Several multi-center clinical trials have provided consistent evidence that implantable defibrillation therapy prolongs patient life. This convincing demonstration of efficacy has led to a nearly exponential growth, over the last decade, in the number of patients receiving implantable devices. Currently, around 0.2 million implantable cardioverter defibrillators (ICDs) are implanted every year throughout the world.
Despite the importance and wide-spread use of this therapy, understanding of mechanisms by which electric shocks halt life-threatening arrhythmias remains incomplete. Further, ICD therapy is clearly suboptimal: to reliably restore sinus rhythm high shock strengths are required which are perceived as extremely painful by most patients, leading to traumatization with a significant impact on quality of life; the high current densities close to the electrode damage adjacent tissue; ICDs sometimes deliver inadequate shocks which may even trigger lethal arrhythmias instead of preventing them.
Recent experimental advances allow a better characterization of the shock-tissue interaction which have led to new mechanistic insights. Nonetheless, current experimental techniques cannot resolve, with sufficient accuracy, electrical events confined to the depth of the myocardial walls which limits observations to the surfaces of the heart. In-silico computer models are a powerful complementary approach to bridge this gap by providing a mechanistic link between elecrical activity observed at endocardial and epicardial surfaces.
The overall objective of this research is, by employing anatomically and functionally realistic in-silico computer simulations of the defibrillation process and the physics of experimental mapping techniques, to shed light on basic mechanisms underlying shock-tissue interactions and to test new hypotheses which may, eventually, pave the road to reliable defibrillation at a fraction of the energy requirements of current ICDs.
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