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Session: Poster session 2 (Odd numbers)
Session starts: Friday 27 January, 10:00
Presentation starts: 10:00

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Evianne Kruithof ()
Matthijs Cluitmans ()
Peter Bovendeerd ()

Abstract:
Myocardial infarction causes cardiac tissue remodeling, which increases the risk of ventricular tachycardia (VT). To optimize therapy selection, computational models are used to study the effect of electrical abnormalities on scar-based VT risk [1]. These models neglect the effect of mechano-electrical interaction, which is explored in this project. Infarct-tissue remodels in both mechanical and electrical terms causing abnormal mechanical deformations and electrical activation patterns over the myocardium. Mechanical remodeling, like formation of stiff fibrosis, alters the strain amplitudes in and around the infarct area. Our hypothesis is that these altered strain amplitudes affect the electrical cell-to-cell communication over time [2], which results in an altered conduction velocity (CV) of the electrical pulse over the heart. This might be of importance to the development of VT, as CV decrease is known to affect VT inducibility. Therefore, in this study, a relation between fiber strain amplitude and CV is proposed. The fiber strain amplitude distribution in the chronically infarcted heart is obtained from a computational model of cardiac mechanics. This distribution is, by means of the proposed relation, transferred into a distribution of CV which serves as input for an electrical model to simulate VT. By incorporating the mechano-electrical interaction, the effect of the infarct on CV was found to extend beyond the fibrotic area, as opposed to traditional models where the effect is limited to this area only. The region of CV slowing was located in and around the fibrotic area, and VT was found to be more easily initiated. Therefore, the implemented mechanism might be promising to assess VT risk. Moreover, if long-term changes in strain are known, this might be a way to predict long-term areas of CV slowing, and thus VT risk, as well. However, further research is needed to investigate if the proposed relation correctly describes strain-induced remodeling of CV.