Fax: 302104000000

EL (ATHENS) coordinator 100˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

lvads    before    clinical    health    induced    unloading    data    function    remodeling    tissue    recovery    therapies    hf    baseline    myocardial    continuous    pulsatile    functional    lvad    failing    heart    human    investigations    outcome    investigation    flow   

 Obiettivo del progetto (Objective)

'Heart failure (HF) represents a major public health problem with high morbidity and mortality. Health care expenditure for HF exceeds those of all cancers and myocardial infarctions combined. We aim to investigate structural, cellular and molecular changes of the failing human heart before and after non-pulsatile,continuous flow,left ventricular assist devices (LVAD) - induced unloading and to correlate them with changes in myocardial function.Tissue analysis will focus on 3 key myocardial remodeling features (fibrosis, microvasculature/endothelium and cardiomyocyte hypertrophy) which appear to be mechanistically associated during the remodeling process that eventually leads to HF (“endothelial to mesenchymal transition”).

This translational investigation will a)formulate a standardized approach to acquire and evaluate myocardial tissue data along with clinical and functional data in HF patients before and after mechanical unloading and b)establish a baseline for the basic biologic effects of continuous flow LVAD unloading on the function and structure of the failing human heart.

We emphasize that two major outcomes are possible, and both are important. The first outcome is that we observe significant degree of improvement in myocardial function induced by non-pulsatile LVADs. In this case our study will provide the basis for identifying the hallmarks that are associated with unloading-induced recovery. The second possible outcome is that the unloading-induced myocardial recovery is minimal or rare. This would further encourage investigations that combine LVAD use with adjuvant therapies. Our results would provide the clinical, functional and pathologic baseline necessary for investigations of the impact of pharmacologic or cell-based or other advanced therapies added to LVADs. In either case we believe our investigation is likely to provide a comprehensive starting point for the new coming era of regenerative medicine and serve as springboard for future studies.'

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