Methodology The KaHMo is based on a general separation of the heart into active and passive parts. While the heart muscle is exerting forces onto the blood and thus forces the flow and can therefore be considered active, the valves and vessels are moved by the forces imposed by the blood flow and are treated as passive. This separation and the treatment of the myocardium in the ventricle walls as active is what makes a patient specific model possible, since then there is no need for a fluid structure interaction approach which would rely on information about the muscle fiber structure not obtainable in vivo. What we can acquire by standard non-invasive measurement and diagnosis is the geometry and the movement of the ventricle walls. In our work this information is gained by MR (magnetic resonance) imaging. From the MR dataset the inner surface of the ventricle (fluid volume) is reconstructed for several points of time during one heart cycle. From this surface a numerical grid is generated for every time step present in the measurement between which the ventricle's motion is interpolated. The real heart valves are passive elements that are moved by the pressure forces exerted by the flow. The movement of the valve is governed by complicated, non- linear and non-isotropic structural mechanics. To our knowledge there is no fluid structure interaction approach currently, which is able to handle this kind of problem. In order to be able to simulate the ventricle flow the valves are modeled by a simplified 2-D projected opening area. Valve opening times are based on the change of the ventricular volume over time. The resulting velocity profiles some diameters behind the valve are matched to the velocity profiles measured by MR flux or Echo Doppler. The non-Newtonian properties of the fluid are taken into account using a modified cross model by Perktold adapted to the properties of blood by as measured by Liepsch. Boundary conditions for the numerical model are firstly the movement of the wall as prescribed, and secondly relative pressure boundaries at the inflow and outflow tracts. While the venous pressure shows only small pulsation and is modeled as a constant relative pressure of 500 Pa, the aortic pressure is highly dependent on the flow itself and cannot be prescribed. The effect of the circulatory system is currently modeled in