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Session: Heart
Session starts: Thursday 26 January, 10:30
Presentation starts: 10:30
Room: Room 558

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Koen Janssens (Eindhoven University of Technology)
Maaike Kraamer ()
Peter Bovendeerd (Eindhoven University of Technology)

Abstract:
Introduction Long-term adverse ventricular remodelling following acute myocardial infarction (MI) can lead to ventricular dilation, diastolic dysfunction, loss of global contractile function and may result in heart failure (HF). Synthetic or tissue engineered patches, disposed over the epicardium, have been suggested as a possible treatment for HF, as they might reduce infarct area, reverse ventricular remodelling and enhance cardiac function. The mechanical properties of these patches and their interaction with the native cardiac tissue are important in device functionality. However, infarct material properties vary over time as the scar tissue matures which may have implications for the support that is to be delivered by the patch. In this study, we aim to quantify the evolution of an acutely infarcted ventricle into a chronically remodelled state in terms of global cardiac function and local myofiber mechanics. Method The finite element model of [1] was extended to model both acute and chronic MI. A droplet shaped region was selected in a thick-walled, truncated ellipsoidal geometry to model an infarct induced by occlusion of the Left Anterior Descending artery. Within this region, active stress generation was eliminated to model acute MI and passive material stiffness was increased to model chronic MI. Pressure-volume plots were used to assess global cardiac function and local stress and strain patterns were analysed to quantify local myofiber function in the infarct, the infarct border zone and the remote region. Results & Conclusions Simulations showed that the relative loss in pump function exceeded the relative loss in the amount healthy tissue by about two-fold, irrespective of infarct age. This disproportional loss was attributed to unfavourable mechanical interactions between healthy and infarcted tissue. With increasing infarct stiffness, myofiber functionality is partially restored in one region of the myocardium though it is depressed in another, resulting in a limited gain in overall cardiac function. These changes were related to the local orientation of myofibers with respect to the infarct region.