UNLOAD FAILING HEART

Impact of continuous flow mechanical unloading on the failing human heart

Coordinatore	NATIONAL AND KAPODISTRIAN UNIVERSITY OF ATHENS    more  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

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 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.'