CARDIODEF

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

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

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 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.