CARDIODEF

Multiscale investigation of drug - implantable cardioverter defibrillator interactions for antiarrhythmic therapy

 Coordinatore THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Ms.
Nome: Gill
Cognome: Wells
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 200˙371 €
 EC contributo 200˙371 €
 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-2011-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-12-01   -   2014-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Ms.
Nome: Gill
Cognome: Wells
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

UK (OXFORD) coordinator 200˙371.80

Mappa

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 Word cloud

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

ventricular    antiarrhythmic    patients    signal    icds    therapy    threshold    drug    energy    ecg    cardioverter    defibrillation    icd    implantable    arrhythmias    interfering    direct    ischemic    interactions    pacing    drugs   

 Obiettivo del progetto (Objective)

'The implantable-cardioverter defibrillator (ICD) is an effective treatment for terminating life threatening ventricular arrhythmias or fibrillations. However, as ICD only serves to terminate tachyarrhythmias and provide pacing support for bradyarrhythmias, concomitant antiarrhythmic drug therapy is common and leads to interactions with the ICD.

Direct drug-ICD interactions include alterations of the pacing threshold (minimum energy needed to achieve a reliable and consistent electrical activation of the heart) and of the defibrillation threshold (the lowest energy level that results in successful defibrillation).

Besides, anti-arrhythmic drugs which work by interfering with ion channel activity, may lead to cardio toxicity and then to ventricular arrhythmias, resulting in increased ICD therapies. Antiarrhythmic drugs can also lead to morphological changes present in the electrogram (EGM) interfering with the ICD function by failures of sensing ventricular events or arrhythmia classification.

The underlying mechanisms of ICD/drug interactions are poorly understood as well as how an ischemic substrate, present in most of the ICD patients, would affect those interactions. Indeed, ICDs are mainly used by patients with a history of previous myocardial infarction (MI) and left ventricle ejection fraction (LVEF) less than 35%. In this framework, this proposal aims at providing a new level of understanding of the interactions between ICD and investigating biomarkers from the electrocardiographic signal (ECG) to predict adverse drug-ICD interactions in ischemic and control patients. The approach will be a combination of modelling and simulation at human tissue level and ECG signal processing. This multidisciplinary project will include direct contact with clinicians to analyse ECG data from ICD patients and pharmacological companies to study the possible cardiotoxicity of class I and III drugs in control and ischemia conditions.'

Introduzione (Teaser)

Sudden cardiac death (SCD), typically caused by arrhythmias, can be averted with implantable cardioverter defibrillators (ICDs). An EU-funded project studied interactions of antiarrhythmic drugs with ICD therapy and ischaemia.

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