title: Towards patient-specific modeling of coronary hemodynamics in healthy and diseased state.
abstract: A model describing the primary relations between the cardiac muscle and coronary circulation might be useful for interpreting coronary hemodynamics in case multiple types of coronary circulatory disease are present. The main contribution of the present study is the coupling of a microstructure-based heart contraction model with a 1D wave propagation model. The 1D representation of the vessels enables patient-specific modeling of the arteries and/or can serve as boundary conditions for detailed 3D models, while the heart model enables the simulation of cardiac disease, with physiology-based parameter changes. Here, the different components of the model are explained and the ability of the model to describe coronary hemodynamics in health and disease is evaluated. Two disease types are modeled: coronary epicardial stenoses and left ventricular hypertrophy with an aortic valve stenosis. In all simulations (healthy and diseased), the dynamics of pressure and flow qualitatively agreed with observations described in literature. We conclude that the model adequately can predict coronary hemodynamics in both normal and diseased state based on patient-specific clinical data.
authors.affiliation: Cardiovascular Biomechanics, Department of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands. a.v.d.horst@tue.nl
authors.forename: Arjen
authors.initials: A
authors.lastname: van der Horst
authors.forename: Frits L
authors.initials: FL
authors.lastname: Boogaard
authors.forename: Marcel
authors.initials: M
authors.lastname: van't Veer
authors.forename: Marcel C M
authors.initials: MC
authors.lastname: Rutten
authors.forename: Nico H J
authors.initials: NH
authors.lastname: Pijls
authors.forename: Frans N
authors.initials: FN
authors.lastname: van de Vosse
mesh_terms: D000465:Algorithms; D001024:Aortic Valve Stenosis / Q000473:pathology; D001783:Blood Flow Velocity; D019295:Computational Biology; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000473:pathology; D003331:Coronary Vessels / Q000502:physiology* / Q000503:physiopathology; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D011312:Pressure