S-SARCOMERE

Sarcomeric-Simulation AppRoach in a COmputational Multiscale EnviRonmEnt

 Coordinatore UNIVERSITY COLLEGE LONDON 

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Greta
Cognome: Borg - Carbott
Email: send email
Telefono: 442077000000
Fax: 442077000000

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 45˙000 €
 EC contributo 45˙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-2007-2-2-ERG
 Funding Scheme MC-ERG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-01-01   -   2011-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Greta
Cognome: Borg - Carbott
Email: send email
Telefono: 442077000000
Fax: 442077000000

UK (LONDON) coordinator 0.00

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 Word cloud

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

quantify    cardiovascular    risk    contraction    cardiac    local    model    forces    models    cavitation    closure    valve    events    cellular    first   

 Obiettivo del progetto (Objective)

'First, a simulation environment of the sarcomere will be developed by using lumped parameter models. This model will be incorporated into existing models of the cardiac contraction to eventually build a multi-scale model of the cardiovascular loop. At a later stage, this model will be coupled to local 3D models of cardiac devices. The study will focus on one specific application in cardiovascular engineering: valve closure force. Whilst forces of closure of prosthetic heart valves are an important characteristic with respect to the design, they are very difficult to quantify. Also, cavitation might be a problem, as could lead to catastrophic failure or blood damage. Closure lasts for only about 35 ms, and there are no adequate models that can predict or quantify the effect of local/cellular events of chemical, biochemical or mechano-electrical nature at the ventricular level on the closure forces. For potentially high-risk patients is possible that pharmacokinetical intervention may reduce the cavitation potential of the valve and risk of fracture. We propose to develop the first coherent multi-scale model of the system taking into account the cellular mechanisms of cardiac contraction, with feedback between electrochemical events in the vessel wall and detail haemodynamic characteristics of the flow'

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